﻿FN Clarivate Analytics Web of Science
VR 1.0
PT J
AU Yang, M
   Liu, JW
   Shao, JH
   Qin, YW
   Ji, QS
   Zhang, XL
   Du, J
AF Yang, Min
   Liu, Jingwei
   Shao, Jianghua
   Qin, Yanwen
   Ji, Qunsheng
   Zhang, Xiaolin
   Du, Jie
TI Cathepsin S-mediated autophagic flux in tumor-associated macrophages
   accelerate tumor development by promoting M2 polarization
SO MOLECULAR CANCER
LA English
DT Article
DE Tumor-associated macrophages; Tumor microenvironment; Cathepsin;
   Autophagy
ID BREAST-CANCER; ENDOPLASMIC-RETICULUM; CYSTEINE CATHEPSINS; DENDRITIC
   CELLS; GROWTH; METASTASIS; EXPRESSION; CARCINOMA; INVASION; STRESS
AB Background: Tumor-associated macrophages (TAMs) are the major component of tumor-infiltrating leukocytes. TAMs are heterogeneous, with distinct phenotypes influenced by the microenvironment surrounding tumor tissues, but relatively little is known about the key molecular in these cells that contribute to malignant phenotypes. Autophagic activity is a critical factor in tumor development that contributes to enhancing cellular fitness and survival in the hostile tumor microenvironment. However, the molecular basis and relations between autophagy and TAMs polarization remain unclear.
   Methods: Cathepsin S (Cat S) expression was analyzed in human colon carcinoma and normal colon tissues. In vivo effects were evaluated using PancO2 subcutaneous tumor model and SL4 hepatic metastasis model. Immunofluorescence staining, flow cytometry and real-time PCR were done to examine TAMs polarization. Western blotting assay, transmission electron microscopy, mCherry-GFP-LC3 transfection and DQ-BSA degradation assays were carried out to determine its role in regulating autophagy.
   Results: In the present study, we showed that the enhanced expression of Cat S correlated with the severity of histologic grade as well as clinical stage, metastasis, and recurrence, which are known indicators of a relatively poor prognosis of human colon carcinoma. Cat S knockout led to decreased tumor growth and metastasis. Moreover, Cat S knockout inhibited M2 macrophage polarization during tumor development. We further demonstrated that Cat S was required for not only autophagic flux but also the fusion processes of autophagosomes and lysosomes in TAMs. Importantly, we found that Cat S contributed to tumor development by regulating the M2 phenotype of TAMs through the activation of autophagy.
   Conclusions: These results indicated that Cat S-mediated autophagic flux is an important mechanism for inducing M2-type polarization of TAMs, which leads to tumor development. These data provide strong evidence for a tumor-promoting role of autophagy in TAMs and suggest Cat S could be a potential target for cancer therapy.
C1 [Yang, Min; Liu, Jingwei; Qin, Yanwen; Du, Jie] Capital Med Univ, Beijing Anzhen Hosp, Beijing, Peoples R China.
   [Yang, Min; Liu, Jingwei; Qin, Yanwen; Du, Jie] Capital Med Univ, Minist Educ, Beijing Inst Heart Lung & Blood Vessel Dis, Key Lab Remodeling Related Cardiovasc Dis, Beijing 100029, Peoples R China.
   [Shao, Jianghua] Nanchang Univ, Affiliated Hosp 2, Nanchang 330006, Jiangxi, Peoples R China.
   [Ji, Qunsheng; Zhang, Xiaolin] AstraZeneca, Innovat Ctr China, Shanghai 201203, Peoples R China.
RP Du, J (corresponding author), Capital Med Univ, Beijing Anzhen Hosp, Beijing, Peoples R China.
EM jdu@bcm.edu
RI Qin, Yanwen/AAM-6961-2020
OI Qin, Yanwen/0000-0002-5185-9726
FU Chinese Ministry of Science and TechnologyMinistry of Science and
   Technology, China [2009CB522205]; Chinese High Technology Research and
   Development ProgramNational High Technology Research and Development
   Program of China [2012AA02A201]; National Science Foundation of
   ChinaNational Natural Science Foundation of China (NSFC) [81170120];
   Beijing Nova ProgramBeijing Municipal Science & Technology Commission
   [Z121107002512041]
FX This study was supported by grants from Chinese Ministry of Science and
   Technology (2009CB522205), Chinese High Technology Research and
   Development Program (2012AA02A201), National Science Foundation of China
   (81170120) and Beijing Nova Program (Z121107002512041).
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NR 59
TC 70
Z9 74
U1 3
U2 18
PU BIOMED CENTRAL LTD
PI LONDON
PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND
SN 1476-4598
J9 MOL CANCER
JI Mol. Cancer
PD MAR 2
PY 2014
VL 13
AR 43
DI 10.1186/1476-4598-13-43
PG 15
WC Biochemistry & Molecular Biology; Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Oncology
GA AF2JL
UT WOS:000334538300001
PM 24580730
OA Green Published, gold
DA 2022-04-25
ER

PT J
AU Rosenfeldt, MT
   Ryan, KM
AF Rosenfeldt, Mathias T.
   Ryan, Kevin M.
TI The role of autophagy in tumour development and cancer therapy
SO EXPERT REVIEWS IN MOLECULAR MEDICINE
LA English
DT Review
ID PROGRAMMED CELL-DEATH; BCL-X-L; REGULATES AUTOPHAGY; BECLIN 1;
   COLON-CANCER; PHOSPHATIDYLINOSITOL 3-KINASE; MICROSATELLITE INSTABILITY;
   EMBRYONIC-DEVELOPMENT; CONJUGATION SYSTEMS; INTERACTING PROTEIN
AB Autophagy is a catabolic membrane-trafficking process that leads to sequestration and degradation of intracellular material within lysosomes. It is executed at basal levels in every cell and promotes cellular homeostasis by regulating organelle and protein turnover. In response to various forms of cellular stress, however, the levels and cargoes of autophagy can be modulated. In nutrient-deprived states, for example, autophagy can be activated to degrade cargoes for cell-autonomous energy production to promote cell survival. In other contexts, in contrast, autophagy has been shown to contribute to cell death. Given these dual effects in regulating cell viability, it is no surprise that autophagy has implications in both the genesis and treatment of malignant disease. In this review, we provide a comprehensive appraisal of the way in which oncogenes and tumour suppressor genes regulate autophagy. In addition, we address the current evidence from human cancer and animal models that has aided our understanding of the role of autophagy in tumour progression. Finally, the potential for targeting autophagy therapeutically is discussed in light of the functions of autophagy at different stages of tumour progression and in normal tissues.
C1 [Rosenfeldt, Mathias T.; Ryan, Kevin M.] Beatson Inst Canc Res, Tumour Cell Death Lab, Glasgow G61 1BD, Lanark, Scotland.
RP Ryan, KM (corresponding author), Beatson Inst Canc Res, Tumour Cell Death Lab, Garscube Estate,Switchback Rd, Glasgow G61 1BD, Lanark, Scotland.
EM k.ryan@beatson.gla.ac.uk
RI Rosenfeldt, Mathias/ABE-4736-2022
OI Rosenfeldt, Mathias/0000-0001-7650-8458; Ryan, Kevin
   M./0000-0002-1059-9681
FU Cancer Research UKCancer Research UK; Association for International
   Cancer Research
FX We are grateful to members of the Tumour Cell Death Laboratory for
   critical reading of the manuscript. We also thank the peer reviewers of
   our article, whose insightful comments improved the clarity and
   comprehensive nature of this review. Work in the Tumour Cell Death
   Laboratory is supported by Cancer Research UK and the Association for
   International Cancer Research.
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NR 116
TC 152
Z9 165
U1 0
U2 9
PU CAMBRIDGE UNIV PRESS
PI NEW YORK
PA 32 AVENUE OF THE AMERICAS, NEW YORK, NY 10013-2473 USA
SN 1462-3994
J9 EXPERT REV MOL MED
JI Expert Rev. Mol. Med.
PD DEC 2
PY 2009
VL 11
AR e36
DI 10.1017/S1462399409001306
PG 20
WC Biochemistry & Molecular Biology; Medicine, Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Research & Experimental Medicine
GA 577UV
UT WOS:000276250400001
PM 19951459
OA Green Published, hybrid
DA 2022-04-25
ER

PT J
AU Mukhopadhyay, S
   Sinha, N
   Das, DN
   Panda, PK
   Naik, PP
   Bhutia, SK
AF Mukhopadhyay, Subhadip
   Sinha, Niharika
   Das, Durgesh Nandini
   Panda, Prashanta Kumar
   Naik, Prajna Paramita
   Bhutia, Sujit Kumar
TI Clinical relevance of autophagic therapy in cancer: Investigating the
   current trends, challenges, and future prospects
SO CRITICAL REVIEWS IN CLINICAL LABORATORY SCIENCES
LA English
DT Review
DE Autophagy; apoptosis; cancer patients; drugs; therapy; oncophagy;
   clinical trials; translational medicine
ID RENAL-CELL-CARCINOMA; ACUTE LYMPHOBLASTIC-LEUKEMIA;
   ENDOPLASMIC-RETICULUM STRESS; DUAL PI3K/MTOR INHIBITOR;
   MEDULLARY-THYROID CANCER; VIVO ANTITUMOR-ACTIVITY; HUMAN OVARIAN-CANCER;
   BREAST-TUMOR CELLS; COLON-CANCER; LUNG-CANCER
AB Oncophagy (cancer-related autophagy) has a complex dual character at different stages of tumor progression. It remains an important clinical problem to unravel the reasons that propel the shift in the role of oncophagy from tumor inhibition to a protective mechanism that shields full-blown malignancy. Most treatment strategies emphasize curbing protective oncophagy while triggering the oncophagy that is lethal to tumor cells. In this review, we focus on the trends in current therapeutics as well as various challenges in clinical trials to address the oncophagic dilemma and evaluate the potential of these developing therapies. A detailed analysis of the clinical and pre-clinical scenario of the anticancer medicines highlights the various inducers and inhibitors of autophagy. The ways in which tumor stage, the microenvironment and combination drug treatment continue to play an important tactical role are discussed. Moreover, autophagy targets also play a crucial role in developing the best possible solution to this oncophagy paradox. In this review, we provide a comprehensive update on the current clinical impact of autophagy-based cancer therapeutic drugs and try to lessen the gap between translational medicine and clinical science.
C1 [Mukhopadhyay, Subhadip; Sinha, Niharika; Das, Durgesh Nandini; Panda, Prashanta Kumar; Naik, Prajna Paramita; Bhutia, Sujit Kumar] Natl Inst Technol Rourkela, Dept Life Sci, Rourkela 769008, Odisha, India.
RP Bhutia, SK (corresponding author), Natl Inst Technol Rourkela, Dept Life Sci, Rourkela 769008, Odisha, India.
EM sbhutia@nitrkl.ac.in
RI Sinha, Niharika/AFF-4328-2022; Naik, Prajna Paramita/AAV-8237-2020;
   MUKHOPADHYAY, SUBHADIP/AAM-2459-2020
OI Sinha, Niharika/0000-0002-5466-4895; Naik, Prajna
   Paramita/0000-0002-6086-3022; 
FU Department of Biotechnology [BT/PR1/5090/GBD/27/309/2011]; Science and
   Engineering Research Board (SERB), the Department of Science and
   Technology [SR/SO/BB-0101/2012]; Council of Scientific and Industrial
   Research (CSIR) Human Resource Development Group, Government of India
   [37(1608)/13/EMR-II]
FX Research support was partly provided by the Rapid Grant for Young
   Investigators (RGYI) Award [Grant Number: BT/PR1/5090/GBD/27/309/2011],
   the Department of Biotechnology [Grant Number:
   BT/PR7791/BRB/10/1187/2013]; the Science and Engineering Research Board
   (SERB), the Department of Science and Technology [Grant Number:
   SR/SO/BB-0101/2012]; the Council of Scientific and Industrial Research
   (CSIR) [Grant Number: 37(1608)/13/EMR-II] Human Resource Development
   Group, Government of India. The funders had no role in study design,
   data collection, and analysis, decision to publish, or preparation of
   the manuscript. We apologize to researchers whose studies on autophagy
   we were unable to cite due to the length of this review.
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NR 230
TC 8
Z9 8
U1 0
U2 23
PU TAYLOR & FRANCIS LTD
PI ABINGDON
PA 2-4 PARK SQUARE, MILTON PARK, ABINGDON OR14 4RN, OXON, ENGLAND
SN 1040-8363
EI 1549-781X
J9 CRIT REV CL LAB SCI
JI Crit. Rev. Clin. Lab. Sci.
PD AUG
PY 2016
VL 53
IS 4
BP 228
EP 252
DI 10.3109/10408363.2015.1135103
PG 25
WC Medical Laboratory Technology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Medical Laboratory Technology
GA DN4IP
UT WOS:000377029000002
PM 26743568
OA Green Submitted
DA 2022-04-25
ER

PT J
AU Song, HT
   Qin, Y
   Yao, GD
   Tian, ZN
   Fu, SB
   Geng, JS
AF Song, Hong-tao
   Qin, Yu
   Yao, Guo-dong
   Tian, Zhen-nan
   Fu, Song-bin
   Geng, Jing-shu
TI Astrocyte Elevated Gene-1 Mediates Glycolysis and Tumorigenesis in
   Colorectal Carcinoma Cells via AMPK Signaling
SO MEDIATORS OF INFLAMMATION
LA English
DT Article
ID CANCER; AEG-1; PROGRESSION; AUTOPHAGY; INHIBITION; PATHOGENESIS;
   METASTASIS; EXPRESSION; SURVIVAL; THERAPY
AB To investigate the role of AEG-1 in glycolysis and tumorigenesis, we construct myc-AEG-1 expression vector and demonstrate a novel mechanism that AEG-1 may increase the activity of AMPK by Thr172 phosphorylation. The higher expression levels of AEG-1 in colorectal carcinoma cells were found but showed significant difference in different cell lines. To study the role of AEG-1 in colorectal cells, myc-AEG-1 vector was constructed and transfected into NCM460 colonic epithelial cells. We observed consistent increasing of glucose consumption and lactate production, typical features of anaerobic glycolysis, suggesting that AEG-1 may promote anaerobic glycolysis. Moreover, we noted that AMPK phosphorylation at Thr172 as well as pPFK2 (Ser466) was increased in NCM460 cells overexpressing AEG-1. Compound C may block AMPK and PFK2 phosphorylation in both control and AEG1-overexpressed cells and decrease the glucose consumption and lactate production. The present findings indicated that reduced AEG-1 protein levels by RNAi may decrease the glucose consumption and lactate production in HCT116 colorectal carcinoma cells. The present identified AEG-1/AMPK/PFK2 glycolysis cascade may be essential to cell proliferation and tumor growth. The present results may provide us with a mechanistic insight into novel targets controlled by AEG-1, and the components in the AEG1/AMPK/PFK2 glycolysis process may be targeted for the clinical treatment of cancer.
C1 [Song, Hong-tao; Qin, Yu; Yao, Guo-dong; Tian, Zhen-nan; Geng, Jing-shu] Harbin Med Univ, Affiliated Tumor Hosp, Dept Pathol, Harbin 150040, Peoples R China.
   [Fu, Song-bin; Geng, Jing-shu] Harbin Med Univ, Dept Med Genet, Harbin 150086, Peoples R China.
RP Geng, JS (corresponding author), Harbin Med Univ, Affiliated Tumor Hosp, Dept Pathol, Harbin 150040, Peoples R China.
EM jingshu0128@163.com
FU Wu Lien-Teh Science Foundation for Youths of Harbin Medical University
   [WLD-QN1117]; Foundation of Heilongjiang Educational Committee
   [12511175]; Foundation of Heilongjiang Provincial Department of Public
   Health [2011-146]; Scientific Research Staring Foundation; Affiliated
   Tumor Hospital of Harbin Medical University [JJ 2010-13]
FX This research was also supported by the Wu Lien-Teh Science Foundation
   for Youths of Harbin Medical University (Grant no. WLD-QN1117), the
   Foundation of Heilongjiang Educational Committee (Grant no. 12511175),
   the Foundation of Heilongjiang Provincial Department of Public Health
   (Grant no. 2011-146), and the Scientific Research Staring Foundation,
   the Affiliated Tumor Hospital of Harbin Medical University (Grant no. JJ
   2010-13).
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NR 38
TC 21
Z9 22
U1 1
U2 10
PU HINDAWI LTD
PI LONDON
PA ADAM HOUSE, 3RD FLR, 1 FITZROY SQ, LONDON, W1T 5HF, ENGLAND
SN 0962-9351
EI 1466-1861
J9 MEDIAT INFLAMM
JI Mediat. Inflamm.
PY 2014
VL 2014
AR 287381
DI 10.1155/2014/287381
PG 9
WC Cell Biology; Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Cell Biology; Immunology
GA AG0WP
UT WOS:000335136700001
PM 24829520
OA Green Published, gold, Green Submitted
DA 2022-04-25
ER

PT J
AU Tesarova, P
   Cabinakova, M
   Mikulova, V
   Zima, T
   Kalousova, M
AF Tesarova, P.
   Cabinakova, M.
   Mikulova, V.
   Zima, T.
   Kalousova, M.
TI RAGE and its ligands in cancer - culprits, biomarkers, or therapeutic
   targets?
SO NEOPLASMA
LA English
DT Review
DE RAGE; cancer; HMGB1; S100 proteins
ID GLYCATION END-PRODUCTS; ALTERNATIVELY SPLICED RAGEV1; SOLUBLE FORM
   SRAGE; ENDPRODUCTS RAGE; MELANOMA GROWTH; RECEPTOR; EXPRESSION; RISK;
   POLYMORPHISM; AGES
AB Receptor for advanced glycation end products (RAGE) plays a central role in the regulation of tissue homeostasis, regeneration and resolution of inflammation, but under pathological conditions RAGE-mediated pathways may induce diminished apoptosis, but enhanced autophagy and cell necrosis. These mechanisms may contribute to malignant transformation, cancer progression and metastases. Soluble RAGE may bind natural RAGE ligands and counteract some of the RAGE-mediated effects. Activation of RAGE was demonstrated in different types of cancer (including colon, pancreatic and breast cancer). Expression of RAGE and serum levels of soluble RAGE may serve as cancer biomarkers and strategies aimed at interfering with RAGE signaling might be promising anticancer drugs.
C1 [Tesarova, P.; Cabinakova, M.] Charles Univ Prague, Dept Oncol, Fac Med 1, Prague, Czech Republic.
   [Tesarova, P.; Cabinakova, M.; Mikulova, V.; Zima, T.; Kalousova, M.] Gen Univ Hosp, Prague, Czech Republic.
   [Mikulova, V.; Zima, T.; Kalousova, M.] Charles Univ Prague, Inst Med Biochem & Lab Diagnost, Fac Med 1, Prague, Czech Republic.
RP Tesarova, P (corresponding author), Charles Univ Prague, Dept Oncol, Fac Med 1, Prague, Czech Republic.
EM tesarova.petra@seznam.cz
RI cabinakova, Michaela/C-1083-2017; Tesarová, P/AAC-3053-2019; Tesarova,
   Petra/A-8718-2017; Zima, Tomas/F-6760-2017; Kalousova, Marta/D-1530-2017
OI cabinakova, Michaela/0000-0003-2766-2090; Tesarova,
   Petra/0000-0003-3607-3474; Zima, Tomas/0000-0001-8518-6972; Kalousova,
   Marta/0000-0001-5928-3074; Mikulova, Veronika/0000-0002-9962-5312
FU  [MH CZ - RVO VFN 64641 VFN 64164];  [PRVOUK - P25/LF1/2]
FX Studies of the authors on RAGE were supported by research projects MH CZ
   - RVO VFN 64641 VFN 64164 and PRVOUK - P25/LF1/2.
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NR 78
TC 18
Z9 18
U1 0
U2 13
PU AEPRESS SRO
PI BRATISLAVA
PA BAJZOVA 7, BRATISLAVA, 821 08, SLOVAKIA
SN 0028-2685
EI 1338-4317
J9 NEOPLASMA
JI Neoplasma
PY 2015
VL 62
IS 3
BP 353
EP 364
DI 10.4149/neo_2015_061
PG 12
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA CM5CV
UT WOS:000357705300002
PM 25967358
OA Bronze
DA 2022-04-25
ER

PT J
AU Pigna, E
   Berardi, E
   Aulino, P
   Rizzuto, E
   Zampieri, S
   Carraro, U
   Kern, H
   Merigliano, S
   Gruppo, M
   Mericskay, M
   Li, ZL
   Rocchi, M
   Barone, R
   Macaluso, F
   Di Felice, V
   Adamo, S
   Coletti, D
   Moresi, V
AF Pigna, Eva
   Berardi, Emanuele
   Aulino, Paola
   Rizzuto, Emanuele
   Zampieri, Sandra
   Carraro, Ugo
   Kern, Helmut
   Merigliano, Stefano
   Gruppo, Mario
   Mericskay, Mathias
   Li, Zhenlin
   Rocchi, Marco
   Barone, Rosario
   Macaluso, Filippo
   Di Felice, Valentina
   Adamo, Sergio
   Coletti, Dario
   Moresi, Viviana
TI Aerobic Exercise and Pharmacological Treatments Counteract Cachexia by
   Modulating Autophagy in Colon Cancer
SO SCIENTIFIC REPORTS
LA English
DT Article
ID QUALITY-OF-LIFE; SKELETAL-MUSCLE; PHYSICAL-ACTIVITY; ENVIRONMENTAL
   ENRICHMENT; MUSCULAR-DYSTROPHY; AMPK; ACTIVATION; DISEASE; HEALTH;
   PHOSPHORYLATION
AB Recent studies have correlated physical activity with a better prognosis in cachectic patients, although the underlying mechanisms are not yet understood. In order to identify the pathways involved in the physical activity-mediated rescue of skeletal muscle mass and function, we investigated the effects of voluntary exercise on cachexia in colon carcinoma (C26)-bearing mice. Voluntary exercise prevented loss of muscle mass and function, ultimately increasing survival of C26-bearing mice. We found that the autophagic flux is overloaded in skeletal muscle of both colon carcinoma murine models and patients, but not in running C26-bearing mice, thus suggesting that exercise may release the autophagic flux and ultimately rescue muscle homeostasis. Treatment of C26-bearing mice with either AICAR or rapamycin, two drugs that trigger the autophagic flux, also rescued muscle mass and prevented atrogene induction. Similar effects were reproduced on myotubes in vitro, which displayed atrophy following exposure to C26-conditioned medium, a phenomenon that was rescued by AICAR or rapamycin treatment and relies on autophagosome-lysosome fusion (inhibited by chloroquine). Since AICAR, rapamycin and exercise equally affect the autophagic system and counteract cachexia, we believe autophagy-triggering drugs may be exploited to treat cachexia in conditions in which exercise cannot be prescribed.
C1 [Pigna, Eva; Berardi, Emanuele; Aulino, Paola; Adamo, Sergio; Coletti, Dario; Moresi, Viviana] Univ Roma La Sapienza, Interuniv Inst Myol, DAHFMO Unit Histol & Med Embryol, Rome, Italy.
   [Berardi, Emanuele] Katholieke Univ Leuven, Res Grp Exercise Physiol, Dept Kinesiol, Leuven, Belgium.
   [Rizzuto, Emanuele] Univ Roma La Sapienza, Dept Mech & Aerosp Engn, Rome, Italy.
   [Zampieri, Sandra] Univ Padua, Dept Biomed Sci, I-35100 Padua, Italy.
   [Zampieri, Sandra; Kern, Helmut] Wilhelminenspital Wien, Dept Phys Med & Rehabil, Ludwig Boltzmann Inst Elect Stimulat & Phys Rehab, Vienna, Austria.
   [Carraro, Ugo] IRCCS Fdn Osped San Camillo, Venice, Italy.
   [Merigliano, Stefano; Gruppo, Mario] Univ Padua, Dept Surg & Gastroenterol Sci, I-35100 Padua, Italy.
   [Mericskay, Mathias; Li, Zhenlin; Coletti, Dario] Univ Paris 06, INSERM, Dept Biol Adaptat & Ageing B2A, CNRS,UMR 8256,ERL,U1164, F-75252 Paris 05, France.
   [Rocchi, Marco] Carlo Bo Univ Urbino, Unit Biostat, Dept Biomol Sci, Urbino, Italy.
   [Barone, Rosario; Macaluso, Filippo; Di Felice, Valentina] Univ Palermo, Dept Expt Biomed & Clin Neurosci BioNeC, I-90133 Palermo, Italy.
RP Adamo, S (corresponding author), Univ Roma La Sapienza, Interuniv Inst Myol, DAHFMO Unit Histol & Med Embryol, Rome, Italy.
EM sergio.adamo@uniroma1.it
RI Gruppo, Mario/ABD-1695-2020; Gruppo, Mario/G-7282-2014; Rocchi, Marco
   BL/AAK-5926-2021; barone, rosario/ABA-6758-2021; Merigliano,
   Stefano/AAY-3023-2021; Barone, Rosario/ABD-8488-2020; Berardi,
   Emanuele/AAC-9753-2019; zampieri, sandra/AAJ-5400-2021; Adamo,
   Sergio/E-9058-2012; Di Felice, Valentina/A-4457-2009; Coletti,
   Dario/U-2219-2018; Di Felice, Valentina/AAG-3740-2021; Rizzuto,
   Emanuele/K-9437-2016; MERICSKAY, Mathias/M-3477-2018
OI Gruppo, Mario/0000-0001-5525-5762; Gruppo, Mario/0000-0001-5525-5762;
   Berardi, Emanuele/0000-0002-0775-9605; zampieri,
   sandra/0000-0001-6970-0011; Adamo, Sergio/0000-0002-1409-0452; Di
   Felice, Valentina/0000-0002-4132-1260; Di Felice,
   Valentina/0000-0002-4132-1260; Moresi, viviana/0000-0003-1912-0339;
   Coletti, Dario/0000-0001-7373-1953; Rizzuto,
   Emanuele/0000-0003-2314-6128; Rocchi, marco/0000-0002-0056-5795; barone,
   rosario/0000-0002-8240-1240; Kern, Helmut/0000-0001-9661-8814; Carraro,
   Ugo/0000-0002-0924-4998; MERICSKAY, Mathias/0000-0002-6779-092X; LI,
   Zhenlin/0000-0002-3706-4505
FU ANRFrench National Research Agency (ANR) [13-BSV1-0005]; NIHUnited
   States Department of Health & Human ServicesNational Institutes of
   Health (NIH) - USA [5R01CA180057-02]; AFMAssociation Francaise contre
   les Myopathies [2012-0773]; UPMC Emergence; IBPS; PRINMinistry of
   Education, Universities and Research (MIUR)Research Projects of National
   Relevance (PRIN) [2012N8YJC3, 2009WBFZYM 001]; European Regional
   Development Fund-Cross Border Cooperation Programme SLOVAKIA-AUSTRIA
   (Interreg-Iva) project "Mobilitat im Alter" MOBIL [00033]; Austrian
   Federal Ministry of Science and Research; Ludwig Boltzmann Society
   (Vienna); NATIONAL CANCER INSTITUTEUnited States Department of Health &
   Human ServicesNational Institutes of Health (NIH) - USANIH National
   Cancer Institute (NCI) [R01CA180057] Funding Source: NIH RePORTER
FX D. Coletti is supported by ANR (# 13-BSV1-0005), NIH (#
   5R01CA180057-02), AFM (# 2012-0773), UPMC Emergence 2011 and IBPS 2015.
   Z. Li is supported by ANR and AFM. We also acknowledge PRIN 2009
   (Project 2009WBFZYM 001) and PRIN 2011 Project # 2012N8YJC3) grants to
   S. Adamo. S. Zampieri, U. Carraro and H. Kern are supported by the
   European Regional Development Fund-Cross Border Cooperation Programme
   SLOVAKIA-AUSTRIA (Interreg-Iva) project "Mobilitat im Alter" MOBIL
   N_00033; Austrian Federal Ministry of Science and Research; Ludwig
   Boltzmann Society (Vienna). The authors are indebted to Carla Ramina for
   her precious technical assistance. They gratefully thank Richard Lowry,
   Ph.D., Professor Emeritus of Psychology at the Vassar College, for his
   web-based, user-friendly tool for performing statistical computation,
   VassarStats, which they used for the statistical analysis, and Daniela
   Annibali for her critical comments.
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NR 59
TC 93
Z9 93
U1 2
U2 23
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 2045-2322
J9 SCI REP-UK
JI Sci Rep
PD MAY 31
PY 2016
VL 6
AR 26991
DI 10.1038/srep26991
PG 14
WC Multidisciplinary Sciences
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Science & Technology - Other Topics
GA DN2GU
UT WOS:000376882900001
PM 27244599
OA Green Submitted, Green Published, gold
DA 2022-04-25
ER

PT J
AU Sui, X
   Chen, R
   Wang, Z
   Huang, Z
   Kong, N
   Zhang, M
   Han, W
   Lou, F
   Yang, J
   Zhang, Q
   Wang, X
   He, C
   Pan, H
AF Sui, X.
   Chen, R.
   Wang, Z.
   Huang, Z.
   Kong, N.
   Zhang, M.
   Han, W.
   Lou, F.
   Yang, J.
   Zhang, Q.
   Wang, X.
   He, C.
   Pan, H.
TI Autophagy and chemotherapy resistance: a promising therapeutic target
   for cancer treatment
SO CELL DEATH & DISEASE
LA English
DT Review
DE autophagy; chemotherapy resistance; cancer; therapy
ID ACTIVATED PROTEIN-KINASE; CELL-DEATH; INDUCED APOPTOSIS;
   HEPATOCELLULAR-CARCINOMA; COLON-CANCER; ER STRESS; INHIBITOR NVP-BEZ235;
   DRUG-RESISTANCE; 3-KINASE/MAMMALIAN TARGET; OVERCOMES RESISTANCE
AB Induction of cell death and inhibition of cell survival are the main principles of cancer therapy. Resistance to chemotherapeutic agents is a major problem in oncology, which limits the effectiveness of anticancer drugs. A variety of factors contribute to drug resistance, including host factors, specific genetic or epigenetic alterations in the cancer cells and so on. Although various mechanisms by which cancer cells become resistant to anticancer drugs in the microenvironment have been well elucidated, how to circumvent this resistance to improve anticancer efficacy remains to be defined. Autophagy, an important homeostatic cellular recycling mechanism, is now emerging as a crucial player in response to metabolic and therapeutic stresses, which attempts to maintain/restore metabolic homeostasis through the catabolic lysis of excessive or unnecessary proteins and injured or aged organelles. Recently, several studies have shown that autophagy constitutes a potential target for cancer therapy and the induction of autophagy in response to therapeutics can be viewed as having a prodeath or a prosurvival role, which contributes to the anticancer efficacy of these drugs as well as drug resistance. Thus, understanding the novel function of autophagy may allow us to develop a promising therapeutic strategy to enhance the effects of chemotherapy and improve clinical outcomes in the treatment of cancer patients.
C1 [Sui, X.; Wang, Z.; Kong, N.; Han, W.; Lou, F.; Yang, J.; Wang, X.; Pan, H.] Zhejiang Univ, Dept Med Oncol, Sir Run Run Shaw Hosp, Hangzhou 310016, Zhejiang, Peoples R China.
   [Chen, R.; Huang, Z.; Zhang, M.; He, C.] Zhejiang Univ, Dept Colorectal Surg, Sir Run Run Shaw Hosp, Hangzhou 310016, Zhejiang, Peoples R China.
   [Zhang, Q.] Zhejiang Prov Peoples Hosp, Dept Gastrointestinal Surg, Hangzhou, Zhejiang, Peoples R China.
   [Wang, X.; He, C.; Pan, H.] Biomed Res Ctr, Hangzhou, Zhejiang, Peoples R China.
   [Wang, X.; He, C.; Pan, H.] Key Lab Biotherapy Zhejiang Prov, Hangzhou, Zhejiang, Peoples R China.
RP Wang, X (corresponding author), Zhejiang Univ, Dept Med Oncol, Sir Run Run Shaw Hosp, Hangzhou 310016, Zhejiang, Peoples R China.
EM wangxzju@163.com; drhechao@yahoo.com.cn; drpanhm@aliyun.com
OI Wang, Xian/0000-0003-0041-7589
FU National Natural Science Foundation of ChinaNational Natural Science
   Foundation of China (NSFC) [81301891, 81272593, 81071651, 81071963];
   Zhejiang Provincial Natural Science Foundation of ChinaNatural Science
   Foundation of Zhejiang Province [LQ13H160008]
FX This study is supported by grants from the National Natural Science
   Foundation of China (grants 81301891, 81272593, 81071651 and 81071963)
   and the Zhejiang Provincial Natural Science Foundation of China (grant
   LQ13H160008).
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NR 121
TC 773
Z9 796
U1 14
U2 167
PU SPRINGERNATURE
PI LONDON
PA CAMPUS, 4 CRINAN ST, LONDON, N1 9XW, ENGLAND
SN 2041-4889
J9 CELL DEATH DIS
JI Cell Death Dis.
PD OCT
PY 2013
VL 4
AR e838
DI 10.1038/cddis.2013.350
PG 12
WC Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Cell Biology
GA 251XK
UT WOS:000326967100024
PM 24113172
OA gold, Green Published
HC Y
HP N
DA 2022-04-25
ER

PT J
AU Jiang, LQ
   Wang, YJ
   Yin, QF
   Liu, GX
   Liu, HH
   Huang, YJ
   Li, B
AF Jiang, Liangqian
   Wang, Yujuan
   Yin, Qifeng
   Liu, Guoxiang
   Liu, Huihui
   Huang, Yajing
   Li, Bing
TI Phycocyanin: A Potential Drug for Cancer Treatment
SO JOURNAL OF CANCER
LA English
DT Review
DE Phycocyanin; Apoptosis; Autophagy; Cancer; Cell cycle arrest
ID NF-KAPPA-B; CYANOBACTERIUM SYNECHOCOCCUS-VULCANUS; SELECTIVE
   CYCLOOXYGENASE-2 INHIBITOR; SELENIUM-CONTAINING PHYCOCYANIN; PROTEIN
   C-PHYCOCYANIN; TRANS-RETINOIC ACID; SPIRULINA-PLATENSIS;
   CRYSTAL-STRUCTURE; IN-VITRO; COLON CARCINOGENESIS
AB Phycocyanin isolated from marine organisms has the characteristics of high efficiency and low toxicity, and it can be used as a functional food. It has been reported that phycocyanin has anti-oxidative function, anti-inflammatory activity, anti-cancer function, immune enhancement function, liver and kidney protection pharmacological effects. Thus, phycocyanin has an important development and utilization as a potential drug, and phycocyanin has become a new hot spot in the field of drug research. So far, there are more and more studies have shown that phycocyanin has the anti-cancer effect, which can block the proliferation of cancer cells and kill cancer cells. Phycocyanin exerts anti-cancer activity by blocking tumor cell cell cycle, inducing tumor cell apoptosis and autophagy, thereby phycocyanin can serve as a promising anti-cancer agent. This review discusses the therapeutic use of phycocyanin and focuses on the latest advances of phycocyanin as a promising anti-cancer drug.
C1 [Jiang, Liangqian; Wang, Yujuan; Yin, Qifeng; Liu, Guoxiang; Liu, Huihui; Li, Bing] Qingdao Univ, Basic Med Coll, Dept Genet & Cell Biol, 308 Ningxia Rd, Qingdao 266071, Peoples R China.
   [Huang, Yajing] Qingdao Univ, Basic Med Coll, 308 Ningxia Rd, Qingdao 266071, Peoples R China.
RP Li, B (corresponding author), Qingdao Univ, Basic Med Coll, Dept Genet & Cell Biol, 308 Ningxia Rd, Qingdao 266071, Peoples R China.
EM jiang8014@163.com; libing_516619@163.com
OI Li, Bing/0000-0002-5545-9674
FU National Natural Science Foundation of ChinaNational Natural Science
   Foundation of China (NSFC) [81471546, 81001346, 81273206]
FX This work was funded by the National Natural Science Foundation of China
   (81471546, 81001346, 81273206).
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   [No title captured], DOI DOI 10.1155/2013/742859
NR 140
TC 65
Z9 69
U1 17
U2 52
PU IVYSPRING INT PUBL
PI LAKE HAVEN
PA PO BOX 4546, LAKE HAVEN, NSW 2263, AUSTRALIA
SN 1837-9664
J9 J CANCER
JI J. Cancer
PY 2017
VL 8
IS 17
BP 3416
EP 3429
DI 10.7150/jca.21058
PG 14
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA FQ6TN
UT WOS:000418497000005
PM 29151925
OA Green Published, Green Submitted, gold
DA 2022-04-25
ER

PT J
AU Heller, L
   Knorrscheidt, A
   Flemming, F
   Wiemann, J
   Sommerwerk, S
   Pavel, IZ
   Al-Harrasi, A
   Csuk, R
AF Heller, Lucie
   Knorrscheidt, Anja
   Flemming, Franziska
   Wiemann, Jana
   Sommerwerk, Sven
   Pavel, Ioana Z.
   Al-Harrasi, Ahmed
   Csuk, Rene
TI Synthesis and proapoptotic activity of oleanolic acid derived amides
SO BIOORGANIC CHEMISTRY
LA English
DT Article
DE Oleanolic acid; Amides; Tumor cells; Cell-cycle arrest; Apoptosis;
   Autophagy
ID URSOLIC ACID; MONODANSYLCADAVERINE MDC; MOLECULAR-MECHANISMS; AUTOPHAGIC
   VACUOLES; COLORECTAL-CANCER; DERIVATIVES; TRITERPENOIDS; OLIVES; CELLS;
   PERSPECTIVES
AB Thirty-one different 3-O-acetyl-OA derived amides have been prepared and screened for their cytotoxic activity. In the SRB assays nearly all the carboxamides displayed good cytotoxicity in the low mu M range for several human tumor cell lines. Low EC50 values were obtained especially for the picolinylamides 14-16, for a N-[2-(dimethylamino)-ethyl] derivative 27 and a N-[2-(pyrrolinyl)-ethyl] carboxamide 28. These compounds were submitted to an extensive biological testing and proved compound 15 to act mainly by an arrest of the tumor cells in the S phase of the cell cycle. Cell death occurred by autophagy while compounds 27 and 28 triggered apoptosis. (C) 2016 Elsevier Inc. All rights reserved.
C1 [Heller, Lucie; Knorrscheidt, Anja; Flemming, Franziska; Wiemann, Jana; Sommerwerk, Sven; Csuk, Rene] Martin Luther Univ Halle Wittenberg, Organ Chem, Kurt Mothes Str 2, D-06120 Halle, Saale, Germany.
   [Pavel, Ioana Z.] Victor Babes Univ Med & Pharm, Dept Pathophysiol, Eftimie Murgu Sq 30004, Timisoara 300173, Romania.
   [Pavel, Ioana Z.] Victor Babes Univ Med & Pharm, Dept Pharmacognosy, Eftimie Murgu Sq 30004, Timisoara 300173, Romania.
   [Al-Harrasi, Ahmed] Univ Nizwa, Chair Omans Med Plants & Marine Nat Prod, POB 33, Birkat Al Mauz, Nizwa, Oman.
RP Csuk, R (corresponding author), Martin Luther Univ Halle Wittenberg, Bereich Organ Chem, Kurt Mothes Str 2, D-06120 Halle, Saale, Germany.
EM rene.csuk@chemie.uni-halle.de
RI Csuk, René/L-1549-2015
OI Csuk, René/0000-0001-7911-290X; Wiemann, Jana/0000-0003-2608-0320;
   Heller, Lucie/0000-0002-6735-7026; Pavel, Ioana
   Zinuca/0000-0002-2223-5228
FU WissenschaftsCampus Halle WCH; Oman Research CouncilMinistry of Higher
   Education, Research & Innovation, OmanThe Research Council Oman
   [ORG/HSS/14/004]
FX We like to thank Dr. R. Kluge for measuring the MS spectra and Dr. D.
   Strohl and his team for the NMR spectra. Thanks are also due to to Mrs.
   J. Wiese, MSc, for measuring the IR spectra and optical rotations and to
   Mrs. J. Pech for the micro-analyses. The cell lines were kindly provided
   by Dr. Th. Muller (Dept. of Haematology/Oncology, Martin-Luther
   Universitat Halle-Wittenberg). Support by the "WissenschaftsCampus Halle
   WCH" and the Oman Research Council (ORG/HSS/14/004) is gratefully
   recognized.
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NR 42
TC 17
Z9 17
U1 1
U2 13
PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 0045-2068
EI 1090-2120
J9 BIOORG CHEM
JI Bioorganic Chem.
PD OCT
PY 2016
VL 68
BP 137
EP 151
DI 10.1016/j.bioorg.2016.08.004
PG 15
WC Biochemistry & Molecular Biology; Chemistry, Organic
WE Science Citation Index Expanded (SCI-EXPANDED); Index Chemicus (IC)
SC Biochemistry & Molecular Biology; Chemistry
GA EC2UA
UT WOS:000387978400015
PM 27518757
DA 2022-04-25
ER

PT J
AU Grimm, WA
   Messer, JS
   Murphy, SF
   Nero, T
   Lodolce, JP
   Weber, CR
   Logsdon, MF
   Bartulis, S
   Sylvester, BE
   Springer, A
   Dougherty, U
   Niewold, TB
   Kupfer, SS
   Ellis, N
   Huo, DH
   Bissonnette, M
   Boone, DL
AF Grimm, Wesley A.
   Messer, Jeannette S.
   Murphy, Stephen F.
   Nero, Thomas
   Lodolce, James P.
   Weber, Christopher R.
   Logsdon, Mark F.
   Bartulis, Sarah
   Sylvester, Brooke E.
   Springer, Amanda
   Dougherty, Urszula
   Niewold, Timothy B.
   Kupfer, Sonia S.
   Ellis, Nathan
   Huo, Dezheng
   Bissonnette, Marc
   Boone, David L.
TI The Thr300Ala variant in ATG16L1 is associated with improved survival in
   human colorectal cancer and enhanced production of type I interferon
SO GUT
LA English
DT Article
ID GENOME-WIDE ASSOCIATION; PROSTATE-CANCER; CROHN-DISEASE; AUTOPHAGY;
   VIRUS; CELLS; SUSCEPTIBILITY; THERAPY; ALPHA; ACTIVATION
AB Objective ATG16L1 is an autophagy gene known to control host immune responses to viruses and bacteria. Recently, a non-synonymous single-nucleotide polymorphism in ATG16L1 (Thr300Ala), previously identified as a risk factor in Crohn's disease (CD), was associated with more favourable clinical outcomes in thyroid cancer. Mechanisms underlying this observation have not been proposed, nor is it clear whether an association between Thr300Ala and clinical outcomes will be observed in other cancers. We hypothesised that Thr300Ala influences clinical outcome in human colorectal cancer (CRC) and controls innate antiviral pathways in colon cancer cells.
   Design We genotyped 460 patients with CRC and assessed for an association between ATG16L1 Thr300Ala and overall survival and clinical stage. Human CRC cell lines were targeted by homologous recombination to examine the functional consequence of loss of ATG16L1, or introduction of the Thr300Ala variant.
   Results We found an association between longer overall survival, reduced metastasis and the ATG16L1 Ala/Ala genotype. Tumour sections from ATG16L1 Ala/Ala patients expressed elevated type I interferons (IFN-I)-inducible, MxA, suggesting that differences in cytokine production may influence disease progression. When introduced into human CRC cells by homologous recombination, the Thr300Ala variant did not affect bulk autophagy, but increased basal production of type I IFN. Introduction of Thr300Ala resulted in increased sensitivity to the dsRNA mimic poly(I:C) through a mitochondrial antiviral signalling (MAVS)-dependent pathway.
   Conclusions The CD-risk allele, Thr300Ala, in ATG16L1 is associated with improved overall survival in human CRC, generating a rationale to genotype ATG16L1 Thr300Ala in patients with CRC. We found that Thr300A alters production of MAVS-dependent type I IFN in CRC cells, providing a mechanism that may influence clinical outcomes.
C1 [Grimm, Wesley A.; Messer, Jeannette S.; Murphy, Stephen F.; Nero, Thomas; Lodolce, James P.; Logsdon, Mark F.; Bartulis, Sarah; Sylvester, Brooke E.; Springer, Amanda; Dougherty, Urszula; Niewold, Timothy B.; Kupfer, Sonia S.; Ellis, Nathan; Huo, Dezheng; Bissonnette, Marc] Univ Chicago, Dept Med, Chicago, IL 60637 USA.
   [Weber, Christopher R.] Univ Chicago, Dept Pathol, Chicago, IL 60637 USA.
   [Boone, David L.] Indiana Univ Sch Med, Dept Microbiol, 1234 N Notre Dame Ave, South Bend, IN 46617 USA.
   [Boone, David L.] Indiana Univ Sch Med, Dept Immunol, 1234 N Notre Dame Ave, South Bend, IN 46617 USA.
RP Boone, DL (corresponding author), Indiana Univ Sch Med, Dept Microbiol, 1234 N Notre Dame Ave, South Bend, IN 46617 USA.; Boone, DL (corresponding author), Indiana Univ Sch Med, Dept Immunol, 1234 N Notre Dame Ave, South Bend, IN 46617 USA.
EM daboone@iu.edu
RI Kupfer, Sonia S/ABD-9416-2021; Niewold, Timothy B/D-2669-2018
OI Weber, Christopher/0000-0002-2117-3184; Messer,
   Jeannette/0000-0002-5072-3835
FU Crohn's and Colitis Foundation of America [0-34493-1362]; Broad medical
   Research Foundation [IBD-0259, F32DK082104];  [AI083375-01];  [DK42086];
   NATIONAL CANCER INSTITUTEUnited States Department of Health & Human
   ServicesNational Institutes of Health (NIH) - USANIH National Cancer
   Institute (NCI) [R01CA164124, U01CA153060] Funding Source: NIH RePORTER;
   NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASESUnited States
   Department of Health & Human ServicesNational Institutes of Health (NIH)
   - USANIH National Institute of Allergy & Infectious Diseases (NIAID)
   [R01AI083375, T32AI007090] Funding Source: NIH RePORTER; NATIONAL
   INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASESUnited States
   Department of Health & Human ServicesNational Institutes of Health (NIH)
   - USANIH National Institute of Diabetes & Digestive & Kidney Diseases
   (NIDDK) [F32DK082104, P30DK042086] Funding Source: NIH RePORTER
FX Grant support: AI083375-01; DK42086; Crohn's and Colitis Foundation of
   America 0-34493-1362; Broad medical Research Foundation IBD-0259 (to
   DLB) F32DK082104 (to JSM).
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NR 50
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U1 0
U2 12
PU BMJ PUBLISHING GROUP
PI LONDON
PA BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON WC1H 9JR, ENGLAND
SN 0017-5749
EI 1468-3288
J9 GUT
JI Gut
PD MAR
PY 2016
VL 65
IS 3
BP 456
EP 464
DI 10.1136/gutjnl-2014-308735
PG 9
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA DF4ME
UT WOS:000371321700014
PM 25645662
OA hybrid, Green Published
DA 2022-04-25
ER

PT J
AU Wang, Z
   Zhang, M
   Shan, R
   Wang, YJ
   Chen, J
   Huang, J
   Sun, LQ
   Zhou, WB
AF Wang, Zhan
   Zhang, Min
   Shan, Rong
   Wang, Yu-Jie
   Chen, Juan
   Huang, Juan
   Sun, Lun-Quan
   Zhou, Wei-Bing
TI MTMR3 is upregulated in patients with breast cancer and regulates
   proliferation, cell cycle progression and autophagy in breast cancer
   cells
SO ONCOLOGY REPORTS
LA English
DT Article
DE breast cancer; myotubularin related protein 3; proliferation; cell
   cycle; autophagy
ID EXPRESSION; MIGRATION; ANLN; CDK2; P21
AB As a member of the myotubularin family, myotubularin related protein 3 (MTMR3) has been demonstrated to participate in tumor development, including oral and colon cancer. However, little is known about its functional roles in breast cancer. In the present study, the expression of MTMR3 in breast cancer was evaluated by immunohistochemical staining of tumor tissues from 172 patients. Online data was then used for survival analysis from the PROGgeneV2 database. In vitro, MTMR3 expression was silenced in MDA-MB-231 cells via lentiviral shRNA transduction. MTT, colony formation and flow cytometry assays were performed in the control and MTMR3-silenced cells to evaluate the cell growth, proliferation and cell cycle phase distribution, respectively. Western blotting was used to evaluate the protein expression levels of autophagy-related markers. The results demonstrated that the expression of MTMR3 in breast cancer tissues was significantly increased compared with adjacent normal tissues. MTMR3 was highly expressed in triple-negative breast cancer and was associated with disease recurrence. MTMR3 knockdown in MDA-MB-231 cells inhibited cell proliferation and induced cell cycle arrest and autophagy. The present results indicated that MTMR3 may have an important role in promoting the progression of breast cancer, and its inhibition may serve as a promising therapeutic target for breast cancer treatment.
C1 [Wang, Zhan; Zhang, Min; Shan, Rong; Wang, Yu-Jie; Zhou, Wei-Bing] Cent South Univ, Xiangya Hosp, Dept Oncol, 87 Xiangya Rd, Changsha 410008, Hunan, Peoples R China.
   [Chen, Juan] Cent South Univ, Xiangya Hosp, Dept Pharm, Changsha 410008, Hunan, Peoples R China.
   [Huang, Juan] Cent South Univ, Xiangya Hosp, Hunan Prov Clin Meditech Res Ctr Breast Canc, Changsha 410008, Hunan, Peoples R China.
   [Sun, Lun-Quan] Cent South Univ, Xiangya Hosp, Ctr Mol Med, Changsha 410008, Hunan, Peoples R China.
RP Zhou, WB (corresponding author), Cent South Univ, Xiangya Hosp, Dept Oncol, 87 Xiangya Rd, Changsha 410008, Hunan, Peoples R China.
EM zhouweibing298@csu.edu.cn
FU National Natural Science Foundation of ChinaNational Natural Science
   Foundation of China (NSFC) [81572612, 81372842, 81803640]; Hunan
   Provincial Natural Science FoundationNatural Science Foundation of Hunan
   Province [2015JJ2183]; Youth Science Foundation of Xiangya Hospital,
   Central South University [2017Q02]; Research Innovation Program for
   Graduate Students of Central South University [2018zzts912]; National
   Key Clinical Specialist Construction Programs of China [2014kll]
FX This study was supported by grants from the National Natural Science
   Foundation of China (grant nos. 81572612, 81372842 and 81803640), the
   Hunan Provincial Natural Science Foundation (grant no. 2015JJ2183), the
   Youth Science Foundation of Xiangya Hospital, Central South University
   (grant no. 2017Q02) and the Research Innovation Program for Graduate
   Students of Central South University (grant no. 2018zzts912). This study
   was also supported by the National Key Clinical Specialist Construction
   Programs of China (grant no. 2014kll).
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NR 44
TC 5
Z9 6
U1 3
U2 4
PU SPANDIDOS PUBL LTD
PI ATHENS
PA POB 18179, ATHENS, 116 10, GREECE
SN 1021-335X
EI 1791-2431
J9 ONCOL REP
JI Oncol. Rep.
PD NOV
PY 2019
VL 42
IS 5
BP 1915
EP 1923
DI 10.3892/or.2019.7292
PG 9
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA JE9BA
UT WOS:000490982300026
PM 31485632
OA Green Published, hybrid
DA 2022-04-25
ER

PT J
AU Zhang, H
   Wang, YB
   Liu, JY
   Kuerban, K
   Li, J
   Iminjan, M
   Ye, L
AF Zhang, Hui
   Wang, Yongbing
   Liu, Jiayang
   Kuerban, Kudelaidi
   Li, Jian
   Iminjan, Mubarak
   Ye, Li
TI Traditional Uyghur medicine Quercus infectoria galls water extract
   triggers apoptosis and autophagic cell death in colorectal cancer cells
SO BMC COMPLEMENTARY MEDICINE AND THERAPIES
LA English
DT Article
DE Quercuse infectoria galls; Colorectal cancer; Apoptosis; Autophagy;
   Reactive oxygen species
ID PATHWAYS; THERAPY
AB Background The water extract of Quercuse infectoria galls (QIG) is the active ingredient of Uyghur medicine Xipayi Kui Jie'an (KJA) which has promising therapeutic effects on Ulcerative Colitis (UC) as an alternative medicine. Considering the relationship between UC and the development of colorectal cancer (CRC), the present work aims to explore the direct anti-CRC activity of QIG extract. Methods CCK8 assay and flow cytometry were used to detect cytotoxicity and apoptosis. Transmission electron microscopy (TEM), flow cytometry, laser confocal and western blotting were performed to examine autophagy. We also adopted Reactive Oxygen Assay kit, as well as transwell and wound healing tests to study the underlying mechanism of QIG against CRC cells. Results First, we found that QIG extract could suppress the viability of CRC cells and trigger caspases-dependent apoptosis. Subsequently, we proved for the first time that QIG extract also triggered autophagic cell death in CRC cells, which together with apoptosis contributed to the cytotoxic effect on CRC cells. Further investigation revealed that QIG-induced cytotoxicity associated with intracellular ROS accumulation which could suppress the AKT/mTOR signaling pathway, and then induce autophagy and inhibit cell growth. Besides, Erk signaling pathway was also involved in the process of autophagic cell death. Moreover, QIG extract also influenced EMT process and inhibited CRC cell migration. Conclusion Altogether, this study provides a basis for the utilization of QIG as an alternative medicine for CRC prevention and treatment.
C1 [Zhang, Hui; Liu, Jiayang; Kuerban, Kudelaidi; Ye, Li] Fudan Univ, Sch Pharm, Dept Biol Med, Shanghai 201203, Peoples R China.
   [Zhang, Hui; Liu, Jiayang; Kuerban, Kudelaidi; Ye, Li] Fudan Univ, Sch Pharm, Shanghai Engn Res Ctr Immunotherapeut, Shanghai 201203, Peoples R China.
   [Wang, Yongbing] Shanghai Univ Med & Hlth Sci, Pudong New Area Peoples Hosp, Shanghai 201200, Peoples R China.
   [Li, Jian] Fudan Univ, Zhongshan Hosp, Minhang Branch, Endoscopy Ctr, Shanghai 200433, Peoples R China.
   [Iminjan, Mubarak] Xinjiang Med Univ, Coll Pharm, Dept Pharmaceut & Phys Chem, Xinjiang 830011, Peoples R China.
RP Ye, L (corresponding author), Fudan Univ, Sch Pharm, Dept Biol Med, Shanghai 201203, Peoples R China.; Ye, L (corresponding author), Fudan Univ, Sch Pharm, Shanghai Engn Res Ctr Immunotherapeut, Shanghai 201203, Peoples R China.; Iminjan, M (corresponding author), Xinjiang Med Univ, Coll Pharm, Dept Pharmaceut & Phys Chem, Xinjiang 830011, Peoples R China.
EM 896612093@qq.com; yelil@fudan.edu.cn
RI kuerban, kudelaidi/AAP-5963-2021
OI Ye, Li/0000-0001-5303-2549
FU Scientific and Innovative Action Plan of Shanghai [18431902800,
   20S11901600]; Key Discipline Construction Project of Pudong Health
   Bureau of Shanghai [PWZxk2017-11]; Shanghai Natural Science Foundation
   ProjectNatural Science Foundation of Shanghai [19ZR1446100]
FX This work was supported by Scientific and Innovative Action Plan of
   Shanghai (No. 18431902800 and 20S11901600), the Key Discipline
   Construction Project of Pudong Health Bureau of Shanghai (No.
   PWZxk2017-11) and Shanghai Natural Science Foundation Project (No.
   19ZR1446100).
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NR 37
TC 0
Z9 0
U1 1
U2 5
PU BMC
PI LONDON
PA CAMPUS, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
EI 2662-7671
J9 BMC COMPLEMENT MED
JI BMC Complement. Med. Ther.
PD DEC 3
PY 2020
VL 20
IS 1
AR 371
DI 10.1186/s12906-020-03167-0
PG 12
WC Integrative & Complementary Medicine
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Integrative & Complementary Medicine
GA PA3WC
UT WOS:000595568800001
PM 33272252
OA gold, Green Published
DA 2022-04-25
ER

PT J
AU Dorr, RT
   Samulitis, BK
   Wisner, L
   Han, HY
   Zhao, Y
   Beroza, P
   Damodaran, K
   Igarashi, S
   Landowski, TH
   Von Hoff, DD
AF Dorr, Robert T.
   Samulitis, Betty K.
   Wisner, Lee
   Han, Haiyong
   Zhao, Yu
   Beroza, Paul
   Damodaran, Komath
   Igarashi, Suzu
   Landowski, Terry H.
   Von Hoff, Daniel D.
TI Characterization of a membrane-active anti-tumor agent, UA8967
SO INVESTIGATIONAL NEW DRUGS
LA English
DT Article
DE DPC4; Membrane integrity; SMAD4; TRAP; UA8967; Autophagy
ID GROWTH; INHIBITOR; APOPTOSIS; PROTEIN
AB Deletions or mutations in the tumor suppressor gene DPC4 (deleted in pancreatic carcinoma locus 4) are common in colon and pancreatic cancers. Using the Target-related Affinity Profiling (TRAP) chemical library screening method, a novel agent, UA8967, was selected for further studies because it showed greater potency in DPC4-deleted HCT-116 colon cancer cells. Cytotoxicity studies in six pancreatic cancer cell lines (MiaPaca-2, Panc-1, BxPC3, CF-PAC1, AsPC1, and T3M4), one normal human pancreatic ductal epithelial line (HPDE-6) and the HCT-116 DPC4(+/+) and HCT-116 DPC4(-/-) colon cancer cells showed IC(50)s ranging from 12-61 mu M for exposure times of 72 h. Analysis of schedule dependence showed no advantage for long drug exposure times. There was also no selective inhibition of DNA, RNA or protein synthesis after exposure to UA8967. At 24-48 h, there was an accumulation of cells in G(0)/G(1)-phase and a proportionate reduction in S-phase cells. Within 1-6 h of exposure, cells were found to undergo an autophagic response, followed at 24 h by a low level of caspase-independent apoptosis with some necrosis. Because of the relatively non-specific mechanistic effects of UA8967, plasma membrane viability was evaluated using uptake of trypan blue and SytoxA (R) Green dyes, and leakage of LDH. There was a dose dependent increase in SytoxA (R) Green staining, trypan blue uptake and LDH leakage with increasing concentrations of UA8967, suggesting that UA8967 is affecting the plasma membrane. The DPC4(-/-) cells were more sensitive to UA8967 but not to DMSO, suggesting a drug-specific effect on cell membrane integrity.
C1 [Dorr, Robert T.; Samulitis, Betty K.; Wisner, Lee; Igarashi, Suzu; Landowski, Terry H.] Univ Arizona, Ctr Canc, Tucson, AZ 85724 USA.
   [Han, Haiyong; Zhao, Yu; Von Hoff, Daniel D.] Translat Genom Res Inst TGEN, Phoenix, AZ 85004 USA.
   [Beroza, Paul; Damodaran, Komath] Telik Inc, Palo Alto, CA 94304 USA.
RP Dorr, RT (corresponding author), Univ Arizona, Ctr Canc, 1515 N Campbell Ave,Rm 4963C, Tucson, AZ 85724 USA.
EM bdorr@azcc.arizona.edu
FU National Institutes of HealthUnited States Department of Health & Human
   ServicesNational Institutes of Health (NIH) - USA [P01-CA109552];
   University of Arizona Cancer Center Support Core Grant [P30-CA023074];
   NATIONAL CANCER INSTITUTEUnited States Department of Health & Human
   ServicesNational Institutes of Health (NIH) - USANIH National Cancer
   Institute (NCI) [P30CA023074, P01CA109552] Funding Source: NIH RePORTER
FX This work was supported by National Institutes of Health grant
   P01-CA109552 (DVH) and the University of Arizona Cancer Center Support
   Core Grant P30-CA023074
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NR 25
TC 1
Z9 1
U1 0
U2 10
PU SPRINGER
PI DORDRECHT
PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS
SN 0167-6997
EI 1573-0646
J9 INVEST NEW DRUG
JI Invest. New Drugs
PD JUN
PY 2013
VL 31
IS 3
BP 576
EP 586
DI 10.1007/s10637-012-9901-z
PG 11
WC Oncology; Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Pharmacology & Pharmacy
GA 140MA
UT WOS:000318657000009
PM 23179338
OA Green Accepted
DA 2022-04-25
ER

PT J
AU Yang, F
   Peng, ZX
   Ji, WD
   Yu, JD
   Qian, C
   Liu, JD
   Fang, GE
AF Yang, Feng
   Peng, Zhang-xiao
   Ji, Wei-dan
   Yu, Ju-dian
   Qian, Chen
   Liu, Jian-dong
   Fang, Guo-en
TI LncRNA CCAT1 Upregulates ATG5 to Enhance Autophagy and Promote Gastric
   Cancer Development by Absorbing miR-140-3p
SO DIGESTIVE DISEASES AND SCIENCES
LA English
DT Article; Early Access
DE Gastric cancer; Autophagy; LncRNA CCAT1; miR-140-3p; ATG5
ID NONCODING RNA CCAT1; C-MYC; PROGRESSION
AB Background Long noncoding RNA colon cancer-associated transcript 1 (LncRNA CCAT1) is highly expressed in gastric cancer tissues and plays a role in autophagy. However, the underlying mechanism still needs to be further clarified. Objective To study the role of LncRNA CCAT1 in regulating autophagy of gastric cancer cells, analyze its downstream targets, and elucidate the mechanism. Methods qPCR detected the expression of LncRNA CCAT1 in gastric cancer cells. The proliferation, migration, and invasion ability of LncRNA CCAT1 and the expression level of autophagy-related proteins in gastric cancer cells were detected. Bioinformatics method predicted the downstream targets of LncRNA CCAT1, and they were verified by dual-luciferase assay. The relationship between LncRNA CCAT1, miR-140, and ATG5 was verified by co-transfection, and the expression levels of ATG5 and ATG5-ATG12 complex proteins were detected. Finally, the role of LncRNA CCAT1 in vivo was confirmed by gastric cancer transplantation model. Results LncRNA CCAT1 was highly expressed in gastric cancer cells. LncRNA CCAT1 can promote the proliferation, migration, invasion, and autophagy activity of gastric cancer cells. LncRNA CCAT1 can bind to miR-140-3p and regulate its expression, while miR-140-3p further regulates the expression of ATG5. Overexpression of LncRNA CCAT1 can promote tumor growth in nude mice. After LncRNA CCAT1 silencing, the positive expression rate of ATG5 in nude mice was low. Conclusion LncRNA CCAT1 may inhibit the expression of miR-140-3p by sponge adsorption, thus weakening its inhibitory effect on ATG5. Eventually, gastric cancer cells were more prone to autophagy under the pressure of stress.
C1 [Yang, Feng; Yu, Ju-dian; Qian, Chen; Liu, Jian-dong] Second Mil Med Univ, Eastern Hepatobiliary Surg Hosp, Dept Gen Surg, Shanghai 201805, Peoples R China.
   [Peng, Zhang-xiao; Ji, Wei-dan] Second Mil Med Univ, Eastern Hepatobiliary Surg Hosp, Mol Tumor Lab, Shanghai 201805, Peoples R China.
   [Fang, Guo-en] Second Mil Med Univ, Changhai Hosp, Dept Gen Surg, 68 Changhai Rd, Shanghai 200433, Peoples R China.
RP Fang, GE (corresponding author), Second Mil Med Univ, Changhai Hosp, Dept Gen Surg, 68 Changhai Rd, Shanghai 200433, Peoples R China.
EM fangguoen56@163.com
FU Shanghai Municipal Health and Family Planning Commission [201840070];
   Science and Technology Commission of Jiading District, Shanghai
   [JDKW-2018-W12]
FX This study was supported by the subject of Shanghai Municipal Health and
   Family Planning Commission (general project) (No. 201840070) and the
   subject of Science and Technology Commission of Jiading District,
   Shanghai (No. JDKW-2018-W12).
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NR 29
TC 2
Z9 2
U1 2
U2 3
PU SPRINGER
PI DORDRECHT
PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS
SN 0163-2116
EI 1573-2568
J9 DIGEST DIS SCI
JI Dig. Dis. Sci.
DI 10.1007/s10620-021-07187-9
EA AUG 2021
PG 17
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA UD2AD
UT WOS:000687014600002
PM 34417924
DA 2022-04-25
ER

PT J
AU Mimura, K
   Sakamaki, JI
   Morishita, H
   Kawazu, M
   Mano, H
   Mizushima, N
AF Mimura, Kaito
   Sakamaki, Jun-Ichi
   Morishita, Hideaki
   Kawazu, Masahito
   Mano, Hiroyuki
   Mizushima, Noboru
TI Genome-wide CRISPR screening reveals nucleotide synthesis negatively
   regulates autophagy
SO JOURNAL OF BIOLOGICAL CHEMISTRY
LA English
DT Article
ID HOPS COMPLEX; COLON-CANCER; 5-FLUOROURACIL; GROWTH; IDENTIFICATION;
   CHEMOTHERAPY; METABOLISM; REPRESSION; INHIBITION; RECEPTOR
AB Macroautophagy (hereafter, autophagy) is a process that directs the degradation of cytoplasmic material in lysosomes. In addition to its homeostatic roles, autophagy undergoes dynamic positive and negative regulation in response to multiple forms of cellular stress, thus enabling the survival of cells. However, the precise mechanisms of autophagy regulation are not fully understood. To identify potential negative regulators of autophagy, we performed a genome-wide CRISPR screen using the quantitative autophagic flux reporter GFP-LC3-RFP. We identified phosphoribosylformylglycinamidine synthase, a component of the de novo purine synthesis pathway, as one such negative regulator of autophagy. Autophagy was activated in cells lacking phosphoribosylformylglycinamidine synthase or phosphoribosyl pyrophosphate amidotransferase, another de novo purine synthesis enzyme, or treated with methotrexate when exogenous levels of purines were insufficient. Purine starvation-induced autophagy activation was concomitant with mammalian target of rapamycin complex 1 (mTORC1) suppression and was profoundly suppressed in cells deficient for tuberous sclerosis complex 2, which negatively regulates mTORC1 through inhibition of Ras homolog enriched in brain, suggesting that purines regulate autophagy through the tuberous sclerosis complex-Ras homolog enriched in brainm-TORC1 signaling axis. Moreover, depletion of the pyrimidine synthesis enzymes carbamoyl-phosphate synthetase 2, aspartate transcarbamylase, and dihydroorotase and dihydroorotate dehydrogenase activated autophagy as well, although mTORC1 activity was not altered by pyrimidine shortage. These results suggest a different mechanism of autophagy induction between purine and pyrimidine starvation. These findings provide novel insights into the regulation of autophagy by nucleotides and possibly the role of autophagy in nucleotide metabolism, leading to further developing anticancer strategies involving nucleotide synthesis and autophagy.
C1 [Mimura, Kaito; Sakamaki, Jun-Ichi; Morishita, Hideaki; Mizushima, Noboru] Univ Tokyo, Grad Sch, Dept Biochem & Mol Biol, Tokyo, Japan.
   [Mimura, Kaito; Sakamaki, Jun-Ichi; Morishita, Hideaki; Mizushima, Noboru] Univ Tokyo, Fac Med, Tokyo, Japan.
   [Kawazu, Masahito; Mano, Hiroyuki] Natl Canc Ctr, Div Cellular Signaling, Tokyo, Japan.
   [Morishita, Hideaki] Juntendo Univ, Dept Physiol, Grad Sch Med, Tokyo 1138421, Japan.
RP Mizushima, N (corresponding author), Univ Tokyo, Grad Sch, Dept Biochem & Mol Biol, Tokyo, Japan.; Mizushima, N (corresponding author), Univ Tokyo, Fac Med, Tokyo, Japan.
EM nmizu@m.u.tokyo.ac.jp
RI Mizushima, Noboru/C-3635-2009; Kawazu, Masahito/AAE-6143-2022
OI Mizushima, Noboru/0000-0002-6258-6444; Kawazu,
   Masahito/0000-0003-4146-3629; Morishita, Hideaki/0000-0003-0860-8371;
   Mimura, Kaito/0000-0002-0053-0218
FU Japan Science and Technology AgencyJapan Science & Technology Agency
   (JST) [JPMJER1702]; MD Scientist Training Program, Faculty of Medicine,
   The University of Tokyo
FX This work was supported by a grant for Exploratory Research for Advanced
   Technology from the Japan Science and Technology Agency (JPMJER1702 to
   N. M.). K. M. was supported by the MD Scientist Training Program,
   Faculty of Medicine, The University of Tokyo.
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NR 68
TC 2
Z9 2
U1 1
U2 4
PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC
PI ROCKVILLE
PA 11200 ROCKVILLE PIKE, SUITE 302, ROCKVILLE, MD, UNITED STATES
SN 0021-9258
EI 1083-351X
J9 J BIOL CHEM
JI J. Biol. Chem.
PD JAN-JUN
PY 2021
VL 296
AR 100780
DI 10.1016/j.jbc.2021.100780
PG 13
WC Biochemistry & Molecular Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology
GA TL2WM
UT WOS:000674717300002
PM 34000301
OA gold, Green Published
DA 2022-04-25
ER

PT J
AU Calvo-Martin, G
   Plano, D
   Encio, I
   Sanmartin, C
AF Calvo-Martin, Gorka
   Plano, Daniel
   Encio, Ignacio
   Sanmartin, Carmen
TI Novel N,N '-Disubstituted Selenoureas as Potential Antioxidant and
   Cytotoxic Agents
SO ANTIOXIDANTS
LA English
DT Article
DE selenoureas; antioxidant; cytotoxicity; radical scavenging; selenium
ID CELL-CYCLE ARREST; BIOLOGICAL EVALUATION; IN-VITRO; ANTIPROLIFERATIVE
   AGENTS; ANTICANCER ACTIVITY; CANCER; DERIVATIVES; SELENIUM; APOPTOSIS;
   FERROCENE
AB A series of 30 novel N,N disubstituted selenoureas were synthesized, characterized, and their antioxidant ability was tested using 2,2-diphenyl-1-picrylhydrazyl (DPPH) and 2,2 '-azino-bis(3-ethylbenzthiazoline-6-sulfonic acid (ABTS) assays. Additionally, their cytotoxic activity was tested in vitro in a panel of three different cancer (breast, lung and colon) and two normal cell lines. Each selenourea entity contains a para-substituted phenyl ring with different electron-withdrawing and electron-donating groups, and different aliphatic and aromatic nuclei. All of the synthesized selenoureas present antioxidant capacity at high concentrations in the DPPH assay, and three of them (2b, 2c and 2d) showed greater radical scavenging capacity than ascorbic acid at lower concentrations. These results were confirmed by the ABTS assay, where these novel selenoureas present even higher antioxidant capacity than the reference compound Trolox. On the other hand, 10 selenoureas present IC50 values below 10 mu M in at least one cancer cell line, resulting in the adamantyl nucleus (6a-6e), the most interesting in terms of activity and selectivity. Outstanding results were found for selenourea 6c, tested in the NCI60 cell line panel and showing an average GI(50) of 1.49 mu M for the 60 cell lines, and LC50 values ranging from 9.33 mu M to 4.27 mu M against 10 of these cancer cell lines. To gain insight into its anticancer activity mechanism, we investigated the cell cycle progression of the promising compound 6c, as well as the type of programmed-cell death in a colon cancer cell line it provokes (HT-29). Compound 6c provoked S phase cell cycle arrest and the induction of cell death was independent of caspase activation, suggesting autophagy, though this assertion requires additional studies. Overall, we envision that this compound can be further developed for the potential treatment of colon cancer.
C1 [Calvo-Martin, Gorka; Plano, Daniel; Sanmartin, Carmen] Univ Navarra, Dept Tecnol & Quim Farmaceut, Irunlarrea 1, E-31008 Pamplona, Spain.
   [Calvo-Martin, Gorka; Plano, Daniel; Encio, Ignacio; Sanmartin, Carmen] Inst Invest Sanit Navarra IdiSNA, Irunlarrea 3, E-31008 Pamplona, Spain.
   [Encio, Ignacio] Univ Publ Navarra, Dept Ciencias Salud, Avda Baranain S-N, E-31008 Pamplona, Spain.
RP Sanmartin, C (corresponding author), Univ Navarra, Dept Tecnol & Quim Farmaceut, Irunlarrea 1, E-31008 Pamplona, Spain.; Sanmartin, C (corresponding author), Inst Invest Sanit Navarra IdiSNA, Irunlarrea 3, E-31008 Pamplona, Spain.
EM gcalvo.3@alumni.unav.es; dplano@unav.es; ignacio.encio@unavarra.es;
   sanmartin@unav.es
RI Plano, Daniel/K-3001-2014; Sanmartin, Carmen/K-1188-2014
OI Plano, Daniel/0000-0002-8266-0445; Encio, Ignacio/0000-0003-1732-1989;
   Sanmartin, Carmen/0000-0003-3431-7826; Calvo-Martin,
   Gorka/0000-0003-2806-5183
FU PIUNA [2014-26, 2018-19]; UNED-Caja Navarra Fundacion La Caixa
FX This research was funded by PIUNA (refs 2014-26 and 2018-19) and
   UNED-Caja Navarra Fundacion La Caixa.
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NR 53
TC 0
Z9 0
U1 3
U2 5
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 2076-3921
J9 ANTIOXIDANTS-BASEL
JI Antioxidants
PD MAY
PY 2021
VL 10
IS 5
AR 777
DI 10.3390/antiox10050777
PG 14
WC Biochemistry & Molecular Biology; Chemistry, Medicinal; Food Science &
   Technology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Pharmacology & Pharmacy; Food Science
   & Technology
GA SG3LO
UT WOS:000653343600001
PM 34068900
OA Green Published, gold
DA 2022-04-25
ER

PT J
AU Goossens, JF
   Bailly, C
AF Goossens, Jean-Francois
   Bailly, Christian
TI Ursodeoxycholic acid and cancer: From chemoprevention to chemotherapy
SO PHARMACOLOGY & THERAPEUTICS
LA English
DT Review
DE Ursodeoxycholic acid; Bile acids; Anticancer drug; Hepatocellular
   carcinoma; Drug design
ID NF-KAPPA-B; EPITHELIAL-MESENCHYMAL TRANSITION; HEPATOCELLULAR-CARCINOMA
   CELLS; PRIMARY SCLEROSING CHOLANGITIS; DERIVATIVES INDUCE APOPTOSIS;
   INFLAMMATORY-BOWEL-DISEASE; PRIMARY BILIARY-CIRRHOSIS; RECEPTOR GPBAR1
   TGR5; PROTEIN-KINASE-C; BILE-ACID
AB Ursodeoxycholic acid (UDCA) is a secondary bile acid issued from the transformation of (cheno)deoxycholic acid by intestinal bacteria, acting as a key regulator of the intestinal barrier integrity and essential for lipid metabolism. UDCA is also a long-established drug, largely used for the dissolution of cholesterol gallstones, the treatment of primary biliary cholangitis and other hepatobiliary disorders. The history of UDCA is briefly retraced here as well as its multifactorial mechanism of action, based on its anti-inflammatory, antioxidant and cytoprotective activities. The present review is centred around the anticancer properties of UDCA and synthetic antitumor derivatives designed over the past 20 years. Paradoxically, depending on the conditions, UDCA exhibits both pro- and anti-apoptotic properties toward different cell types. In particular, the UDCA drug can protect epithelial cells from damages and apoptosis while inducing inhibition of proliferation and apoptotic and/or autophagic death of cancer cells. The effects of UDCA on cancer cell migration, cancer stem cells and drug-induced dysbiosis are also evoked. The drug has revealed modest activities against colon and gastric cancers but may be useful to improve treatments of hepatocellular carcinoma, notably in combination with other drugs such as sorafenib. UDCA can also protect from damages induced by cancer chemotherapeutic agents. The potential of UDCA in cancer, as a chemo-protecting or chemotherapeutic agent, is highlighted here as well as the design of tumour-active derivatives, including UDCA-drug conjugates. A repurposing of UDCA in oncology should be further considered. (C) 2019 Elsevier Inc. All rights reserved.
C1 [Goossens, Jean-Francois] Univ Lille, CHU Lille, GRITA Grp Rech Formes Injectables & Technol Assoc, EA 7365, F-59000 Lille, France.
   [Bailly, Christian] Oncowitan, F-59290 Lille, Wasquehal, France.
RP Bailly, C (corresponding author), Oncowitan, F-59290 Lille, Wasquehal, France.
EM christian.bailly@inserm.fr
RI BAILLY, Christian/AAK-2799-2021; Bailly, Christian/V-4707-2019
OI BAILLY, Christian/0000-0002-2973-9357; 
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NR 148
TC 36
Z9 40
U1 3
U2 21
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0163-7258
J9 PHARMACOL THERAPEUT
JI Pharmacol. Ther.
PD NOV
PY 2019
VL 203
AR 107396
DI 10.1016/j.pharmthera.2019.107396
PG 13
WC Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA JO0ZL
UT WOS:000497315100009
PM 31356908
DA 2022-04-25
ER

PT J
AU Frank, D
   Vaux, DL
   Murphy, JM
   Vince, JE
   Lindqvist, LM
AF Frank, Daniel
   Vaux, David L.
   Murphy, James M.
   Vince, James E.
   Lindqvist, Lisa M.
TI Activated MLKL attenuates autophagy following its translocation to
   intracellular membranes
SO JOURNAL OF CELL SCIENCE
LA English
DT Article
DE Necroptosis; Autophagy; MLKL; LC3
ID MIXED LINEAGE KINASE; DOMAIN-LIKE; CELL-DEATH; MEDIATES NECROPTOSIS;
   FAMILY-MEMBERS; PROTEIN; PHOSPHORYLATION; NECROSIS; TNF; DOWNSTREAM
AB Necroptosis is an inflammatory form of programmed cell death mediated by the pseudokinase mixed-lineage kinase domain-like protein (MLKL). Upon phosphorylation by receptor-interacting protein kinase-3 (RIPK3), MLKL oligomerizes, and translocates to and disrupts the plasma membrane, thereby causing necroptotic cell lysis. Herein, we show that activation of necroptosis in mouse dermal fibroblasts (MDFs) and HT-29 human colorectal cancer cells results in accumulation of the autophagic marker, lipidated LC3B (also known as MAP1LC3B), in an MLKL-dependent manner. Unexpectedly, the necroptosis-induced increase in lipidated LC3B was due to inhibition of autophagic flux, not the activation of autophagy. Inhibition of autophagy by MLKL correlated with a decrease in autophagosome and/or autolysosome function, and required the association of activated MLKL with intracellular membranes. Collectively, our findings uncover an additional role for the MLKL pseudokinase, namely to inhibit autophagy during necroptosis.
C1 [Frank, Daniel; Vaux, David L.; Murphy, James M.; Lindqvist, Lisa M.] Walter & Eliza Hall Inst Med Res, Cell Signalling & Cell Death Div, 1G Royal Parade, Melbourne, Vic 3052, Australia.
   [Frank, Daniel; Vaux, David L.; Murphy, James M.; Vince, James E.; Lindqvist, Lisa M.] Univ Melbourne, Dept Med Biol, Parkville, Vic 3050, Australia.
   [Vince, James E.] Walter & Eliza Hall Inst Med Res, Inflammat Div, 1G Royal Parade, Melbourne, Vic 3052, Australia.
   [Lindqvist, Lisa M.] CSL Ltd, Res & Clin Bioanalyt, 30 Flemington Rd, Parkville, Vic 3052, Australia.
RP Lindqvist, LM (corresponding author), Walter & Eliza Hall Inst Med Res, Cell Signalling & Cell Death Div, 1G Royal Parade, Melbourne, Vic 3052, Australia.; Vince, JE; Lindqvist, LM (corresponding author), Univ Melbourne, Dept Med Biol, Parkville, Vic 3050, Australia.; Vince, JE (corresponding author), Walter & Eliza Hall Inst Med Res, Inflammat Div, 1G Royal Parade, Melbourne, Vic 3052, Australia.; Lindqvist, LM (corresponding author), CSL Ltd, Res & Clin Bioanalyt, 30 Flemington Rd, Parkville, Vic 3052, Australia.
EM vince@wehi.edu.au; Lisa.Lindqvist@csl.com.au
RI Vaux, David L/C-7249-2013
OI Vaux, David L/0000-0003-2703-1651; vince, james/0000-0001-7166-2798;
   Frank, Daniel/0000-0003-4998-2220
FU Australian National Health and Medical Research Council (NHMRC)National
   Health and Medical Research Council (NHMRC) of Australia [461221,
   1101405, 1145788]; NHMRCNational Health and Medical Research Council
   (NHMRC) of Australia [1105754, 1141466, 1020136, 361646]; Melbourne
   Research Scholarship (MRS); Victorian State Government Operational
   Infrastructure Support Grant
FX This work was supported by Australian National Health and Medical
   Research Council (NHMRC) Program 461221 (D.L.V.), and Project 1101405
   (J.E.V.) and 1145788 (J.M.M., J.E.V. and L.M.L.) grants. J.M.M.
   (1105754) and J.E.V. (1141466) were supported by NHMRC Career
   Development Fellowships, while D.L.V. held an NHMRC Fellowship
   (1020136). D.F. was supported by Melbourne Research Scholarship (MRS).
   This work was also made possible through an Independent Research
   Institutes Infrastructure Support Scheme Grant (361646) from the NHMRC
   and a Victorian State Government Operational Infrastructure Support
   Grant.
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NR 42
TC 22
Z9 22
U1 3
U2 6
PU COMPANY BIOLOGISTS LTD
PI CAMBRIDGE
PA BIDDER BUILDING, STATION RD, HISTON, CAMBRIDGE CB24 9LF, ENGLAND
SN 0021-9533
EI 1477-9137
J9 J CELL SCI
JI J. Cell Sci.
PD MAR
PY 2019
VL 132
IS 5
AR jcs220996
DI 10.1242/jcs.220996
PG 11
WC Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Cell Biology
GA HP1GO
UT WOS:000461414300010
PM 30709919
OA Bronze
DA 2022-04-25
ER

PT J
AU Zheng, HC
AF Zheng, Hua-Chuan
TI The molecular mechanisms of chemoresistance in cancers
SO ONCOTARGET
LA English
DT Review
DE cancer; chemoresistance; molecular mechanisms; chemotherapy
ID EPITHELIAL-MESENCHYMAL TRANSITION; CELL-LIKE PROPERTIES; BREAST-CANCER;
   CONFERS CHEMORESISTANCE; DRUG-RESISTANCE; DOWN-REGULATION; REGULATES
   CHEMORESISTANCE; COLON-CANCER; LUNG-CANCER; STEM-CELLS
AB Overcoming intrinsic and acquired drug resistance is a major challenge in treating cancer patients because chemoresistance causes recurrence, cancer dissemination and death. This review summarizes numerous molecular aspects of multi-resistance, including transporter pumps, oncogenes (EGFR, PI3K/Akt, Erk and NF-kappa B), tumor suppressor gene (p53), mitochondrial alteration, DNA repair, autophagy, epithelial-mesenchymal transition (EMT), cancer stemness, and exosome. The chemoresistance-related proteins are localized to extracellular ligand, membrane receptor, cytosolic signal messenger, and nuclear transcription factors for various events, including proliferation, apoptosis, EMT, autophagy and exosome. Their cross-talk frequently appears, such as the regulatory effects of EGFR-Akt-NF-kappa B signal pathway on the transcription of Bcl-2, Bcl-xL and survivin or EMT-related stemness. It is essential for the realization of the target, individualized and combine therapy to clarify these molecular mechanisms, explore the therapy target, screen chemosensitive population, and determine the efficacy of chemoreagents by cell culture and orthotopic model.
C1 [Zheng, Hua-Chuan] China Med Univ, Dept Expt Oncol, Shengjing Hosp, Shenyang 110004, Peoples R China.
   [Zheng, Hua-Chuan] China Med Univ, Anim Ctr, Shengjing Hosp, Shenyang 110004, Peoples R China.
RP Zheng, HC (corresponding author), China Med Univ, Dept Expt Oncol, Shengjing Hosp, Shenyang 110004, Peoples R China.; Zheng, HC (corresponding author), China Med Univ, Anim Ctr, Shengjing Hosp, Shenyang 110004, Peoples R China.
EM zheng_huachuan@hotmail.com
FU Liaoning BaiQianWan Talents Program; Key Scientific and Technological
   Project of Liaoning Province [2015408001]; National Natural Scientific
   Foundation of ChinaNational Natural Science Foundation of China (NSFC)
   [81472544, 81672700]; Award for Liaoning Distinguished Professor
FX This study was supported by Liaoning BaiQianWan Talents Program, Award
   for Liaoning Distinguished Professor, A Key Scientific and Technological
   Project of Liaoning Province (2015408001), and National Natural
   Scientific Foundation of China (81472544; 81672700).
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NR 123
TC 295
Z9 300
U1 22
U2 98
PU IMPACT JOURNALS LLC
PI ORCHARD PARK
PA 6666 E QUAKER ST, STE 1, ORCHARD PARK, NY 14127 USA
EI 1949-2553
J9 ONCOTARGET
JI Oncotarget
PD AUG 29
PY 2017
VL 8
IS 35
BP 59950
EP 59964
DI 10.18632/oncotarget.19048
PG 15
WC Oncology; Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Cell Biology
GA FF4RD
UT WOS:000408941900171
PM 28938696
OA Green Published, gold
HC Y
HP N
DA 2022-04-25
ER

PT J
AU Li, ZW
   Zhuang, M
   Zhang, LC
   Zheng, XN
   Yang, P
   Li, ZY
AF Li, Zongwei
   Zhuang, Ming
   Zhang, Lichao
   Zheng, Xingnan
   Yang, Peng
   Li, Zhuoyu
TI Acetylation modification regulates GRP78 secretion in colon cancer cells
SO SCIENTIFIC REPORTS
LA English
DT Article
ID PROTEIN LYSINE ACETYLATION; TUMOR MICROENVIRONMENT; EXTRACELLULAR
   VESICLES; EXOSOMES; MICROVESICLES; ACTIVATION; AUTOPHAGY; VPS34;
   FIBROBLASTS; PROGRESSION
AB High glucose-regulated protein 78 (GRP78) expression contributes to the acquisition of a wide range of phenotypic cancer hallmarks, and the pleiotropic oncogenic functions of GRP78 may result from its diverse subcellular distribution. Interestingly, GRP78 has been reported to be secreted from solid tumour cells, participating in cell-cell communication in the tumour microenvironment. However, the mechanism underlying this secretion remains elusive. Here, we report that GRP78 is secreted from colon cancer cells via exosomes. Histone deacetylase (HDAC) inhibitors blocked GRP78 release by inducing its aggregation in the ER. Mechanistically, HDAC inhibitor treatment suppressed HDAC6 activity and led to increased GRP78 acetylation; acetylated GRP78 then bound to VPS34, a class III phosphoinositide-3 kinase, consequently preventing the sorting of GRP78 into multivesicular bodies (MVBs). Of note, we found that mimicking GRP78 acetylation by substituting the lysine at residue 633, one of the deacetylated sites of HDAC6, with a glutamine resulted in decreased GRP78 secretion and impaired tumour cell growth in vitro. Our study thus reveals a hitherto-unknown mechanism of GRP78 secretion and may also provide implications for the therapeutic use of HDAC inhibitors.
C1 [Li, Zongwei; Zhang, Lichao; Yang, Peng; Li, Zhuoyu] Shanxi Univ, Inst Biotechnol, Key Lab Chem Biol & Mol Engn, Natl Minist Educ, Taiyuan 030006, Peoples R China.
   [Li, Zongwei] Univ Texas MD Anderson Canc Ctr, Dept Lymphoma & Myeloma, Div Canc Med, Ctr Canc Immunol Res, Houston, TX 77030 USA.
   [Zhuang, Ming] Shanghai Jiao Tong Univ, Sch Med, Xinhua Hosp, Dept Gen Surg, Shanghai 200092, Peoples R China.
   [Zheng, Xingnan] Univ N Carolina, Lineberger Comprehens Canc Ctr, Sch Med, Chapel Hill, NC 27599 USA.
RP Li, ZY (corresponding author), Shanxi Univ, Inst Biotechnol, Key Lab Chem Biol & Mol Engn, Natl Minist Educ, Taiyuan 030006, Peoples R China.
EM lzy@sxu.edu.cn
RI Li, Zongwei/AAM-4135-2021
FU National Natural Science Foundation of ChinaNational Natural Science
   Foundation of China (NSFC) [31201072, 31271516]; Shanxi Province Science
   Foundation for Outstanding Youths [201601D021007]; Zhejiang Province
   Science Foundation [LY15H280008]
FX This study was supported by the National Natural Science Foundation of
   China (No. 31201072, No. 31271516), the Shanxi Province Science
   Foundation for Outstanding Youths (201601D021007), and the Zhejiang
   Province Science Foundation (LY15H280008).
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NR 41
TC 34
Z9 34
U1 1
U2 13
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 2045-2322
J9 SCI REP-UK
JI Sci Rep
PD JUL 27
PY 2016
VL 6
AR 30406
DI 10.1038/srep30406
PG 11
WC Multidisciplinary Sciences
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Science & Technology - Other Topics
GA DS3BB
UT WOS:000380656700001
PM 27460191
OA Green Published, gold
DA 2022-04-25
ER

PT J
AU Yun, S
   Han, YS
   Lee, JH
   Kim, S
   Lee, SH
AF Yun, Seungpil
   Han, Yong-Seok
   Lee, Jun Hee
   Kim, Sangmin
   Lee, Sang Hun
TI Enhanced Susceptibility to 5-Fluorouracil in Human Colon Cancer Cells by
   Silencing of GRP78
SO ANTICANCER RESEARCH
LA English
DT Article
DE Colon cancer; 5-FU; GRP78; ER stress; apoptosis
ID ENDOPLASMIC-RETICULUM STRESS; UNFOLDED PROTEIN RESPONSE; ER STRESS;
   HEPATOCELLULAR-CARCINOMA; HEME OXYGENASE-1; PROSTATE-CANCER; ROS;
   AUTOPHAGY; HYDROETHIDINE; ACTIVATION
AB Background: Glucose-regulated protein (GRP78), also known as immunoglobulin heavy chain binding protein and as heat shock 70 kDa protein 5, is present in the endoplasmic reticulum (ER) membrane. GRP78 is generally expressed at low concentrations, but is increased by physiological stress. GRP78 is thought to protect against tissue or organ damage under pathological conditions, such as neurotoxic stress, myocardial infarction, or arteriosclerosis. In addition, in tumors, GRP78 expression is much higher than in normal tissues. Furthermore, high levels of GRP78 expression have been shown to increase the risk of malignancy and metastasis in prostate and colon cancer. Because both anticancer drugs and down-regulation of GRP78 expression inhibit cancer progression and growth, we hypothesized that down-regulation of GRP78 expression might lead to enhanced susceptibility of cancer cells to cytotoxic action of 5-fluorouracil (5-FU). Materials and Methods: GRP78 expression was suppressed in LoVo colon cancer cells by utilizing small-interfering RNA (si-GRP78), and the cells were subsequently used to study the antiproliferative and anticancer effects of 5-FU treatment. The signaling pathways responsible for the increase of LoVo cell susceptibility to 5-FU treatment after exposure to GRP78 siRNA were determined by western blot. Results: GRP78 silencing significantly inhibited cell viability and increased apoptosis of LoVo cells. Furthermore, combined treatment with 5-FU and GRP78 siRNA for 12 h reduced cell viability, and increased apoptosis and generation reactive oxygen species more strongly than either of the two treatments applied separately. In order to examine the role of ER stress in increased susceptibility of LoVo cells to 5-FU after pretreatment with GRP78 siRNA, we analyzed expression levels of ER stress marker proteins, such as phosphorylated protein kinase-like endoplasmic reticulum kinase (PERK), phosphorylated eukaryotic initiation factor 2 alpha (eIF2 alpha), activating transcription factor 4 (ATF4), phosphorylated inositol-requiring enzyme 1 alpha (IRE1 alpha), phosphorylated p38, and C/EBP homologous protein (CHOP). Treatment with 5-FU alone increased the expression of ER stress marker proteins, whereas combined exposure to both 5-FU and GRP78 siRNA led to an even stronger effect on these markers. Similar to the pattern of modulation of ER stress protein expression, the levels of apoptosis-related proteins were also more strongly affected by combined exposure to 5-FU and GRP78 siRNA than by single treatments. In particular, expression of Bcl-2-associated X protein (BAX), cleaved caspase-3, and cleaved poly (ADP-ribose) polymerase 1 (PARP1) were increased, whereas the expression of B-cell lymphoma 2 (BCL2) was reduced by these treatments. Conclusion: GRP78 silencing and incubation with 5-FU have synergistic effects on the inhibition of LoVo colon cancer cell growth via the induction of ER stress-dependent apoptosis.
C1 [Yun, Seungpil; Kim, Sangmin] Johns Hopkins Univ, Sch Med, Dept Neurol, Neuroregenerat & Stem Cell Programs,Inst Cell Eng, Baltimore, MD 21205 USA.
   [Han, Yong-Seok; Lee, Sang Hun] Soonchunhyang Univ, Seoul Hosp, Med Sci Res Inst, Seoul, South Korea.
   [Han, Yong-Seok; Lee, Sang Hun] Soonchunhyang Univ, Dept Med Biosci, Asan, South Korea.
   [Lee, Jun Hee] Univ Alabama Birmingham, Birmingham Sch Med, Dept Pharmacol & Toxicol, Birmingham, AL USA.
RP Lee, SH (corresponding author), Soonchunhyang Univ, Soonchunhyang Med Sci Res Inst, Seoul Hosp, 59 Daesagwan Ro,657 Hannam Dong, Seoul 140887, South Korea.
EM jhlee0407@sch.ac.kr; ykckss1114@nate.com
RI lee, sang hun/Q-4650-2019
OI lee, sang hun/0000-0002-9005-5966
FU Soonchunhyang University; National Research Foundation grant - Korean
   governmentNational Research Foundation of Korea
   [NRF-2016R1D1A3B01007727]; Korean Health Technology R&D Project,
   Ministry of Health and Welfare, Republic of Korea [HI14C2253]
FX This study was supported by the Soonchunhyang University Research Fund,
   a National Research Foundation grant funded by the Korean government
   (NRF-2016R1D1A3B01007727), and a grant from the Korean Health Technology
   R&D Project, Ministry of Health and Welfare, Republic of Korea
   (HI14C2253). The funders had no role in study design, data collection or
   analysis, decision to publish, or preparation of the article.
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NR 33
TC 13
Z9 14
U1 0
U2 14
PU INT INST ANTICANCER RESEARCH
PI ATHENS
PA EDITORIAL OFFICE 1ST KM KAPANDRITIOU-KALAMOU RD KAPANDRITI, PO BOX 22,
   ATHENS 19014, GREECE
SN 0250-7005
EI 1791-7530
J9 ANTICANCER RES
JI Anticancer Res.
PD JUN
PY 2017
VL 37
IS 6
BP 2975
EP 2984
DI 10.21873/anticanres.11651
PG 10
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA EW0LG
UT WOS:000402181600025
PM 28551635
OA Bronze
DA 2022-04-25
ER

PT J
AU Walker, T
   Mitchell, C
   Park, MA
   Yacoub, A
   Graf, M
   Rahmani, M
   Houghton, PJ
   Voelkel-Johnson, C
   Grant, S
   Dent, P
AF Walker, Teneille
   Mitchell, Clint
   Park, Margaret A.
   Yacoub, Adly
   Graf, Martin
   Rahmani, Mohamed
   Houghton, Peter J.
   Voelkel-Johnson, Christina
   Grant, Steven
   Dent, Paul
TI Sorafenib and Vorinostat Kill Colon Cancer Cells by CD95-Dependent and
   -Independent Mechanisms
SO MOLECULAR PHARMACOLOGY
LA English
DT Article
ID HISTONE DEACETYLASE INHIBITOR; HUMAN-LEUKEMIA-CELLS; SUBEROYLANILIDE
   HYDROXAMIC ACID; PRIMARY RODENT HEPATOCYTES; SIGNAL-REGULATED KINASE;
   INDUCED APOPTOSIS; DOWN-REGULATION; TUMOR-CELLS;
   HEPATOCELLULAR-CARCINOMA; SYNERGISTIC INTERACTIONS
AB We examined the interaction between the multikinase inhibitor sorafenib and histone deacetylase inhibitors. Sorafenib and vorinostat synergized ( sorafenib + vorinostat) to kill HCT116 and SW480 cells. In SW480 cells, sorafenib + vorinostat increased CD95 plasma membrane levels and promoted death-inducing signal complex ( DISC) formation, and drug toxicity was blocked by knockdown of CD95 or overexpression of cellular FLICE-like inhibitory protein (c-FLIP-s). In SW620 cells that are patient-matched to SW480 cells, sorafenib + vorinostat toxicity was significantly lower, which correlated with a lack of CD95 activation and lower expression of ceramide synthase 6 (LASS6). Overexpression of LASS6 in SW620 cells enhanced drug-induced CD95 activation and enhanced tumor cell killing, whereas knockdown of LASS6 in SW480 cells suppressed CD95 activation. Knocking down LASS6 expression also suppressed CD95 activation in hepatoma, pancreatic, and ovarian cancer cells. In HCT116 cells, sorafenib + vorinostat treatment caused DISC formation without reducing c-FLIP-s expression and did not increase CD95 plasma membrane levels; sorafenib + vorinostat exposure killed HCT116 cells via an intrinsic pathway/caspase 9-dependent mechanism. In HCT116 cells, knockdown of CD95 enhanced sorafenib + vorinostat lethality, which correlated with less drug-induced CD95-dependent autophagy. Sorafenib + vorinostat treatment activated the c-Jun NH2-terminal kinase pathway, which was causal in promoting dissociation of Beclin1 from BCL-2, and in promoting autophagy. Knockdown of Beclin1 expression blocked autophagy and enhanced drug toxicity. Our data demonstrate that treatment of colon cancer cells with sorafenib + vorinostat activates CD95 via de novo ceramide synthesis that promotes viability via autophagy or degrades survival via either the extrinsic or intrinsic pathways.
C1 [Walker, Teneille; Mitchell, Clint; Park, Margaret A.; Grant, Steven; Dent, Paul] Virginia Commonwealth Univ, Dept Biochem, Richmond, VA 23298 USA.
   [Rahmani, Mohamed; Grant, Steven] Virginia Commonwealth Univ, Dept Med, Richmond, VA 23298 USA.
   [Yacoub, Adly] Virginia Commonwealth Univ, Dept Radiat Oncol, Richmond, VA 23298 USA.
   [Graf, Martin] Virginia Commonwealth Univ, Dept Neurosurg, Richmond, VA 23298 USA.
   [Grant, Steven; Dent, Paul] Virginia Commonwealth Univ, Inst Mol Med, Richmond, VA 23298 USA.
   [Voelkel-Johnson, Christina] Med Univ S Carolina, Dept Microbiol & Immunol, Charleston, SC 29425 USA.
   [Houghton, Peter J.] St Jude Childrens Hosp, Dept Mol Pharmacol, Memphis, TN 38105 USA.
RP Dent, P (corresponding author), Virginia Commonwealth Univ, Dept Biochem & Mol Biol, Massey Canc Ctr, 401 Coll St,Room 280A,Box 980035, Richmond, VA 23298 USA.
EM pdent@vcu.edu
OI Rahmani, Mohamed/0000-0002-3992-8039
FU NATIONAL CANCER INSTITUTEUnited States Department of Health & Human
   ServicesNational Institutes of Health (NIH) - USANIH National Cancer
   Institute (NCI) [R01CA063753, P01CA104177, R01CA108520, R01CA093738]
   Funding Source: NIH RePORTER; NATIONAL INSTITUTE OF DIABETES AND
   DIGESTIVE AND KIDNEY DISEASESUnited States Department of Health & Human
   ServicesNational Institutes of Health (NIH) - USANIH National Institute
   of Diabetes & Digestive & Kidney Diseases (NIDDK) [R01DK052825] Funding
   Source: NIH RePORTER; NCI NIH HHSUnited States Department of Health &
   Human ServicesNational Institutes of Health (NIH) - USANIH National
   Cancer Institute (NCI) [R01-CA108520, R01-CA77141, P01-CA104177,
   R01-CA93738, R01-CA63753, R01 CA093738] Funding Source: Medline; NIDDK
   NIH HHSUnited States Department of Health & Human ServicesNational
   Institutes of Health (NIH) - USANIH National Institute of Diabetes &
   Digestive & Kidney Diseases (NIDDK) [R01-DK52825, R01 DK052825] Funding
   Source: Medline
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NR 54
TC 69
Z9 74
U1 0
U2 10
PU AMER SOC PHARMACOLOGY EXPERIMENTAL THERAPEUTICS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3995 USA
SN 0026-895X
EI 1521-0111
J9 MOL PHARMACOL
JI Mol. Pharmacol.
PD AUG
PY 2009
VL 76
IS 2
BP 342
EP 355
DI 10.1124/mol.109.056523
PG 14
WC Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA 472SV
UT WOS:000268153400011
PM 19483104
OA Green Published
DA 2022-04-25
ER

PT J
AU Cai, XM
   Wei, B
   Li, LL
   Chen, XF
   Yang, J
   Li, XF
   Jiang, XZ
   Lv, M
   Li, MY
   Lin, YM
   Xu, Q
   Guo, WJ
   Gu, YH
AF Cai, Xiaomin
   Wei, Bin
   Li, Lele
   Chen, Xiaofeng
   Yang, Jing
   Li, Xiaofei
   Jiang, Xiaozheng
   Lv, Mu
   Li, Mingyang
   Lin, Yumeng
   Xu, Qiang
   Guo, Wenjie
   Gu, Yanhong
TI Therapeutic Potential of Apatinib Against Colorectal Cancer by
   Inhibiting VEGFR2-Mediated Angiogenesis and beta-Catenin Signaling
SO ONCOTARGETS AND THERAPY
LA English
DT Article
DE apatinib; colorectal cancer; VEGFR2; angiogenesis; beta-catenin
ID STEM-CELLS; COLON; ACTIVATION; APOPTOSIS; AUTOPHAGY; DRIVEN; PLUS
AB Purpose: Apatinib is an inhibitor of VEGFR2 (vascular endothelial growth factor receptor 2) that has attracted a great deal of attention due to its promotion of anticancer activity. In the present study, we investigated the therapeutic effects of apatinib against colorectal cancer (CRC) and examined the underlying mechanism.
   Materials and Methods: Both in vivo and in vitro assays were conducted to study the effect of apatinib on CRC. To elucidate the associated mechanism, RNA-seq (transcriptome) analysis was conducted on apatinib-treated HCT116 cells.
   Results: Apatinib showed antiproliferative and proapoptotic effects, induced G0/G1 arrest and blocked cell migration and invasion in CRC. An analysis of the mechanism associated with apatinib activity demonstrated that by interacting with VEGFR2, apatinib decreased p-Src, p-Akt, and p-GSK3 beta levels, which further increased beta-catenin ubiquitination and reduced the nuclear translocation of beta-catenin. Furthermore, apatinib strongly suppressed CT26 cell growth in mouse xenograft models by inhibiting beta-catenin signaling and angiogenesis.
   Conclusion: Overall, the results of the present study here indicated that by inhibiting the VEGFR2-beta-catenin-mediated malignant phenotype, apatinib significantly suppresses the growth of CRC, suggesting that the use of apatinib is a promising therapeutic strategy for CRC.
C1 [Cai, Xiaomin; Wei, Bin; Li, Lele; Chen, Xiaofeng; Yang, Jing; Li, Xiaofei; Jiang, Xiaozheng; Lv, Mu; Li, Mingyang; Gu, Yanhong] Nanjing Med Univ, Affiliated Hosp 1, Dept Oncol, 300 Guangzhou Rd, Nanjing 210029, Peoples R China.
   [Wei, Bin] Nanjing Med Univ, Affiliated Huaian 1 Peoples Hosp, Dept Oncol, Huaian 223300, Peoples R China.
   [Lin, Yumeng; Xu, Qiang; Guo, Wenjie] Nanjing Univ, Sch Life Sci, State Key Lab Pharmaceut Biotechnol, 163 Xianlin Ave, Nanjing 210023, Peoples R China.
RP Gu, YH (corresponding author), Nanjing Med Univ, Affiliated Hosp 1, Dept Oncol, 300 Guangzhou Rd, Nanjing 210029, Peoples R China.; Guo, WJ (corresponding author), Nanjing Univ, Sch Life Sci, State Key Lab Pharmaceut Biotechnol, 163 Xianlin Ave, Nanjing 210023, Peoples R China.
EM guowj@nju.edu.cn; guyhphd@163.com
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NR 48
TC 3
Z9 3
U1 1
U2 3
PU DOVE MEDICAL PRESS LTD
PI ALBANY
PA PO BOX 300-008, ALBANY, AUCKLAND 0752, NEW ZEALAND
SN 1178-6930
J9 ONCOTARGETS THER
JI OncoTargets Ther.
PY 2020
VL 13
BP 11031
EP 11044
DI 10.2147/OTT.S266549
PG 14
WC Biotechnology & Applied Microbiology; Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biotechnology & Applied Microbiology; Oncology
GA OH7TG
UT WOS:000582795800017
PM 33154652
OA Green Published, gold
DA 2022-04-25
ER

PT J
AU Gao, C
   Cao, WP
   Bao, L
   Zuo, W
   Xie, GM
   Cai, TT
   Fu, W
   Zhang, J
   Wu, W
   Zhang, X
   Chen, YG
AF Gao, Chan
   Cao, Weipeng
   Bao, Lan
   Zuo, Wei
   Xie, Guoming
   Cai, Tiantian
   Fu, Wei
   Zhang, Jian
   Wu, Wei
   Zhang, Xu
   Chen, Ye-Guang
TI Autophagy negatively regulates Wnt signalling by promoting Dishevelled
   degradation
SO NATURE CELL BIOLOGY
LA English
DT Article
ID TUMOR-SUPPRESSOR PROTEIN; REQUIRES DIRECT BINDING; CATENIN PATHWAY;
   BETA-CATENIN; UBIQUITINATION; GENE; TUMORIGENESIS; LIGASE; INHIBITION;
   ACTIVATION
AB In eukaryotic cells, autophagy is a highly conserved self-digestion process to promote cell survival in response to nutrient starvation and other metabolic stresses. Autophagy is regulated by cell signalling such as the mTOR (mammalian target of rapamycin) pathway. However, the significance of autophagy in modulation of signal transduction is unclear. Here we show that autophagy negatively regulates Wnt signalling by promoting Dishevelled (Dvl) degradation. Von Hippel-Lindau protein-mediated ubiquitylation is critical for the binding of Dvl2 to p62, which in turn facilitates the aggregation and the LC3-mediated autophagosome recruitment of Dvl2 under starvation; the ubiquitylated Dvl2 aggregates are ultimately degraded through the autophagy-lysosome pathway. Moreover, a reverse correlation between Dvl expression and autophagy is observed in late stages of colon cancer development, indicating that autophagy may contribute to the aberrant activation of Wnt signalling in tumour formation.
C1 [Gao, Chan; Cao, Weipeng; Zuo, Wei; Xie, Guoming; Chen, Ye-Guang] Tsinghua Univ, State Key Lab Biomembrane & Membrane Biotechnol, Beijing 100084, Peoples R China.
   [Gao, Chan; Cao, Weipeng; Zuo, Wei; Xie, Guoming; Cai, Tiantian; Wu, Wei; Chen, Ye-Guang] Tsinghua Univ, Sch Life Sci, Beijing 100084, Peoples R China.
   [Bao, Lan; Zhang, Xu] Chinese Acad Sci, Shanghai Inst Biol Sci, Shanghai 200031, Peoples R China.
   [Fu, Wei] Peking Univ, Hosp 3, Dept Gen Surg, Beijing 100191, Peoples R China.
   [Zhang, Jian] Chinese Acad Sci, Inst Genet & Dev Biol, Beijing 100101, Peoples R China.
RP Chen, YG (corresponding author), Tsinghua Univ, State Key Lab Biomembrane & Membrane Biotechnol, Beijing 100084, Peoples R China.
EM ygchen@tsinghua.edu.cn
RI Gao, Chan/D-7964-2013; Chen, Ye-Guang/L-6998-2019
FU National Natural Science Foundation of ChinaNational Natural Science
   Foundation of China (NSFC) [30930050, 30921004]; 973 ProgramNational
   Basic Research Program of China [2006CB943401, 2010CB833706]
FX We thank Terje Johansen for p62 constructs, Long Yu for human LC3
   construct, Noboru Mizushima for Atg5<SUP>-/-</SUP> MEFs, Masaaki Komatsu
   for Atg7<SUP>-/-</SUP> MEFs, and Li Yu, Rod Nusse, Daniel J. Klionsky,
   Juan Liang and Zhao Chen for suggestions. This work was supported by
   grants from the National Natural Science Foundation of China (30930050
   and 30921004) and the 973 Program (2006CB943401 and 2010CB833706) to
   Y.-G.C.
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NR 57
TC 283
Z9 294
U1 3
U2 52
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 1465-7392
EI 1476-4679
J9 NAT CELL BIOL
JI Nat. Cell Biol.
PD AUG
PY 2010
VL 12
IS 8
BP 781
EP +
DI 10.1038/ncb2082
PG 20
WC Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Cell Biology
GA 634EF
UT WOS:000280561600010
PM 20639871
DA 2022-04-25
ER

PT J
AU Sequeira, D
   Baptista, PV
   Valente, R
   Piedade, MFM
   Garcia, MH
   Morais, TS
   Fernandes, AR
AF Sequeira, Diogo
   Baptista, Pedro V.
   Valente, Ruben
   Piedade, M. Fatima M.
   Garcia, M. Helena
   Morais, Tania S.
   Fernandes, Alexandra R.
TI Cu(I) complexes as new antiproliferative agents against sensitive and
   doxorubicin resistant colorectal cancer cells: synthesis,
   characterization, and mechanisms of action
SO DALTON TRANSACTIONS
LA English
DT Article
AB Cancer is one of the worst health issues worldwide, representing the second leading cause of death. Current chemotherapeutic drugs face some challenges like the acquired resistance of the tumoral cells and low specificity leading to unwanted side effects. There is an urgent need to develop new compounds that may target resistant cells. The synthesis and characterization of two Cu(I) complexes of general formula [Cu(PP)(LL)][BF4], where PP is a phosphane ligand (triphenylphosphine or 1,2-bis(diphenylphosphano) ethane) and LL = is a heteroaromatic bidentate ligand (4,4'-dimethyl-2,2'-bipyridine and 6,3-(2-pyridyl)-5,6-diphenyl-1,2,4-triazine). The new compounds were fully characterized by spectroscopic techniques (NMR, FTIR and UV-vis.), elemental analysis (C, H, N and S) and two structures were determined by single X-ray diffraction studies. The antiproliferative potential of the new Cu(I) complexes were studied in tumor (breast adenocarcinoma, ovarian carcinoma and in colorectal carcinoma sensitive and resistant to doxorubicin) and normal (fibroblasts) cell lines. Complexes 1-4 did not show any antiproliferative potential. Amongst the complexes 5-8, complex 8 shows high cytotoxic potential against colorectal cancer sensitive and resistant to doxorubicin and low cytotoxicity towards healthy cells. We show that complexes 5-8 can cleave pDNA and, in particular, the in vitro pDNA cleavage is due to an oxidative mechanism. This oxidative mechanism corroborates the induction of reactive oxygen species (ROS), that triggers HCT116 cell death via apoptosis, as proved by the increased expression of BAX protein relative to BCL-2 protein and the depolarization of mitochondrial membrane potential, and via autophagy. Additionally, complex 8 can block the cell cycle in the G1 phase, also exhibiting a cytostatic potential. Proteomic analysis confirmed the apoptotic, autophagic and cytostatic potential of complex 8, as well as its ability to produce ROS and cause DNA damage. The interference of the complex in folding and protein synthesis and its ability to cause post-translational modifications was also verified. Finally, it was observed that the complex causes a reduction in cellular metabolism. The results herein demonstrated the potential of Cu(I) complexes in targeting doxorubicin sensitive and resistant cells which is positive and must be further explored using in vivo animal models.
C1 [Sequeira, Diogo; Baptista, Pedro V.; Valente, Ruben; Fernandes, Alexandra R.] Univ Nova Lisboa, Fac Ciencias & Tecnol, Dept Ciencias Vida, UCIBIO, Lisbon, Portugal.
   [Piedade, M. Fatima M.; Garcia, M. Helena; Morais, Tania S.] Univ Lisbon, Fac Ciencias, Dept Quim & Bioquim, DQB FCUL, Lisbon, Portugal.
   [Piedade, M. Fatima M.] Univ Lisbon, Inst Super Tecn, Ctr Quim Estrutural, CCQE IST, Lisbon, Portugal.
   [Garcia, M. Helena; Morais, Tania S.] Univ Lisbon, Fac Ciencias, Ctr Quim Estrutural, CQE FCUL, Lisbon, Portugal.
RP Fernandes, AR (corresponding author), Univ Nova Lisboa, Fac Ciencias & Tecnol, Dept Ciencias Vida, UCIBIO, Lisbon, Portugal.; Morais, TS (corresponding author), Univ Lisbon, Fac Ciencias, Dept Quim & Bioquim, DQB FCUL, Lisbon, Portugal.; Morais, TS (corresponding author), Univ Lisbon, Fac Ciencias, Ctr Quim Estrutural, CQE FCUL, Lisbon, Portugal.
EM tsmorais@ciencias.ulisboa.pt; ma.fernandes@fct.unl.pt
RI Morais, Tânia S./D-8824-2011; Garcia, Maria Helena/H-2175-2013;
   Fernandes, Alexandra/C-7465-2011; Baptista, Pedro/A-1237-2009
OI Morais, Tânia S./0000-0003-0233-8243; Garcia, Maria
   Helena/0000-0002-4344-2218; Valente, Ruben/0000-0001-6534-4128;
   Fernandes, Alexandra/0000-0003-2054-4438; Baptista,
   Pedro/0000-0001-5255-7095
FU Applied Molecular Biosciences Unit - UCIBIO - FCT [UIDB/04378/2020];
   Centro de Quimica Estrutural - FCT [UIDB/00100/2020]; FCTPortuguese
   Foundation for Science and TechnologyEuropean Commission
   [CEECIND/00630/2017]
FX This work was supported by the Applied Molecular Biosciences Unit -
   UCIBIO and Centro de Quimica Estrutural which are financed by national
   funds from FCT (UIDB/04378/2020 and UIDB/00100/2020, respectively). T.
   S. Morais thanks FCT for CEECIND 2017 Initiative for the project
   CEECIND/00630/2017 (acknowledging FCT, as well as POPH and FSE-European
   Social Fund). M. Silva and C. Fonseca are also acknowledged for
   preliminary fluorescence microscopy and viability data, respectively.
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NR 73
TC 2
Z9 2
U1 4
U2 13
PU ROYAL SOC CHEMISTRY
PI CAMBRIDGE
PA THOMAS GRAHAM HOUSE, SCIENCE PARK, MILTON RD, CAMBRIDGE CB4 0WF, CAMBS,
   ENGLAND
SN 1477-9226
EI 1477-9234
J9 DALTON T
JI Dalton Trans.
PD FEB 7
PY 2021
VL 50
IS 5
BP 1845
EP 1865
DI 10.1039/d0dt03566a
PG 21
WC Chemistry, Inorganic & Nuclear
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Chemistry
GA QE6SV
UT WOS:000616337100034
PM 33470993
DA 2022-04-25
ER

PT J
AU Rong, L
   Li, ZD
   Leng, X
   Li, HY
   Ma, YP
   Chen, YK
   Song, FZ
AF Rong, Li
   Li, Zhaodong
   Leng, Xue
   Li, Haiyu
   Ma, Yongping
   Chen, Yaokai
   Song, Fangzhou
TI Salidroside induces apoptosis and protective autophagy in human gastric
   cancer AGS cells through the PI3K/Akt/mTOR pathway
SO BIOMEDICINE & PHARMACOTHERAPY
LA English
DT Article
DE Salidroside; Gastric cancer; Apoptosis; Autophagy; PI3K/AKT/mTOR
ID MTOR PATHWAY; DISEASE; CHINA
AB Salidroside, a natural active ingredient extracted from Rhodiola rosea, has been shown to exert antitumor activity against breast cancer Dong Young et al. [1], colon cancer Sun et al. [2] and bladder cancer Tian et al. [3]. However, the effect of salidroside on apoptosis and autophagy in gastric cancer remains unclear. In our research, we observed the biological effect of salidroside on human gastric cancer AGS cells. Our results demonstrated that salidroside inhibited the growth of AGS cells both in vivo and in vitro and exerted a proapoptotic effect on AGS cells as confirmed by flow cytometry, Hoechst staining and western blot analysis. Additionally, we found that salidroside decreased the phosphorylation of PI3K and Akt and that pretreatment with the PI3K/Akt agonist IGF-1 could weaken the proapoptotic effect of salidroside. Interestingly, the exposure of AGS cells to salidroside induced autophagy as indicated by transmission electron microscopy, mRFP-GFP-LC3 transfection and western blot analysis, suggesting that salidroside promoted autophagy in gastric cancer AGS cells. Furthermore, treatment with the autophagy inhibitor chloroquine enhanced salidroside-induced cell apoptosis, indicating that the autophagy mediated by salidroside may protect AGS cells from death. Additionally, we found that salidroside decreased the level of p-mTOR protein in a concentration-dependent manner and that pretreatment with IGF-1 decreased the expression of autophagy proteins, suggesting that salidroside induced autophagy through the PI3K/Akt/mTOR pathway. The above findings indicate that salidroside inhibited the growth of gastric cancer and induced apoptosis and protective autophagy through the PI3K/Akt/mTOR pathway. In summary, our study provides novel insights regarding the activity of salidroside against gastric cancer and contributes to the clinical application of salidroside combined with autophagy inhibitors as a chemotherapeutic strategy for human gastric cancer.
C1 [Rong, Li; Li, Zhaodong; Leng, Xue; Li, Haiyu; Ma, Yongping; Song, Fangzhou] Chongqing Med Univ, Basic Med Coll, 1 Med Coll Rd, Chongqing 400016, Peoples R China.
   [Rong, Li; Li, Haiyu; Chen, Yaokai] Chongqing Publ Hlth Med Ctr, 109 Baoyu Rd, Chongqing 400036, Peoples R China.
RP Song, FZ (corresponding author), Chongqing Med Univ, Basic Med Coll, 1 Med Coll Rd, Chongqing 400016, Peoples R China.; Chen, YK (corresponding author), Chongqing Publ Hlth Med Ctr, 109 Baoyu Rd, Chongqing 400036, Peoples R China.
EM l3883886491@163.com; 19702119@qq.com; 904561548@qq.com;
   lihaiyu@stu.cqmu.edu.cn; 93404551@qq.com; yaokaichen@hotmail.com;
   fzsongcq@163.com
OI Song, Fang/0000-0002-4083-3889
FU TCM Science and Technology Project of Chongqing Health and Family
   Planning Commission [ZY201702048]; Chongqing natural science
   foundationNatural Science Foundation of Chongqing
   [cstc2019jcyj-msxmX0428]; National Science and Technology Major Project
   of China [2018ZX10302104]
FX 1. TCM Science and Technology Project of Chongqing Health and Family
   Planning Commission, Project number: ZY201702048.; 2. Chongqing natural
   science foundation, Project number:cstc2019jcyj-msxmX0428; 3. The
   National Science and Technology Major Project of China during the 13th
   five-year plan period. Project number: 2018ZX10302104.
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NR 31
TC 34
Z9 35
U1 4
U2 20
PU ELSEVIER FRANCE-EDITIONS SCIENTIFIQUES MEDICALES ELSEVIER
PI ISSY-LES-MOULINEAUX
PA 65 RUE CAMILLE DESMOULINS, CS50083, 92442 ISSY-LES-MOULINEAUX, FRANCE
SN 0753-3322
EI 1950-6007
J9 BIOMED PHARMACOTHER
JI Biomed. Pharmacother.
PD FEB
PY 2020
VL 122
AR 109726
DI 10.1016/j.biopha.2019.109726
PG 9
WC Medicine, Research & Experimental; Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Research & Experimental Medicine; Pharmacology & Pharmacy
GA KA7VF
UT WOS:000506005800044
PM 31918283
OA gold
DA 2022-04-25
ER

PT J
AU Liu, J
   Zhang, Y
   Qu, JL
   Xu, L
   Hou, KZ
   Zhang, JD
   Qu, XJ
   Liu, YP
AF Liu, Jing
   Zhang, Ye
   Qu, Jinglei
   Xu, Ling
   Hou, Kezuo
   Zhang, Jingdong
   Qu, Xiujuan
   Liu, Yunpeng
TI beta-Elemene-induced autophagy protects human gastric cancer cells from
   undergoing apoptosis
SO BMC CANCER
LA English
DT Article
ID MAMMALIAN TARGET; COLON-CANCER; TUMOR-CELLS; P38 MAPK; DEATH;
   INHIBITION; ACTIVATION; PI3K/AKT; ANTIBODY; THERAPY
AB Background: beta-Elemene, a compound found in an herb used in traditional Chinese medicine, has shown promising anti-cancer effects against a broad spectrum of tumors. The mechanism by which beta elemene kills cells remains unclear. The aim of the present study is to investigate the anti-tumor effect of beta-elemene on human gastric cancer cells and the molecular mechanism involved.
   Results: beta-Elemene inhibited the viability of human gastric cancer MGC803 and SGC7901 cells in a dose-dependent manner. The suppression of cell viability was due to the induction of apoptosis. A robust autophagy was observed in the cells treated with beta-elemene; it was characterized by the increase of punctate LC3 dots, the cellular morphology, and the increased levels of LC3 II protein. Further study showed that beta elemene treatment up-regulated Atg5-Atg12 conjugated protein but had little effect on other autophagy-related proteins. PI3K/Akt/mTOR/p70S6K1 activity was inhibited by beta-elemene. Knockdown of Beclin 1 with small interfering RNA, or co-treatment with the autophagy inhibitor, 3-methyladenine or chlorochine enhanced significantly the antitumor effects of beta-elemene.
   Conclusions: Our data provides the first evidence that beta-elemene induces protective autophagy and prevents human gastric cancer cells from undergoing apoptosis. A combination of beta-elemene with autophagy inhibitor might thus be a useful therapeutic option for advanced gastric cancer.
C1 [Liu, Jing; Zhang, Ye; Qu, Jinglei; Xu, Ling; Hou, Kezuo; Zhang, Jingdong; Qu, Xiujuan; Liu, Yunpeng] China Med Univ, Hosp 1, Dept Med Oncol, Shenyang 110001, Peoples R China.
RP Qu, XJ (corresponding author), China Med Univ, Hosp 1, Dept Med Oncol, Shenyang 110001, Peoples R China.
EM qu_xiujuan2001@yahoo.co.jp; cmuliuyunpeng@yahoo.cn
FU Chinese National Foundation of National Sciences [30770993]; China
   Postdoctor Foundation of Science [20070411081]; The First Hospital of
   China Medical University [fsfh1002]; CSCO-King Kong Elemene
FX YL (Chinese National Foundation of National Sciences grants 30770993);
   XQ (China Postdoctor Foundation of Science grants 20070411081); JL (Fund
   for Scientific Research of The First Hospital of China Medical
   University, fsfh1002); YZ (The Doctor Startup Fund Program Funded by
   CSCO-King Kong Elemene).
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NR 33
TC 110
Z9 121
U1 2
U2 39
PU BMC
PI LONDON
PA CAMPUS, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 1471-2407
J9 BMC CANCER
JI BMC Cancer
PD MAY 20
PY 2011
VL 11
AR 183
DI 10.1186/1471-2407-11-183
PG 10
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA 778CK
UT WOS:000291676600001
PM 21595977
OA Green Published, gold
DA 2022-04-25
ER

PT J
AU Zuo, Q
   Liao, L
   Yao, ZT
   Liu, YP
   Wang, DK
   Li, SJ
   Yin, XF
   He, QY
   Xu, WW
AF Zuo, Qian
   Liao, Long
   Yao, Zi-Ting
   Liu, Ya-Ping
   Wang, Ding-Kang
   Li, Shu-Jun
   Yin, Xing-Feng
   He, Qing-Yu
   Xu, Wen-Wen
TI Targeting PP2A with lomitapide suppresses colorectal tumorigenesis
   through the activation of AMPK/Beclin1-mediated autophagy
SO CANCER LETTERS
LA English
DT Article
DE Lomitapide; Colorectal cancer; PP2A inhibitor; AMPK; Autophagy
ID CANCER; CARCINOMA; AMPK; ASSOCIATION; INHIBITION; MODULATION; APOPTOSIS;
   PATHWAY; CELLS; MAP
AB Colorectal cancer (CRC) is one of the most common malignancies worldwide, and effective therapy remains a challenge. In this study, we take advantage of a drug repurposing strategy to screen small molecules with novel anticancer activities in a small-molecule library consisting of 1056 FDA-approved drugs. We show, for the first time, that lomitapide, a lipid-lowering agent, exhibits antitumor properties in vitro and in vivo. Activated autophagy is characterized as a key biological process in lomitapide-induced CRC repression. Mechanistically, lomitapide stimulated mitochondrial dysfunction-mediated AMPK activation, resulting in increased AMPK phosphorylation and enhanced Beclin1/Atg14/Vps34 interactions, provoking autophagy induction. Autophagy inhibition or AMPK silencing significantly abrogated lomitapide-induced cell death, indicating the significance of AMPK-regulated autophagy in the antitumor activities of lomitapide. More importantly, PP2A was identified as a direct target of lomitapide by limited proteolysis-mass spectrometry (LiP-SMap), and the bioactivity of lomitapide was attenuated in PP2A-deficient cells, suggesting that the anticancer effect of lomitapide occurs in a PP2Adependent manner. Taken together, the results of the study reveal that lomitapide can be repositioned as a potential therapeutic drug for CRC treatment.
C1 [Zuo, Qian; Liao, Long; Yao, Zi-Ting; Liu, Ya-Ping; Wang, Ding-Kang; Li, Shu-Jun; Yin, Xing-Feng; He, Qing-Yu] Jinan Univ, Coll Life Sci & Technol, Inst Life & Hlth Engn, MOE Key Lab Tumor Mol Biol, Guangzhou 510632, Peoples R China.
   [Zuo, Qian; Liao, Long; Yao, Zi-Ting; Liu, Ya-Ping; Wang, Ding-Kang; Li, Shu-Jun; Yin, Xing-Feng; He, Qing-Yu] Jinan Univ, Coll Life Sci & Technol, Inst Life & Hlth Engn, Key Lab Funct Prot Res Guangdong Higher Educ Inst, Guangzhou 510632, Peoples R China.
   [Xu, Wen-Wen] Jinan Univ, Coll Life Sci & Technol, Natl Engn Res Ctr Genet Med, Inst Biomed,MOE Key Lab Tumor Mol Biol, Guangzhou 510632, Peoples R China.
   [Xu, Wen-Wen] Jinan Univ, Coll Life Sci & Technol, Natl Engn Res Ctr Genet Med, Inst Biomed,Guangdong Prov Key Lab Bioengn Med, Guangzhou 510632, Peoples R China.
RP Xu, WW (corresponding author), Jinan Univ, Natl Engn Res Ctr Genet Med, Inst Biomed, Guangdong Prov Key Lab Bioengn Med, Guangzhou 510632, Peoples R China.
EM xuwen6966@163.com
FU National Natural Science Foundation of China of ChinaNational Natural
   Science Foundation of China (NSFC) [82073196, 81803551, 31770888];
   National Key R&D Program of China [2017YFA0505100]; Guangdong Natural
   Science Research Grant International joint project [2021A0505030035];
   Guangdong Natural Science Research Grant [2021A1515011158,
   2020A1515110760]; Fundamental Research Funds for the Central
   UniversitiesFundamental Research Funds for the Central Universities
   [21620429]
FX This research was supported by National Natural Science Foundation of
   China of China (82073196, 81803551, 31770888) , National Key R&D Program
   of China (2017YFA0505100) , Guangdong Natural Science Research Grant
   International joint project (2021A0505030035) , Guangdong Natural
   Science Research Grant (2021A1515011158, 2020A1515110760) , and the
   Fundamental Research Funds for the Central Universities (21620429) .
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NR 57
TC 0
Z9 0
U1 9
U2 14
PU ELSEVIER IRELAND LTD
PI CLARE
PA ELSEVIER HOUSE, BROOKVALE PLAZA, EAST PARK SHANNON, CO, CLARE, 00000,
   IRELAND
SN 0304-3835
EI 1872-7980
J9 CANCER LETT
JI Cancer Lett.
PD NOV 28
PY 2021
VL 521
BP 281
EP 293
DI 10.1016/j.canlet.2021.09.010
EA SEP 2021
PG 13
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA WB3UH
UT WOS:000703500300001
PM 34509534
DA 2022-04-25
ER

PT J
AU Krmpot, AJ
   Janjetovic, KD
   Misirkic, MS
   Vucicevic, LM
   Pantelic, DV
   Vasiljevic, DM
   Popadic, DM
   Jelenkovic, BM
   Trajkovic, VS
AF Krmpot, Aleksandar J.
   Janjetovic, Kristina D.
   Misirkic, Maja S.
   Vucicevic, Ljubica M.
   Pantelic, Dejan V.
   Vasiljevic, Darko M.
   Popadic, Dusan M.
   Jelenkovic, Branislav M.
   Trajkovic, Vladimir S.
TI Protective Effect of Autophagy in Laser-Induced Glioma Cell Death In
   Vitro
SO LASERS IN SURGERY AND MEDICINE
LA English
DT Article
DE apoptosis; cancer; necrosis; phototherapy
ID TUMOR-NECROSIS-FACTOR; COLORECTAL LIVER METASTASES; PHOTODYNAMIC
   THERAPY; INDUCED APOPTOSIS; CANCER-CELLS; MAMMALIAN-CELLS; PKC
   ACTIVATION; IRRADIATION; PROLIFERATION; THERMOTHERAPY
AB Background and Objective: Laser phototherapy could be potentially used for cancer treatment, but the mechanisms of laser-induced cell death are not completely understood. Autophagy is the process in which the damaged cellular proteins and organelles are engulfed by and destroyed in acidified multiple-membrane vesicles. The aim of the present study was to investigate the role of autophagy in laser-induced tumor cell death in vitro.
   Study Design/Materials and Methods: The monolayers of U251 human glioma tumor cells were exposed to 532 nm laser light from a single mode frequency-doubled Nd-YVO4 laser. A flattened Gaussian radial profile of laser beam (0.5-4W) was used to uniformly illuminate entire colony of cells for various amounts of time (15-120 seconds) in the absence of cell culture medium. The cells were grown for 24 hours and the cell viability was determined by crystal violet or MTT assay. The presence of autophagy was assessed after 16 hours by fluorescence microscopy/flow cytometric analysis of acridine orange-stained autophagolysosomes and Western blot analysis of the autophagosome-associated LC3-II protein. The concentration of the principal pro-autophagic protein beclin-1 was determined after 6 hours by cell-based ELISA.
   Results: The intracytoplasmic accumulation of autophagic vesicles, increase in LC3-II and up-regulation of beclin-1 expression were clearly observed under irradiation conditions that caused approximately 50% cytotoxicity. Postirradiation addition of three different autophagy inhibitors (bafilomycin A1, chloroquine, or wortmannin) further increased the laser-induced cytotoxicity, without affecting non-irradiated cells.
   Conclusions: These data indicate that beclin-1-dependent induction of autophagy can protect glioma cells from laser-mediated cytotoxicity. Lasers Surg. Med. 42:338-347, 2010. (C) 2010 Wiley-Liss, Inc.
C1 [Janjetovic, Kristina D.; Misirkic, Maja S.; Vucicevic, Ljubica M.; Popadic, Dusan M.; Trajkovic, Vladimir S.] Univ Belgrade, Sch Med, Inst Microbiol & Immunol, Belgrade 11000, Serbia.
   [Krmpot, Aleksandar J.; Pantelic, Dejan V.; Vasiljevic, Darko M.; Jelenkovic, Branislav M.] Univ Belgrade, Inst Phys, Belgrade 11080, Serbia.
   [Janjetovic, Kristina D.; Misirkic, Maja S.; Vucicevic, Ljubica M.; Popadic, Dusan M.] Inst Biol Res, Belgrade 11000, Serbia.
RP Trajkovic, VS (corresponding author), Univ Belgrade, Sch Med, Inst Microbiol & Immunol, Dr Subotica 1, Belgrade 11000, Serbia.
EM krmpot@phy.bg.ac.rs; vtrajkovic@eunet.rs
RI Jelenkovic, Brana/AAE-8831-2020; Vasiljević, Darko/R-8265-2019; Krmpot,
   Aleksandar/C-4975-2011; Vasiljević, Darko/ABA-3894-2020
OI Vasiljević, Darko/0000-0001-6737-6000; Misirkic Marjanovic,
   Maja/0000-0002-0510-826X; Krmpot, Aleksandar/0000-0003-2751-7395;
   Janjetovic, Kristina/0000-0003-1387-480X; Vucicevic,
   Ljubica/0000-0003-2802-2773; Popadic, Dusan/0000-0002-7502-1709;
   Trajkovic, Vladimir/0000-0002-8061-2968
FU Ministry of Science of the Republic of SerbiaMinistry of Education,
   Science & Technological Development, Serbia [145073, 141003]
FX Contract grant sponsor: Ministry of Science of the Republic of Serbia;
   Contract grant numbers: 145073, 141003.
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NR 58
TC 10
Z9 11
U1 1
U2 12
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0196-8092
EI 1096-9101
J9 LASER SURG MED
JI Lasers Surg. Med.
PD APR
PY 2010
VL 42
IS 4
BP 338
EP 347
DI 10.1002/lsm.20911
PG 10
WC Dermatology; Surgery
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Dermatology; Surgery
GA 592UZ
UT WOS:000277407500008
PM 20432283
DA 2022-04-25
ER

PT J
AU Ortiz, LMG
   Lombardi, P
   Tillhon, M
   Scovassi, AI
AF Ortiz, Luis Miguel Guaman
   Lombardi, Paolo
   Tillhon, Micol
   Scovassi, Anna Ivana
TI Berberine, an Epiphany Against Cancer
SO MOLECULES
LA English
DT Review
DE apoptosis; autophagy; berberine; cancer; traditional medicine
ID ACTIVATED PROTEIN-KINASE; DNA TOPOISOMERASE-I; INDUCED
   GROWTH-INHIBITION; LEUKEMIA HL-60 CELLS; INDUCED APOPTOSIS;
   DOWN-REGULATION; ALKALOID BERBERINE; CARCINOMA-CELLS; COLON-CANCER;
   LUNG-CANCER
AB Alkaloids are used in traditional medicine for the treatment of many diseases. These compounds are synthesized in plants as secondary metabolites and have multiple effects on cellular metabolism. Among plant derivatives with biological properties, the isoquinoline quaternary alkaloid berberine possesses a broad range of therapeutic uses against several diseases. In recent years, berberine has been reported to inhibit cell proliferation and to be cytotoxic towards cancer cells. Based on this evidence, many derivatives have been synthesized to improve berberine efficiency and selectivity; the results so far obtained on human cancer cell lines support the idea that they could be promising agents for cancer treatment. The main properties of berberine and derivatives will be illustrated.
C1 [Ortiz, Luis Miguel Guaman; Tillhon, Micol; Scovassi, Anna Ivana] Ist Genet Mol CNR, I-27100 Pavia, Italy.
   [Ortiz, Luis Miguel Guaman] Univ Tecn Particular Loja, Dept Ciencias Salud, Calle Paris 1101608, Loja, Ecuador.
   [Lombardi, Paolo] Naxospharma, I-20026 Novate Milanese, Italy.
RP Scovassi, AI (corresponding author), Ist Genet Mol CNR, Via Abbiategrasso 207, I-27100 Pavia, Italy.
EM lmguaman@utpl.edu.ec; p.lombardi@naxospharma.eu; tillhon@igm.cnr.it;
   scovassi@igm.cnr.it
RI Ortiz, Luis Miguel Guaman/X-9496-2019; Tillhon, Micol/AAQ-6994-2020
OI Ortiz, Luis Miguel Guaman/0000-0003-2919-4905; Lombardi,
   Paolo/0000-0002-7971-7404; Scovassi, Anna Ivana/0000-0003-3484-9881
FU SENESCYT (Quito, Ecuador); Universidad Tecnica Particular de Loja (Loja,
   Ecuador); Italian AIRCFondazione AIRC per la ricerca sul cancro
FX LMGO is a PhD student (Dottorato in Genetica, Biologia Cellulare e
   Molecolare, University of Pavia, Italy) supported by SENESCYT (Quito,
   Ecuador) and Universidad Tecnica Particular de Loja (Loja, Ecuador); MT
   is a post-doc supported by Italian AIRC. The authors acknowledge
   Lucrezia Lombardi for English revision of the text.
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NR 127
TC 150
Z9 164
U1 10
U2 65
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 1420-3049
J9 MOLECULES
JI Molecules
PD AUG
PY 2014
VL 19
IS 8
BP 12349
EP 12367
DI 10.3390/molecules190812349
PG 19
WC Biochemistry & Molecular Biology; Chemistry, Multidisciplinary
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Chemistry
GA AO6ZW
UT WOS:000341502600092
PM 25153862
OA gold, Green Published
DA 2022-04-25
ER

PT J
AU Deng, YL
   Li, S
   Wang, M
   Chen, XT
   Tian, L
   Wang, LQ
   Yang, WY
   Chen, LZ
   He, F
   Yin, WY
AF Deng, Yuanle
   Li, Sha
   Wang, Meng
   Chen, Xiaotong
   Tian, Li
   Wang, Liqun
   Yang, Wenyu
   Chen, Lezhang
   He, Fang
   Yin, Wenya
TI Flavonoid-rich extracts from okra flowers exert antitumor activity in
   colorectal cancer through induction of mitochondrial
   dysfunction-associated apoptosis, senescence and autophagy
SO FOOD & FUNCTION
LA English
DT Article
ID CELL-PROLIFERATION; COLON-CANCER; P53; INVASION; METASTASIS;
   POLYMORPHISMS; MORTALITY; MIGRATION; SURVIVAL; MMP-2
AB Okra flowers contain a higher content of total flavonoids than most other flowers; however little research has been conducted on their potential benefits, including antitumor activity. In this study, we extracted and purified flavonoids from okra flower (AFE), and aimed to evaluate the effect of AFE and its underlying mechanism on colorectal cancer (CRC) cell growth in vitro and in vivo. Here, we identify that AFE is a safe, natural antioxidant and exerts significant antitumor efficacy on the inhibition of CRC cell proliferation and metastasis as well as tumour growth in vivo. We further reveal that AFE inhibits CRC cell proliferation by inducing mitochondrial dysfunction, which results from the activation of p53 and induction of apoptosis and senescence, and inhibits autophagic degradation. Furthermore, AFE inhibited migration and invasion of CRC cells by regulating the balance of MMP2/TIMP2 and MMP9 expression levels. Of note, administration of AFE as a preventive agent achieves a more effective antitumor effect than the therapeutic agent in a xenograft mouse model. Our results reveal, for the first time, that AFE is a safe, natural antioxidant with significant antitumor efficacy, which has great potential in the application for CRC prevention and treatment.
C1 [Deng, Yuanle; Li, Sha; Chen, Xiaotong; Tian, Li; Wang, Liqun; He, Fang; Yin, Wenya] Sichuan Univ, West China Sch Publ Hlth, Chengdu 610041, Sichuan, Peoples R China.
   [Deng, Yuanle; Li, Sha; Chen, Xiaotong; Tian, Li; Wang, Liqun; He, Fang; Yin, Wenya] Sichuan Univ, West China Hosp 4, Chengdu 610041, Sichuan, Peoples R China.
   [Wang, Meng; Yang, Wenyu] Xihua Univ, Sch Food Sci & Bioengn, Pharmaceut Engn, Chengdu 610039, Sichuan, Peoples R China.
   [Chen, Lezhang] Sichuan Huitai Agr Technol Co LTD, Chengdu, Peoples R China.
RP He, F; Yin, WY (corresponding author), Sichuan Univ, West China Sch Publ Hlth, Chengdu 610041, Sichuan, Peoples R China.; He, F; Yin, WY (corresponding author), Sichuan Univ, West China Hosp 4, Chengdu 610041, Sichuan, Peoples R China.
EM hf18602880124@163.com; yinwenya@scu.edu.cn
OI Yin, Wenya/0000-0001-7698-6871; Deng, Yuanle/0000-0002-5748-585X
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NR 71
TC 6
Z9 6
U1 2
U2 18
PU ROYAL SOC CHEMISTRY
PI CAMBRIDGE
PA THOMAS GRAHAM HOUSE, SCIENCE PARK, MILTON RD, CAMBRIDGE CB4 0WF, CAMBS,
   ENGLAND
SN 2042-6496
EI 2042-650X
J9 FOOD FUNCT
JI Food Funct.
PD DEC 1
PY 2020
VL 11
IS 12
BP 10448
EP 10466
DI 10.1039/d0fo02081h
PG 19
WC Biochemistry & Molecular Biology; Food Science & Technology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Food Science & Technology
GA PG8DY
UT WOS:000599960700015
PM 33241810
DA 2022-04-25
ER

PT J
AU Chowchaikong, N
   Nilwarangkoon, S
   Laphookhieo, S
   Tanunyutthawongse, C
   Watanapokasin, R
AF Chowchaikong, Nittiya
   Nilwarangkoon, Sirinun
   Laphookhieo, Surat
   Tanunyutthawongse, Chantra
   Watanapokasin, Ramida
TI p38 inhibitor inhibits the apoptosis of cowanin-treated human colorectal
   adenocarcinoma cells
SO INTERNATIONAL JOURNAL OF ONCOLOGY
LA English
DT Article
DE cowanin; colorectal cancer; apoptosis; mitogen-activated protein kinase;
   p38 inhibitor
ID ACTIVATED PROTEIN-KINASE; SIGNALING PATHWAYS; BCL-2 FAMILY; CANCER;
   DEATH; COLON; MITOCHONDRIAL; REGULATORS; XANTHONES; AUTOPHAGY
AB Colorectal cancer, which is the third most common type of cancer diagnosed in both men and women, is the leading cause of cancer-related deaths worldwide. Cowanin is a pure compound extracted from Garcinia cowa Roxb., a tree species present in Thailand, Malaysia and Myanmar. The crude extract has been demonstrated to have antitumor activity, inflammation induction, antibacterial activity, anti-inflammatory activity and antimalarial activity. In the present study, the effects of cowanin on apoptosis induction and on the apoptosis-related and mitogen-activated protein kinase (MAPK) pathways were investigated in the LoVo human colorectal cancer cell line. The cytotoxicity of cowanin in LoVo cells was determined by MTT assay. Hoechst 33342 and JC-1 staining were used to determine nuclear morphological changes and mitochondrial membrane potential, respectively. The expression levels of BCL2 apoptosis regulator (Bcl-2) family, MAPK and AKT serine/threonine kinase 1 (Akt) pathway proteins following cowanin treatment were determined by western blot analysis. The results demonstrated that cowanin inhibited cell proliferation and induced cell death via the apoptosis pathway. Cowanin treatment increased BCL2 associated X (Bax) and decreased Bcl-2 expression. In addition, cowanin activated caspase-9, -7 and poly-ADP-ribose-polymerase expression. Furthermore, cowanin decreased the levels of phosphorylated extracellular signal-regulated kinase (p-ERK), p-Akt, p-3-phosphoinositide-dependent protein kinase-1, while it increased p-p38 expression, thus resulting in the induction of apoptosis. In conclusion, cowanin inhibited cell proliferation and induced apoptosis of LoVo cells via the MAPK and Akt signaling pathways. Notably, inhibition of p38 by using a p38 inhibitor (SB203580) prevented the cowanin-induced apoptosis in LoVo cells. These results suggested that cowanin may be a potential candidate for the treatment of colorectal cancer and provided important information on the molecular mechanisms underlying its antitumor activity.
C1 [Chowchaikong, Nittiya; Nilwarangkoon, Sirinun; Tanunyutthawongse, Chantra; Watanapokasin, Ramida] Srinakharinwirot Univ, Fac Med, Dept Biochem, 114 Sukhumvit 23, Bangkok 10110, Thailand.
   [Laphookhieo, Surat] Mae Fah Luang Univ, Fac Sci, Dept Chem, Muang 57100, Chiang Rai, Thailand.
RP Watanapokasin, R (corresponding author), Srinakharinwirot Univ, Fac Med, Dept Biochem, 114 Sukhumvit 23, Bangkok 10110, Thailand.
EM ramidaw@g.swu.ac.th
RI laphookhieo, surat/AAA-9701-2019
OI laphookhieo, surat/0000-0002-4757-2781
FU Royal Golden Jubilee (RGJ) Ph.D. Program from the Thailand Research Fund
   (TRF) [PHD/0143/2553]
FX This study was supported by the Royal Golden Jubilee (RGJ) Ph.D. Program
   (grant no. PHD/0143/2553) from the Thailand Research Fund (TRF).
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NR 50
TC 6
Z9 6
U1 3
U2 10
PU SPANDIDOS PUBL LTD
PI ATHENS
PA POB 18179, ATHENS, 116 10, GREECE
SN 1019-6439
EI 1791-2423
J9 INT J ONCOL
JI Int. J. Oncol.
PD JUN
PY 2018
VL 52
IS 6
BP 2031
EP 2040
DI 10.3892/ijo.2018.4353
PG 10
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA GF8RW
UT WOS:000432241200024
PM 29620273
OA Bronze
DA 2022-04-25
ER

PT J
AU Hai, Y
   Shinsky, SA
   Porter, NJ
   Christianson, DW
AF Hai, Yang
   Shinsky, Stephen A.
   Porter, Nicholas J.
   Christianson, David W.
TI Histone deacetylase 10 structure and molecular function as a polyamine
   deacetylase
SO NATURE COMMUNICATIONS
LA English
DT Article
ID INTERACTIVE TREE; ONLINE TOOL; LIFE ITOL; N-8-ACETYLSPERMIDINE;
   INHIBITION; SPERMIDINE; SUBSTRATE; AUTOPHAGY; DISPLAY; ELECTROSTATICS
AB Cationic polyamines such as spermidine and spermine are critical in all forms of life, as they regulate the function of biological macromolecules. Intracellular polyamine metabolism is regulated by reversible acetylation and dysregulated polyamine metabolism is associated with neoplastic diseases such as colon cancer, prostate cancer and neuroblastoma. Here we report that histone deacetylase 10 (HDAC10) is a robust polyamine deacetylase, using recombinant enzymes from Homo sapiens (human) and Danio rerio (zebrafish). The 2.85 angstrom-resolution crystal structure of zebrafish HDAC10 complexed with a transition-state analogue inhibitor reveals that a glutamate gatekeeper and a sterically constricted active site confer specificity for N-8-acetylspermidine hydrolysis and disfavour acetyllysine hydrolysis. Both HDAC10 and spermidine are known to promote cellular survival through autophagy. Accordingly, this work sets a foundation for studying the chemical biology of autophagy through the structure-based design of inhibitors that may also serve as new leads for cancer chemotherapy.
C1 [Hai, Yang; Shinsky, Stephen A.; Porter, Nicholas J.; Christianson, David W.] Univ Penn, Dept Chem, Roy & Diana Vagelos Labs, 231 South 34th St, Philadelphia, PA 19104 USA.
   [Hai, Yang] Univ Calif Los Angeles, Dept Chem & Biomol Engn, Los Angeles, CA 90095 USA.
RP Christianson, DW (corresponding author), Univ Penn, Dept Chem, Roy & Diana Vagelos Labs, 231 South 34th St, Philadelphia, PA 19104 USA.
EM chris@sas.upenn.edu
RI Hai, Yang/N-6388-2015
OI Hai, Yang/0000-0002-2039-5367; Shinsky, Stephen/0000-0001-5437-1729;
   Porter, Nicholas/0000-0002-9803-5310
FU NIHUnited States Department of Health & Human ServicesNational
   Institutes of Health (NIH) - USA [GM49758]; Department of Chemistry at
   the University of Pennsylvania; NATIONAL INSTITUTE OF GENERAL MEDICAL
   SCIENCESUnited States Department of Health & Human ServicesNational
   Institutes of Health (NIH) - USANIH National Institute of General
   Medical Sciences (NIGMS) [R01GM049758] Funding Source: NIH RePORTER
FX We thank C. Decroos and R. Marmorstein for helpful discussions, and we
   thank the NIH for grant GM49758 in support of this research. N.J.P.
   thanks the Department of Chemistry at the University of Pennsylvania for
   the award of a graduate research fellowship. In addition, we thank V.
   Stojanoff and S. Russi at BL 14-1 and T. Doukov at beamline 12-2 of the
   Stanford Synchrotron Radiation Lightsource for assistance with data
   collection.
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TC 79
Z9 80
U1 1
U2 26
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 2041-1723
J9 NAT COMMUN
JI Nat. Commun.
PD MAY 18
PY 2017
VL 8
AR 15368
DI 10.1038/ncomms15368
PG 9
WC Multidisciplinary Sciences
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Science & Technology - Other Topics
GA EV1MG
UT WOS:000401509800001
PM 28516954
OA Green Published, gold
DA 2022-04-25
ER

PT J
AU Zhu, QW
   Zhang, QC
   Gu, M
   Zhang, KW
   Xia, T
   Zhang, SY
   Chen, WH
   Yin, HM
   Yao, H
   Fan, Y
   Pan, S
   Xie, HJ
   Liu, HT
   Cheng, TY
   Zhang, PP
   Zhang, T
   You, B
   You, YW
AF Zhu, Qingwen
   Zhang, Qicheng
   Gu, Miao
   Zhang, Kaiwen
   Xia, Tian
   Zhang, Siyu
   Chen, Wenhui
   Yin, Haimeng
   Yao, Hui
   Fan, Yue
   Pan, Si
   Xie, Haijing
   Liu, Huiting
   Cheng, Tianyi
   Zhang, Panpan
   Zhang, Ting
   You, Bo
   You, Yiwen
TI MIR106A-5pupregulation suppresses autophagy and accelerates malignant
   phenotype in nasopharyngeal carcinoma
SO AUTOPHAGY
LA English
DT Article
DE Autophagy; BTG3; malignant phenotype; MIR106A-5p; nasopharyngeal
   carcinoma
ID ENHANCES RADIOSENSITIVITY; PROMOTES PROLIFERATION; COLORECTAL-CANCER;
   GASTRIC-CANCER; CELLS; METASTASIS; EXPRESSION; INHIBITION; INVASION;
   GROWTH
AB Dysregulated microRNAs (miRNAs) are involved in carcinoma progression, metastasis, and poor prognosis. We demonstrated that in nasopharyngeal carcinoma (NPC), transactivatedMIR106A-5ppromotes a malignant phenotype by functioning as a macroautophagy/autophagy suppressor by targetingBTG3(BTG anti-proliferation factor 3) and activating autophagy-regulating MAPK signaling.MIR106A-5pexpression was markedly increased in NPC cases based on quantitative real-time PCR, miRNA microarray, and TCGA database analysis findings. Moreover,MIR106A-5pwas correlated with advanced stage, recurrence, and poor clinical outcomes in NPC patients. In addition to three-dimensional cell culture assays, zebrafish and BALB/c mouse tumor models revealed that overexpressedMIR106A-5ptargetedBTG3and accelerated the NPC malignant phenotype by inhibiting autophagy. BTG3 promoted autophagy, and its expression was correlated with poor prognosis in NPC. Attenuation of autophagy, mediated by theMIR106A-5p-BTG3 axis, occurred because of MAPK pathway activation.MIR106A-5poverexpression in NPC was due to increased transactivation by EGR1 and SOX9. Our findings may lead to novel insights into the pathogenesis of NPC.
C1 [Zhu, Qingwen; Zhang, Qicheng; Gu, Miao; Zhang, Kaiwen; Xia, Tian; Zhang, Siyu; Chen, Wenhui; Yin, Haimeng; Yao, Hui; Fan, Yue; Pan, Si; Xie, Haijing; Liu, Huiting; Cheng, Tianyi; Zhang, Panpan; Zhang, Ting; You, Bo; You, Yiwen] Nantong Univ, Affiliated Hosp, Dept Otorhinolaryngol Head & Neck Surg, Nantong, Jiangsu, Peoples R China.
   [Zhu, Qingwen; Zhang, Qicheng; Gu, Miao; Zhang, Kaiwen; Xia, Tian; Zhang, Siyu; Chen, Wenhui; Yin, Haimeng; Yao, Hui; Fan, Yue; Pan, Si; Xie, Haijing; Liu, Huiting; Cheng, Tianyi; Zhang, Panpan; Zhang, Ting; You, Bo; You, Yiwen] Nantong Univ, Affiliated Hosp, Inst Otolaryngol Head & Neck Surg, Nantong, Jiangsu, Peoples R China.
RP You, B; You, YW (corresponding author), Nantong Univ, Affiliated Hosp, Dept Otorhinolaryngol Head & Neck Surg, Nantong, Jiangsu, Peoples R China.
EM oubo19891014@163.com; youyiwen_nantong@163.com
FU National Natural Science Foundation of ChinaNational Natural Science
   Foundation of China (NSFC) [81972554, 81672682, 81602385]; Clinical
   Frontier Technology of Jiangsu [BE2017680]; CSCO Clinical Oncology
   Research Foundation of Beijing [Y-HS2017-074]; Clinical Medical Center
   of Nantong [HS2016001]; innovative research project for postgraduate
   students of Jiangsu province [SJCX19_0871, SJCX19_0872, SJCX18_0822]
FX This work was supported by grants from the National Natural Science
   Foundation of China (Grant No. 81972554, No. 81672682, No. 81602385),
   the Clinical Frontier Technology of Jiangsu (Grant No. BE2017680), the
   CSCO Clinical Oncology Research Foundation of Beijing (Grant No.
   Y-HS2017-074), the Clinical Medical Center of Nantong (Grant No.
   HS2016001), the innovative research project for postgraduate students of
   Jiangsu province (Grant No. SJCX19_0871, No. SJCX19_0872, No.
   SJCX18_0822).
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NR 56
TC 9
Z9 9
U1 7
U2 12
PU TAYLOR & FRANCIS INC
PI PHILADELPHIA
PA 530 WALNUT STREET, STE 850, PHILADELPHIA, PA 19106 USA
SN 1554-8627
EI 1554-8635
J9 AUTOPHAGY
JI Autophagy
PD JUL 3
PY 2021
VL 17
IS 7
BP 1667
EP 1683
DI 10.1080/15548627.2020.1781368
EA JUL 2020
PG 17
WC Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Cell Biology
GA TX3WW
UT WOS:000547416600001
PM 32627648
OA Green Published, hybrid
DA 2022-04-25
ER

PT J
AU Momtazi-borojeni, AA
   Abdollahi, E
   Ghasemi, F
   Caraglia, M
   Sahebkar, A
AF Momtazi-borojeni, Amir A.
   Abdollahi, Elham
   Ghasemi, Faezeh
   Caraglia, Michele
   Sahebkar, Amirhossein
TI The novel role of pyrvinium in cancer therapy
SO JOURNAL OF CELLULAR PHYSIOLOGY
LA English
DT Review
DE cancer; cancer stem cell; pyrvinium
ID ANDROGEN RECEPTOR INHIBITION; BETA-CATENIN; STEM-CELLS; PROSTATE-CANCER;
   PHOSPHATIDYLINOSITOL 3-KINASE; AUTOPHAGY ADDICTION; ANTITUMOR-ACTIVITY;
   TUMOR-SUPPRESSOR; REPAIR PATHWAYS; GENE-EXPRESSION
AB Pyrvinium pamoate (PP) is a quinoline-derived cyanine dye which was officially approved by FDA for its anthelmintic properties and therapeutic function against animal-like protists such as Cryptosporidium parvum and Plasmodium falciparum in the 1950s. In the last 10 years, several studies have shown the novel activity of pyrvinium in tumor therapy. Some investigations have indicated that pyrvinium could delay or inhibit tumor cell proliferation in cancer models including colon, breast, lung and prostate cancer, and some hematological malignancies. In this review, we discuss multiple critical signaling pathways and mechanisms underlying the anticancer effects of PP. In details, pyrvinium acts through the following main mechanisms: (i) energy and autophagy depletion; and (ii) inhibition of Akt and Wnt--catenin-dependent pathways. Interestingly, pyrvinium has also shown potent anti-cancer stem cell activity. The overwhelming insights into the mechanism of anticancer properties of PP can help establishing novel and future anti-tumor treatment strategies.
C1 [Momtazi-borojeni, Amir A.] Mashhad Univ Med Sci, Nanotechnol Res Ctr, Bu Ali Res Inst, Mashhad, Iran.
   [Momtazi-borojeni, Amir A.] Mashhad Univ Med Sci, Fac Med, Dept Med Biotechnol, Student Res Comm, Mashhad, Iran.
   [Abdollahi, Elham] Mashhad Univ Med Sci, Dept Med Immunol, Sch Med, Mashhad, Iran.
   [Abdollahi, Elham] Mashhad Univ Med Sci, Student Res Comm, Mashhad, Iran.
   [Ghasemi, Faezeh] Arak Univ Med Sci, Fac Med, Dept Med Biotechnol, Arak, Iran.
   [Caraglia, Michele] Univ Campania L Vanvitelli, Dept Biochem Biophys & Gen Pathol, Via L De Crecchio, Naples, Italy.
   [Sahebkar, Amirhossein] Mashhad Univ Med Sci, Biotechnol Res Ctr, Mashhad, Iran.
RP Sahebkar, A (corresponding author), Mashhad Univ Med Sci, Sch Med, Dept Med Biotechnol, POB 91779-48564, Mashhad, Iran.
EM sahebkara@mums.ac.ir
RI Momtazi-Borojeni, Amir Abaas/AAC-6972-2019; Sahebkar,
   Amirhossein/B-5124-2018; Caraglia, Michele/AAK-4569-2020; Abdollahi,
   Elham/AAA-2731-2020
OI Momtazi-Borojeni, Amir Abaas/0000-0002-4376-1083; Caraglia,
   Michele/0000-0003-2408-6091; Abdollahi, Elham/0000-0002-8176-3557
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NR 127
TC 37
Z9 37
U1 1
U2 58
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0021-9541
EI 1097-4652
J9 J CELL PHYSIOL
JI J. Cell. Physiol.
PD APR
PY 2018
VL 233
IS 4
BP 2871
EP 2881
DI 10.1002/jcp.26006
PG 11
WC Cell Biology; Physiology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Cell Biology; Physiology
GA FR0AL
UT WOS:000418723200022
PM 28500633
DA 2022-04-25
ER

PT J
AU Tuorkey, MJ
AF Tuorkey, Muobarak J.
TI Cancer Therapy with Phytochemicals: Present and Future Perspectives
SO BIOMEDICAL AND ENVIRONMENTAL SCIENCES
LA English
DT Review
ID KINASE-C-DELTA; ROTTLERIN INDUCES AUTOPHAGY; APOPTOTIC CELL-DEATH;
   PANCREATIC-CANCER; PKC-DELTA; COLON-CANCER; IN-VITRO; SPARSTOLONIN B;
   UP-REGULATION; REDUCING MATRIX-METALLOPROTEINASE-9
AB Recently, a wide range of food-derived phytochemical compounds and their synthetic derivatives have been proposed for cancer treatment. Unfortunately, data available in related literature focus on the anti-cancer properties of compounds derived from edible plants, while very little is known about those derived from non-edible plants. And thus, the underlying mechanisms of their anti-cancer effects are yet to be elucidated. This review collates the available data on the anti-cancer activities of six phytochemical-derived compounds from edible and non-edible plants, i.e. rottlerin, berbamine, sparstolonin B, sulforaphane, plumbagin and 6-shogaol. These compounds are used as bioactive markers for cytotoxicity against tumors. As such, understanding their mode of action will provide the rationale for the combination strategies of these compounds with other drugs in the battle against cancer.
C1 [Tuorkey, Muobarak J.] Damanhour Univ, Fac Sci, Div Physiol, Dept Zool, Damanhour 22111, Egypt.
RP Tuorkey, MJ (corresponding author), Damanhour Univ, Fac Sci, Div Physiol, Dept Zool, Damanhour 22111, Egypt.
EM physio_mj_tuorkey@yahoo.com
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NR 98
TC 43
Z9 44
U1 0
U2 27
PU CHINESE CENTER DISEASE CONTROL & PREVENTION
PI BEIJING
PA 155 CHANGBAI RD, CHANGPING DISTRICT, BEIJING, 102206, PEOPLES R CHINA
SN 0895-3988
J9 BIOMED ENVIRON SCI
JI Biomed. Environ. Sci.
PD NOV
PY 2015
VL 28
IS 11
BP 808
EP 819
DI 10.1016/S0895-3988(15)30111-2
PG 12
WC Environmental Sciences; Public, Environmental & Occupational Health
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Environmental Sciences & Ecology; Public, Environmental & Occupational
   Health
GA DC3YW
UT WOS:000369157400004
PM 26695359
DA 2022-04-25
ER

PT S
AU Ashrafizadeh, M
   Tavakol, S
   Mohammadinejad, R
   Ahmadi, Z
   Yaribeygi, H
   Jamialahmadi, T
   Johnston, TP
   Sahebkar, A
AF Ashrafizadeh, Milad
   Tavakol, Shima
   Mohammadinejad, Reza
   Ahmadi, Zahra
   Yaribeygi, Habib
   Jamialahmadi, Tannaz
   Johnston, Thomas P.
   Sahebkar, Amirhossein
BE Barreto, GE
   Sahebkar, A
TI Paving the Road Toward Exploiting the Therapeutic Effects of
   Ginsenosides: An Emphasis on Autophagy and Endoplasmic Reticulum Stress
SO PHARMACOLOGICAL PROPERTIES OF PLANT-DERIVED NATURAL PRODUCTS AND
   IMPLICATIONS FOR HUMAN HEALTH
SE Advances in Experimental Medicine and Biology
LA English
DT Article; Book Chapter
DE Ginsenoside; Endoplasmic reticulum stress; Autophagy; Apoptosis; Cancer
   therapy
ID TUMOR-NECROSIS-FACTOR; RG1 PROTECTS CARDIOMYOCYTES; COLON-CANCER CELLS;
   ER STRESS; INDUCED APOPTOSIS; OXIDATIVE STRESS; PC12 CELLS; IN-VITRO;
   HYPOXIA/REOXYGENATION INJURY; DIABETIC CARDIOMYOPATHY
AB Programmed cell death processes such as apoptosis and autophagy strongly contribute to the onset and progression of cancer. Along with these lines, modulation of cell death mechanisms to combat cancer cells and elimination of resistance to apoptosis is of great interest. It appears that modulation of autophagy and endoplasmic reticulum (ER) stress with specific agents would be beneficial in the treatment of several disorders. Interestingly, it has been suggested that herbal natural products may be suitable candidates for the modulation of these processes due to few side effects and significant therapeutic potential. Ginsenosides are derivatives of ginseng and exert modulatory effects on the molecular mechanisms associated with autophagy and ER stress. Ginsenosides act as smart phytochemicals that confer their effects by up-regulating ATG proteins and converting LC3-I to -II, which results in maturation of autophagosomes. Not only do ginsenosides promote autophagy but they also possess protective and therapeutic properties due to their capacity to modulate ER stress and up- and down-regulate and/or dephosphorylate UPR transducers such as IRE1, PERK, and ATF6. Thus, it would appear that ginsenosides are promising agents to potentially restore tissue malfunction and possibly eliminate cancer.
C1 [Ashrafizadeh, Milad] Sabanci Univ, Fac Engn & Nat Sci, Istanbul, Turkey.
   [Ashrafizadeh, Milad] Sabanci Univ Nanotechnol Res & Applicat Ctr SUNUM, Istanbul, Turkey.
   [Tavakol, Shima] Iran Univ Med Sci, Cellular & Mol Res Ctr, Tehran, Iran.
   [Mohammadinejad, Reza] Kerman Univ Med Sci, Inst Neuropharmacol, Neurosci Res Ctr, Kerman, Iran.
   [Ahmadi, Zahra] Islamic Azad Univ, Dept Basic Sci, Shoushtar Branch, Shoushtar, Iran.
   [Yaribeygi, Habib] Semnan Univ Med Sci, Physiol Res Ctr, Semnan, Iran.
   [Jamialahmadi, Tannaz] Islamic Azad Univ, Dept Food Sci & Technol, Quchan Branch, Quchan, Iran.
   [Jamialahmadi, Tannaz] Mashhad Univ Med Sci, Fac Med, Dept Nutr, Mashhad, Razavi Khorasan, Iran.
   [Johnston, Thomas P.] Univ Missouri Kansas City, Sch Pharm, Div Pharmacol & Pharmaceut Sci, Kansas City, MO USA.
   [Sahebkar, Amirhossein] Mashhad Univ Med Sci, Appl Biomed Res Ctr, Mashhad, Razavi Khorasan, Iran.
   [Sahebkar, Amirhossein] Mashhad Univ Med Sci, Pharmaceut Technol Inst, Biotechnol Res Ctr, Mashhad, Razavi Khorasan, Iran.
   [Sahebkar, Amirhossein] Mashhad Univ Med Sci, Sch Pharm, Mashhad, Razavi Khorasan, Iran.
   [Sahebkar, Amirhossein] Polish Mothers Mem Hosp Res Inst PMMHRI, Lodz, Poland.
RP Yaribeygi, H (corresponding author), Semnan Univ Med Sci, Physiol Res Ctr, Semnan, Iran.; Sahebkar, A (corresponding author), Mashhad Univ Med Sci, Appl Biomed Res Ctr, Mashhad, Razavi Khorasan, Iran.; Sahebkar, A (corresponding author), Mashhad Univ Med Sci, Pharmaceut Technol Inst, Biotechnol Res Ctr, Mashhad, Razavi Khorasan, Iran.; Sahebkar, A (corresponding author), Mashhad Univ Med Sci, Sch Pharm, Mashhad, Razavi Khorasan, Iran.; Sahebkar, A (corresponding author), Polish Mothers Mem Hosp Res Inst PMMHRI, Lodz, Poland.
EM habib.yari@yahoo.com; sahebkara@mums.ac.ir
RI Yaribeygi, Habib/R-8998-2019
OI Yaribeygi, Habib/0000-0002-1706-6212; Jami, Tannaz/0000-0001-9521-3153
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NR 218
TC 2
Z9 2
U1 3
U2 3
PU SPRINGER INTERNATIONAL PUBLISHING AG
PI CHAM
PA GEWERBESTRASSE 11, CHAM, CH-6330, SWITZERLAND
SN 0065-2598
EI 2214-8019
BN 978-3-030-64872-5; 978-3-030-64871-8
J9 ADV EXP MED BIOL
JI Adv.Exp.Med.Biol.
PY 2021
VL 1308
BP 137
EP 160
DI 10.1007/978-3-030-64872-5_12
D2 10.1007/978-3-030-64872-5
PG 24
WC Chemistry, Medicinal; Medicine, Research & Experimental; Pharmacology &
   Pharmacy
WE Book Citation Index – Science (BKCI-S); Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy; Research & Experimental Medicine
GA BR3MG
UT WOS:000647701200012
PM 33861443
DA 2022-04-25
ER

PT J
AU Khaket, TP
   Singh, MP
   Khan, I
   Kang, SC
AF Khaket, Tejinder Pal
   Singh, Mahendra Pal
   Khan, Imran
   Kang, Sun Chul
TI In vitro and in vivo studies on potentiation of curcumin-induced
   lysosomal-dependent apoptosis upon silencing of cathepsin C in
   colorectal cancer cells
SO PHARMACOLOGICAL RESEARCH
LA English
DT Article
DE Cathepsins; Autophagy; Endoplasmic reticulum stress; Apoptosis
ID AUTOPHAGY INDUCTION; PROTEIN-SYNTHESIS; DEATH; INHIBITION; INVASION;
   GROWTH; JNK; PERMEABILIZATION; REGULATOR; MIGRATION
AB Cathepsins are lysosomal acid hydrolases that make crucial contributions to tumor progression through a variety of signaling mechanisms, including autophagy, cell survival, chemotherapeutic resistance, and metastasis. Herein, we report that cathepsin C (CTSC) silencing upregulates the anticancer potential of curcumin in colorectal cancer cells (CRCs) both in vitro and in athymic mice xenografts. Curcumin treatment enhances CTSC level in CRCs; however, CTSC silencing with subsequent curcumin treatment (sequential treatment) induces ER stress and autophagic dysregulation accompanied by lysosomal permeabilization and ROS generation. This lysosomal permeabilization triggered the cytosolic CTSB mediated BID-dependent mitochondrial membrane permeabilization and thereby caspase-dependent apoptosis. This phenotype can be rescued by CTSB inhibition and NAC, which further supported the involvement of ROS and CTSB in apoptosis following sequential treatment. Indeed, the sequential CTSC silencing and curcumin treatment also significantly curtailed tumor volume as well as ameliorated cytosolic cyt c and tBID protein levels in tumor tissues compared to those in control and individual treatments of CTSC targeting and on curcumin treatment in nude mice xenografts. The results reveal that CTSC can controls the curcumin-induced cytotoxic insult through autophagy maintenance both in vitro and in athymic mice xenografts, thereby providing an insight into the role of CTSC in chemoprevention of CRCs.
C1 [Khaket, Tejinder Pal; Singh, Mahendra Pal; Khan, Imran; Kang, Sun Chul] Daegu Univ, Dept Biotechnol, Gyongsan 38453, Gyeongbuk, South Korea.
   [Khaket, Tejinder Pal] Ohio State Univ, Comprehens Canc Ctr, Dept Radiat Oncol, Columbus, OH 43210 USA.
   [Singh, Mahendra Pal] Mayo Clin, Dept Immunol, Rochester, MN 55905 USA.
   [Khan, Imran] Univ Minnesota, Hormel Inst, 801 16th Ave NE, Austin, MN 55912 USA.
RP Kang, SC (corresponding author), Daegu Univ, Coll Engn, Dept Biotechnol, Gyongsan 38453, Gyeongbuk, South Korea.
EM sckang@daegu.ac.kr
RI Singh, Mahendra Pal/J-8391-2019
FU National Research Foundation of Korea (NRF)National Research Foundation
   of Korea [NRF 2019R1A2B5B01070543]
FX This work was supported by the National Research Foundation of Korea
   (NRF) NRF 2019R1A2B5B01070543.
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NR 58
TC 4
Z9 4
U1 2
U2 7
PU ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD
PI LONDON
PA 24-28 OVAL RD, LONDON NW1 7DX, ENGLAND
SN 1043-6618
EI 1096-1186
J9 PHARMACOL RES
JI Pharmacol. Res.
PD NOV
PY 2020
VL 161
AR 105156
DI 10.1016/j.phrs.2020.105156
PG 15
WC Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA PI3JG
UT WOS:000600990100043
PM 32835867
DA 2022-04-25
ER

PT J
AU Woo, Y
   Lee, HJ
   Jung, YM
   Jung, YJ
AF Woo, Yunseo
   Lee, Hyo-Ji
   Jung, Young Mee
   Jung, Yu-Jin
TI Regulated Necrotic Cell Death in Alternative Tumor Therapeutic
   Strategies
SO CELLS
LA English
DT Review
DE apoptosis; autophagy; necrosis; necroptosis; pyroptosis; ferroptosis;
   therapy-resistant tumors
ID DOMAIN-LIKE PROTEIN; COLON-CANCER CELLS; INFLAMMASOME ACTIVATION;
   DEPENDENT NECROPTOSIS; MOLECULAR-MECHANISMS; AUTOPHAGY INHIBITION;
   PROGRAMMED NECROSIS; NLRP3 INFLAMMASOME; OXIDATIVE STRESS;
   POOR-PROGNOSIS
AB The treatment of tumors requires the induction of cell death. Radiotherapy, chemotherapy, and immunotherapy are administered to kill cancer cells; however, some cancer cells are resistant to these therapies. Therefore, effective treatments require various strategies for the induction of cell death. Regulated cell death (RCD) is systematically controlled by intracellular signaling proteins. Apoptosis and autophagy are types of RCD that are morphologically different from necrosis, while necroptosis, pyroptosis, and ferroptosis are morphologically similar to necrosis. Unlike necrosis, regulated necrotic cell death (RNCD) is caused by disruption of the plasma membrane under the control of specific proteins and induces tissue inflammation. Various types of RNCD, such as necroptosis, pyroptosis, and ferroptosis, have been used as therapeutic strategies against various tumor types. In this review, the mechanisms of necroptosis, pyroptosis, and ferroptosis are described in detail, and a potential effective treatment strategy to increase the anticancer effects on apoptosis- or autophagy-resistant tumor types through the induction of RNCD is suggested.
C1 [Woo, Yunseo; Lee, Hyo-Ji; Jung, Yu-Jin] Kangwon Natl Univ, Dept Biol Sci, Chunchon 24341, South Korea.
   [Woo, Yunseo; Lee, Hyo-Ji; Jung, Young Mee; Jung, Yu-Jin] Kangwon Natl Univ, Kangwon Radiat Convergence Res Support Ctr, Chunchon 24341, South Korea.
   [Jung, Young Mee] Kangwon Natl Univ, Dept Chem, Chunchon 24341, South Korea.
   [Jung, Yu-Jin] Kangwon Natl Univ, BIT Med Convergence Grad Program, Chunchon 24341, South Korea.
RP Jung, YJ (corresponding author), Kangwon Natl Univ, Dept Biol Sci, Chunchon 24341, South Korea.; Jung, YJ (corresponding author), Kangwon Natl Univ, Kangwon Radiat Convergence Res Support Ctr, Chunchon 24341, South Korea.; Jung, YJ (corresponding author), Kangwon Natl Univ, BIT Med Convergence Grad Program, Chunchon 24341, South Korea.
EM yunseo@kangwon.ac.kr; koko7912@kangwon.ac.kr; ymjung@kangwon.ac.kr;
   yjjung@kangwon.ac.kr
OI Jung, Young Mee/0000-0003-4362-0990; Lee, Hyo-Ji/0000-0001-9892-8365;
   Jung, Yu-Jin/0000-0002-4942-677X
FU Basic Science Research Program through the National Research Foundation
   of Korea (NRF) - Ministry of Education, Science, and Technology
   [2018R1D1A1B07049097]; Korea Basic Science Institute (National Research
   Facilities and Equipment Center) - Ministry of Education
   [2020R1A6C101A195]
FX This research was supported by a grant from the Basic Science Research
   Program through the National Research Foundation of Korea (NRF), which
   is funded by the Ministry of Education, Science, and Technology
   (2018R1D1A1B07049097), and by a Korea Basic Science Institute (National
   Research Facilities and Equipment Center) grant funded by the Ministry
   of Education (2020R1A6C101A195).
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NR 162
TC 15
Z9 15
U1 3
U2 12
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 2073-4409
J9 CELLS-BASEL
JI Cells
PD DEC
PY 2020
VL 9
IS 12
AR 2709
DI 10.3390/cells9122709
PG 17
WC Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Cell Biology
GA PJ5YY
UT WOS:000601844000001
PM 33348858
OA Green Published, gold
DA 2022-04-25
ER

PT J
AU Prabhu, V
   Srivastava, P
   Yadav, N
   Amadori, M
   Schneider, A
   Seshadri, A
   Pitarresi, J
   Scott, R
   Zhang, HH
   Koochekpour, S
   Gogada, R
   Chandra, D
AF Prabhu, Varun
   Srivastava, Pragya
   Yadav, Neelu
   Amadori, Michael
   Schneider, Andrea
   Seshadri, Athul
   Pitarresi, Jason
   Scott, Rachael
   Zhang, Honghao
   Koochekpour, Shahriar
   Gogada, Raghu
   Chandra, Dhyan
TI Resveratrol depletes mitochondrial DNA and inhibition of autophagy
   enhances resveratrol-induced caspase activation
SO MITOCHONDRION
LA English
DT Article
DE Resveratrol; Mitochondria; Autophagy; Apoptosis; Mitochondrial DNA
ID BREAST-CANCER CELLS; CHRONIC MYELOGENOUS LEUKEMIA; ISOLATED RAT
   HEPATOCYTES; INDUCED APOPTOSIS; AMPK ACTIVATION; IN-VIVO; DEATH;
   MECHANISMS; BAX; CHEMOPREVENTION
AB We recently demonstrated that resveratrol induces caspase-dependent apoptosis in multiple cancer cell types. Whether apoptosis is also regulated by other cell death mechanisms such as autophagy is not clearly defined. Here we show that inhibition of autophagy enhanced resveratrol-induced caspase activation and apoptosis. Resveratrol inhibited colony formation and cell proliferation in multiple cancer cell types. Resveratrol treatment induced accumulation of LC3-II, which is a key marker for autophagy. Pretreatment with 3-methyladenine (3-MA), an autophagy inhibitor, increased resveratrol-mediated caspase activation and cell death in breast and colon cancer cells. Inhibition of autophagy by silencing key autophagy regulators such as ATG5 and Beclin-1 enhanced resveratrol-induced caspase activation. Mechanistic analysis revealed that Beclin-1 did not interact with proapoptotic proteins Bax and Bak; however, Beclin-1 was found to interact with p53 in the cytosol and mitochondria upon resveratrol treatment. Importantly, resveratrol depleted ATPase 8 gene, and thus, reduced mitochondrial DNA (mtDNA) content, suggesting that resveratrol induces damage to mtDNA causing accumulation of dysfunctional mitochondria triggering autophagy induction. Together, our findings indicate that induction of autophagy during resveratrol-induced apoptosis is an adaptive response. (C) 2012 Elsevier B.V. and Mitochondria Research Society. All rights reserved.
C1 [Prabhu, Varun; Srivastava, Pragya; Yadav, Neelu; Amadori, Michael; Schneider, Andrea; Seshadri, Athul; Pitarresi, Jason; Scott, Rachael; Zhang, Honghao; Koochekpour, Shahriar; Gogada, Raghu; Chandra, Dhyan] Roswell Pk Canc Inst, Dept Pharmacol & Therapeut, Buffalo, NY 14263 USA.
RP Chandra, D (corresponding author), Roswell Pk Canc Inst, Dept Pharmacol & Therapeut, Elm & Carlton St, Buffalo, NY 14263 USA.
EM dhyan.chandra@roswellpark.org
RI Gogada, Raghu/AAG-6624-2019
OI Gogada, Raghu/0000-0003-0933-7999; Chandra, Dhyan/0000-0001-7272-9384;
   Zhang, Honghao/0000-0002-2338-6992
FU National Institutes of HealthUnited States Department of Health & Human
   ServicesNational Institutes of Health (NIH) - USA [CA123142]; National
   Cancer InstituteUnited States Department of Health & Human
   ServicesNational Institutes of Health (NIH) - USANIH National Cancer
   Institute (NCI) [CA016056]; American Cancer SocietyAmerican Cancer
   Society [RSG-12-214-01 - CCG]; NATIONAL CANCER INSTITUTEUnited States
   Department of Health & Human ServicesNational Institutes of Health (NIH)
   - USANIH National Cancer Institute (NCI) [K01CA123142, P30CA016056]
   Funding Source: NIH RePORTER
FX This work was supported by National Institutes of Health K01 award
   CA123142 to Dhyan Chandra and National Cancer Institute Center Support
   Grant CA016056 to Roswell Park Cancer Institute. Dhyan Chandra was
   supported by a Research Scholar Grant, RSG-12-214-01 - CCG from the
   American Cancer Society. We thank Dr. Bert Vogelstein for providing
   HCT116 cells. Varun Prabhu was an MS student at University at Buffalo.
   We apologize to all colleagues whose work could not be cited due to
   space constraints.
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NR 56
TC 26
Z9 31
U1 0
U2 19
PU ELSEVIER SCI LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND
SN 1567-7249
J9 MITOCHONDRION
JI Mitochondrion
PD SEP
PY 2013
VL 13
IS 5
SI SI
BP 493
EP 499
DI 10.1016/j.mito.2012.10.010
PG 7
WC Cell Biology; Genetics & Heredity
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Cell Biology; Genetics & Heredity
GA 210YF
UT WOS:000323870600013
PM 23088850
OA Green Accepted
DA 2022-04-25
ER

PT J
AU Ferreira, PMP
   de Sousa, RWR
   Ferreira, JRD
   Militao, GCG
   Bezerra, DP
AF Pinheiro Ferreira, Paulo Michel
   Ramos de Sousa, Rayran Walter
   de Oliveira Ferreira, Jose Roberto
   Gadelha Militao, Gardenia Carmen
   Bezerra, Daniel Pereira
TI Chloroquine and hydroxychloroquine in antitumor therapies based on
   autophagy-related mechanisms
SO PHARMACOLOGICAL RESEARCH
LA English
DT Review
DE Cell death; Chemoresistance; Immunomodulatory properties; Clinical
   option
ID MIXED LINEAGE KINASE; COLON-CANCER CELLS; CPG-DNA; INHIBITION;
   RESISTANCE; P53; DEATH; RIP3; DRUG; CYTOTOXICITY
AB Chloroquine (CQ) and hydroxychloroquine (HCQ) are the most common drugs used to relieve acute and chronic inflammatory diseases. In this article, we present a review about the use of CQ and HCQ in antitumor therapies based on autophagy mechanisms. These molecules break/discontinue autophagosome-lysosome fusions in initial phases and enhance antiproliferative action of chemotherapeutics. Their sensitizing effects of chemotherapy when used as an adjuvant option in clinical trials against cancer. However, human related-MDR genes are also under risk to develop chemo or radioresistance because cancer cells have ability to throw 4-aminoquinolines out from digestive vacuoles well. Additionally, they also have antitumor mechanism unrelated to autophagy, including cell death from apoptosis and necroptosis and immunomodulatory/anti-inflammatory properties. However, the link between some anticancer mechanisms, clinical efficacy and pharmacological safety has not yet been fully defined.
C1 [Pinheiro Ferreira, Paulo Michel; Ramos de Sousa, Rayran Walter] Univ Fed Piaui, Dept Biophys & Physiol, Lab Expt Cancerol, BR-64049550 Teresina, Brazil.
   [de Oliveira Ferreira, Jose Roberto] State Univ Hlth Sci Alagoas, Ctr Integrat Sci, BR-57010382 Maceio, Alagoas, Brazil.
   [Gadelha Militao, Gardenia Carmen] Univ Fed Pernambuco, Dept Physiol & Pharmacol, BR-50670901 Recife, PE, Brazil.
   [Bezerra, Daniel Pereira] Oswaldo Cruz Fdn IGM FIOCRUZ BA, Goncalo Moniz Inst, BR-40296710 Salvador, BA, Brazil.
RP Ferreira, PMP (corresponding author), Univ Fed Piaui, Dept Biophys & Physiol, Lab Expt Cancerol LabCanc, Ctr Hlth Sci, Univ Ave, BR-64049550 Teresina, Piaui, Brazil.
EM pmpf@ufpi.edu.br
RI Ferreira, Paulo Michel Pinheiro/J-6783-2012
OI Ferreira, Paulo Michel Pinheiro/0000-0001-6862-6497
FU Brazilian agency "Conselho Nacional de Desenvolvimento Cientifico e
   Tecnologico" (CNPq)Conselho Nacional de Desenvolvimento Cientifico e
   Tecnologico (CNPQ) [303247/2019-3, 313350/2018-3]
FX Dr Paulo Michel Pinheiro Ferreira and Dr Daniel Pereira Bezerra are
   grateful to the Brazilian agency "Conselho Nacional de Desenvolvimento
   Cientifico e Tecnologico" (CNPq) for their personal scholarships
   (#303247/2019-3 and #313350/2018-3, respectively).
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   ANN SURG ONCOL
   BIOCHEM PHARMACOL
   ANN INTERN MED
NR 83
TC 4
Z9 4
U1 7
U2 9
PU ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD
PI LONDON
PA 24-28 OVAL RD, LONDON NW1 7DX, ENGLAND
SN 1043-6618
EI 1096-1186
J9 PHARMACOL RES
JI Pharmacol. Res.
PD MAR
PY 2021
VL 168
AR 105582
DI 10.1016/j.phrs.2021.105582
EA APR 2021
PG 9
WC Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA SJ4FE
UT WOS:000655486900007
PM 33775862
DA 2022-04-25
ER

PT J
AU Vecera, L
   Gabrhelik, T
   Prasil, P
   Stourac, P
AF Vecera, L.
   Gabrhelik, T.
   Prasil, P.
   Stourac, P.
TI The role of cannabinoids in the treatment of cancer
SO BRATISLAVA MEDICAL JOURNAL-BRATISLAVSKE LEKARSKE LISTY
LA English
DT Review
DE cannabinoids; cannabinoid receptor; cancer; oncological diseases; cancer
   treatment
ID EPITHELIAL-MESENCHYMAL TRANSITION; PROTEIN-COUPLED RECEPTOR; CELL
   LUNG-CANCER; TUMOR-GROWTH; IN-VIVO; INDUCED APOPTOSIS; CB2 RECEPTOR;
   COLON-CANCER; CHOLANGIOCARCINOMA GROWTH; INHIBITS ANGIOGENESIS
AB AIM: The aim of this review article is to summarize current knowledge about the role of cannabinoids and cannabinoid receptors in tumor disease modulation and to evaluate comprehensively the use of cannabinoids in cancer patients.
   METHOD: According to the PRISMA protocol, we have included data from a total of 105 articles.
   RESULTS: Cannabinoids affect cancer progression by three mechanisms. The most important mechanism is the stimulation of autophagy and affecting the signaling pathways leading to apoptosis. The most important mechanism of this process is the accumulation of ceramide. Cannabinoids also stimulate apoptosis by mechanisms independent of autophagy. Other mechanisms by which cannabinoids affect tumor growth are inhibition of tumor angiogenesis, invasiveness, metastasis, and the modulation of the anti-tumor immune response.
   CONCLUSION: In addition to the symptomatic therapy of cancer patients, the antitumor effects of cannabinoids (whether in monotherapy or in combination with other cancer therapies) have promising potential in the treatment of cancer patients. More clinical trials are needed to demonstrate the antitumor effect of cannabinoids (Tab. 1, Fig. 1, Ref. 167).
C1 [Vecera, L.; Gabrhelik, T.; Prasil, P.; Stourac, P.] Tomas Bata Hosp Zlin, Dept Emergency Med, Zlin, Czech Republic.
   [Vecera, L.; Stourac, P.] Masaryk Univ, Univ Hosp Brno, Med Fac, Dept Paediat Anaesthesiol & Intens Care Med, Brno, Czech Republic.
   [Gabrhelik, T.] Tomas Bata Hosp Zlin, Dept Anaesthesiol Resuscitat & Intens Care Med, Havlickovo Nabrezi 600, Zlin 76275, Czech Republic.
   [Prasil, P.] Dist Hosp Amstetten, Dept Anaesthesia & Intens Care Med, Amstetten, Austria.
RP Gabrhelik, T (corresponding author), Tomas Bata Hosp Zlin, Dept Anaesthesiol Resuscitat & Intens Care Med, Havlickovo Nabrezi 600, Zlin 76275, Czech Republic.
EM Tomas.Gabrhelik@bnzlin.cz
RI Stourac, Petr/J-3610-2012
OI Stourac, Petr/0000-0003-1944-5926
FU  [NV18-03-00470]
FX This work was supported by grant no: NV18-03-00470.
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NR 164
TC 6
Z9 6
U1 4
U2 12
PU COMENIUS UNIV
PI BRATISLAVA I
PA SCH MEDICINE, SPITALSKA 24, BRATISLAVA I, SK-813 72, SLOVAKIA
SN 0006-9248
EI 1336-0345
J9 BRATISL MED J
JI Bratisl. Med. J.
PY 2020
VL 121
IS 1
BP 79
EP 95
DI 10.4149/BLL_2020_012
PG 17
WC Medicine, General & Internal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC General & Internal Medicine
GA KD5SP
UT WOS:000507926100012
PM 31950844
OA gold
DA 2022-04-25
ER

PT J
AU Hidayat, AFA
   Chan, CK
   Mohamad, J
   Kadir, HA
AF Hidayat, Ahmad Fadhlurrahman Ahmad
   Chan, Chim Kei
   Mohamad, Jamaludin
   Kadir, Habsah Abdul
TI Dioscorea bulbifera induced apoptosis through inhibition of ERK 1/2 and
   activation of JNK signaling pathways in HCT116 human colorectal
   carcinoma cells
SO BIOMEDICINE & PHARMACOTHERAPY
LA English
DT Article
DE Apoptosis; Colon cancer; Dioscorea bulbifera; ERK1/2 and JNK
ID REGULATED KINASE-1/2; REACTIVE OXYGEN; CANCER-CELLS; MAPK;
   PHOSPHORYLATION; INDUCTION; AUTOPHAGY; CASPASES; TUBERS; L.
AB Dioscorea bulbifera, also known as air potato, has been cultivated as food crop mainly in tropical countries in Asia and Australia. The tubers are edible and have often been used in Traditional Chinese Medicine (TCM) and Ayurvedic medicine to treat cancer, diabetes, thyroid disease, and inflammation. This study aimed to investigate the effects of D. bulbifera on HCT116 human colorectal carcinoma cells and to unravel the plausible mechanisms underlying its apoptotic effects. The ethanol crude and fractions (hexane, ethyl acetate and water) of D. bulbifera were subjected to cell viability MTT assay against various cancer cell lines. The lowest IC50 of the extract and fractions on selected cancer cells were selected for further apoptosis assay and western blot analysis. HCT116 cancer cells were treated with D. bulbifera and stained with Annexin/PI or Hoechst 33342/PI for preliminary confirmation of apoptosis. The dissipation of mitochondria membrane potential (MMP) was determined by flow cytometry. The protein expressions of apoptosis-related proteins such as Bcl-2 family, caspases, Fas, PARP, ERK1/2 and JNK were detected by western blot analysis. Moreover, the HCT116 cells were treated with UO126 and SP600125 inhibitors to verify the involvement of ERK1/2 and JNK protein expressions in inducing apoptotic cell death. Based on the result, D. bulbifera ethyl acetate fraction (DBEAF) exhibited the most compelling cytotoxicity on HCT116 cells with an IC50 of 37.91 +/- 1.30 mu g/mL. The induction of apoptosis was confirmed by phosphatidylserine externalization and chromatin condensation. Depolarization of MMP further conferred the induction of apoptosis was through the regulation of Bcl-2 family proteins. Activation of caspase cascades (caspase-3, -9, -8 and -10) was elicited followed by the observation of cleaved PARP accumulation in DBEAFtreated cells. Furthermore, death receptor, Fas was activated upon exposure to DBEAF. Collective apoptotic evidences suggested the involvement of intrinsic and extrinsic pathways by DBEAF in HCT116 cells. Interestingly, the attenuation of ERK1/2 phosphorylation accompanied by the activation of JNK was detected in DBEAF-treated cells. In conclusion, the findings revealed that DBEAF induced apoptosis through intrinsic and extrinsic pathways involving ERK1/2 and JNK.
C1 [Hidayat, Ahmad Fadhlurrahman Ahmad; Chan, Chim Kei; Kadir, Habsah Abdul] Univ Malaya, Fac Sci, Inst Biol Sci, Biomol Res Grp,Biochem Program, Kuala Lumpur 50603, Malaysia.
   [Mohamad, Jamaludin] Univ Malaya, Fac Sci, Inst Biol Sci, Biohlth Program, Kuala Lumpur 50603, Malaysia.
RP Kadir, HA (corresponding author), Univ Malaya, Fac Sci, Inst Biol Sci, Biomol Res Grp,Biochem Program, Kuala Lumpur 50603, Malaysia.
EM habsah@um.edu.my
RI MOHAMAD, J/B-8690-2010
OI Chan, Chim kei/0000-0002-1606-8814
FU Fundamental Research Grant Scheme (FRGS) from the Ministry of Education,
   Malaysia [FP009-2014B]
FX This study was supported by the Fundamental Research Grant Scheme (FRGS)
   FP009-2014B from the Ministry of Education, Malaysia.
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   Yarla N.S., 2016, SEMIN CANC BIOL
NR 38
TC 13
Z9 13
U1 3
U2 25
PU ELSEVIER FRANCE-EDITIONS SCIENTIFIQUES MEDICALES ELSEVIER
PI ISSY-LES-MOULINEAUX
PA 65 RUE CAMILLE DESMOULINS, CS50083, 92442 ISSY-LES-MOULINEAUX, FRANCE
SN 0753-3322
EI 1950-6007
J9 BIOMED PHARMACOTHER
JI Biomed. Pharmacother.
PD AUG
PY 2018
VL 104
BP 806
EP 816
DI 10.1016/j.biopha.2018.05.073
PG 11
WC Medicine, Research & Experimental; Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Research & Experimental Medicine; Pharmacology & Pharmacy
GA GL1BQ
UT WOS:000436830700092
PM 29860114
DA 2022-04-25
ER

PT J
AU Garufi, A
   Ricci, A
   Trisciuoglio, D
   Iorio, E
   Carpinelli, G
   Pistritto, G
   Cirone, M
   D'Orazi, G
AF Garufi, A.
   Ricci, A.
   Trisciuoglio, D.
   Iorio, E.
   Carpinelli, G.
   Pistritto, G.
   Cirone, M.
   D'Orazi, G.
TI Glucose restriction induces cell death in parental but not in
   homeodomain-interacting protein kinase 2-depleted RKO colon cancer
   cells: molecular mechanisms and implications for tumor therapy
SO CELL DEATH & DISEASE
LA English
DT Article
DE HIPK2; glucose; tumor; cell death; autophagy; zinc supplementation
ID P53 ACTIVITY; HIPK2; HYPOXIA; ACTIVATION; APOPTOSIS; AUTOPHAGY;
   TRANSCRIPTION; TOLERANCE; GENE; DEPRIVATION
AB Tumor cell tolerance to nutrient deprivation can be an important factor for tumor progression, and may depend on deregulation of both oncogenes and oncosuppressor proteins. Homeodomain-interacting protein kinase 2 (HIPK2) is an oncosuppressor that, following its activation by several cellular stress, induces cancer cell death via p53-dependent or -independent pathways. Here, we used genetically matched human RKO colon cancer cells harboring wt-HIPK2 (HIPK2(+/+)) or stable HIPK2 siRNA interference (siHIPK2) to investigate in vitro whether HIPK2 influenced cell death in glucose restriction. We found that glucose starvation induced cell death, mainly due to c-Jun NH2-terminal kinase activation, in HIPK2(+/+)cells compared with siHIPK2 cells that did not die. 1 H-nuclear magnetic resonance quantitative metabolic analyses showed a marked glycolytic activation in siHIPK2 cells. However, treatment with glycolysis inhibitor 2-deoxy-D-glucose induced cell death only in HIPK2(+/+) cells but not in siHIPK2 cells. Similarly, siGlut-1 interference did not re-establish siHIPK2 cell death under glucose restriction, whereas marked cell death was reached only after zinc supplementation, a condition known to reactivate misfolded p53 and inhibit the pseudohypoxic phenotype in this setting. Further siHIPK2 cell death was reached with zinc in combination with autophagy inhibitor. We propose that the metabolic changes acquired by cells after HIPK2 silencing may contribute to induce resistance to cell death in glucose restriction condition, and therefore be directly relevant for tumor progression. Moreover, elimination of such a tolerance might serve as a new strategy for cancer therapy.
C1 [Garufi, A.; D'Orazi, G.] Regina Elena Inst Canc Res, Dept Expt Oncol, Mol Oncogenesis Lab, Rome, Italy.
   [Ricci, A.; Iorio, E.; Carpinelli, G.] Ist Super Sanita, Dept Cell Biol & Neurosci, I-00161 Rome, Italy.
   [Trisciuoglio, D.] Regina Elena Inst Canc Res, Expt Chemotherapy Lab, Rome, Italy.
   [Pistritto, G.] Univ Roma Tor Vergata, Dept Neurosci, Pharmacol Sect, Rome, Italy.
   [Cirone, M.] Sapienza Univ, Ist Pasteur Fdn Cenci Bolognetti, Dept Expt Med, Rome, Italy.
   [D'Orazi, G.] Univ G DAnnunzio, Dept Med Oral & Biotechnol Sci, I-66013 Chieti, Italy.
RP D'Orazi, G (corresponding author), Univ G DAnnunzio, Dept Med Oral & Biotechnol Sci, Via Vestini 31, I-66013 Chieti, Italy.
EM gdorazi@unich.it
RI Iorio, Egidio/M-7077-2017; D'Orazi, Gabriella/T-2792-2019; Garufi,
   Alessia/AAT-3363-2020; trisciuoglio, daniela/AAL-4002-2021;
   trisciuoglio, Daniela/H-2131-2016
OI Iorio, Egidio/0000-0001-6673-3838; D'Orazi,
   Gabriella/0000-0001-6876-9105; trisciuoglio,
   Daniela/0000-0002-7007-7914; Garufi, Alessia/0000-0001-9354-993X
FU Associazione Italiana per la Ricerca sul Cancro (AIRC)Fondazione AIRC
   per la ricerca sul cancro [IG 11377]; My First AIRC grantFondazione AIRC
   per la ricerca sul cancro [MFAG 11502]
FX This study was supported by grant form Associazione Italiana per la
   Ricerca sul Cancro (AIRC, IG 11377, to GD) and My First AIRC grant (MFAG
   11502, to DT). We are greatly indebted to Drs. L Di Renzo and G Bossi
   for their helpful advice, stimulating discussion and for sharing
   reagents. GD dedicates this study to the memory of Professor David Givol
   who with a combination of intelligence, passion, vision, and
   organization was a precious and challenging collaborator and an
   unforgettable friend. We also dedicate this study to the memory of
   Professor Rita Levi Montalcini. May her outstanding contribution to
   science be an immortal legacy and an example for us all.
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NR 59
TC 26
Z9 26
U1 1
U2 7
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 2041-4889
J9 CELL DEATH DIS
JI Cell Death Dis.
PD MAY
PY 2013
VL 4
AR e639
DI 10.1038/cddis.2013.163
PG 11
WC Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Cell Biology
GA 156LR
UT WOS:000319824100028
PM 23703384
OA Green Published, gold
DA 2022-04-25
ER

PT J
AU Zhao, YL
   Zhou, Y
   Wang, MF
AF Zhao, Yueliang
   Zhou, Yue
   Wang, Mingfu
TI Brosimone I, an isoprenoid-substituted flavonoid, induces cell cycle
   G(1) phase arrest and apoptosis through ROS-dependent endoplasmic
   reticulum stress in HCT116 human colon cancer cells
SO FOOD & FUNCTION
LA English
DT Article
ID ER STRESS; AMPK; AUTOPHAGY; GROWTH; DEATH; CALCIUM; HOMEOSTASIS;
   INHIBITION; QUERCETIN; ACTIVATOR
AB Brosimone I is an isoprenoid-substituted flavonoid from Artocarpus heterophyllus. Here, we reported for the first time that brosimone I induced cell cycle G(1) phase arrest and apoptosis in HCT116 human colon cancer cells. Brosimone I treatment increased the cytosolic Ca2+ level, and subsequently activated the CaMKK-AMPK pathway. STO-609, a CaMKK inhibitor, and compound C, an AMPK-specific inhibitor, attenuated brosimone I-induced loss of cell viability in HCT116 cells. Furthermore, brosimone I enhanced ER stress. Salubrinal, an ER stress inhibitor, reduced brosimone I-induced cell growth inhibition. In addition, brosimone I was found to increase ROS generation and the inhibition of ROS formation by NAC, a ROS inhibitor, attenuated brosimone I-induced cell death, cytosolic Ca2+ increase, and ER stress markers. Collectively, our findings reveal that brosimone I induces cell cycle G(1) phase arrest and apoptosis via the induction of ROS-mediated increased cytosolic Ca2+, ER stress, and the activation of the CaMKK-AMPK signaling pathway.
C1 [Zhao, Yueliang; Wang, Mingfu] Shanghai Ocean Univ, Coll Food Sci & Technol, Shanghai 201306, Peoples R China.
   [Zhao, Yueliang] Minist Agr, Lab Qual & Safety Risk Assessment Aquat Prod Stor, Shanghai 201306, Peoples R China.
   [Zhao, Yueliang; Zhou, Yue; Wang, Mingfu] Univ Hong Kong, Sch Biol Sci, Pokfulam Rd, Hong Kong, Peoples R China.
RP Wang, MF (corresponding author), Shanghai Ocean Univ, Coll Food Sci & Technol, Shanghai 201306, Peoples R China.; Wang, MF (corresponding author), Univ Hong Kong, Sch Biol Sci, Pokfulam Rd, Hong Kong, Peoples R China.
EM mfwang@hku.hk
RI Wang, Mingfu/D-3136-2009; Wang, Mingfu/AAT-3292-2021
OI Wang, Mingfu/0000-0003-1469-3963; 
FU Hong Kong Research Grants Council (GRF Project)Hong Kong Research Grants
   Council [17154816]
FX The research was supported by the Hong Kong Research Grants Council (GRF
   Project No.: 17154816). The authors would like to thank Ms Iris M. Y.
   Tse for her technical support and kind advice on this research.
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NR 50
TC 7
Z9 7
U1 4
U2 16
PU ROYAL SOC CHEMISTRY
PI CAMBRIDGE
PA THOMAS GRAHAM HOUSE, SCIENCE PARK, MILTON RD, CAMBRIDGE CB4 0WF, CAMBS,
   ENGLAND
SN 2042-6496
EI 2042-650X
J9 FOOD FUNCT
JI Food Funct.
PD MAY 1
PY 2019
VL 10
IS 5
BP 2729
EP 2738
DI 10.1039/c8fo02315h
PG 10
WC Biochemistry & Molecular Biology; Food Science & Technology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Food Science & Technology
GA HZ8ZR
UT WOS:000469145900038
PM 31038133
DA 2022-04-25
ER

PT J
AU Han, WD
   Sun, J
   Feng, LF
   Wang, KF
   Li, D
   Pan, Q
   Chen, Y
   Jin, W
   Wang, X
   Pan, HM
   Jin, HC
AF Han, Weidong
   Sun, Jie
   Feng, Lifeng
   Wang, KaiFeng
   Li, Da
   Pan, Qin
   Chen, Yan
   Jin, Wei
   Wang, Xian
   Pan, Hongming
   Jin, Hongchuan
TI Autophagy Inhibition Enhances Daunorubicin-Induced Apoptosis in K562
   Cells
SO PLOS ONE
LA English
DT Article
ID COLON-CANCER CELLS; SIGNALING PATHWAYS; DRUG-RESISTANCE; JNK ACTIVATION;
   DEPENDENT ERK; DEATH; INDUCTION; PROTEIN; THERAPY
AB Anthracycline daunorubicin (DNR) is one of the major antitumor agents widely used in the treatment of myeloid leukemia. Unfortunately, the clinical efficacy of DNR was limited because of its cytotoxity at high dosage. As a novel cytoprotective mechanism for tumor cell to survive under unfavorable conditions, autophagy has been proposed to play a role in drug resistance of tumor cells. Whether DNR can activate to impair the sensitivity of cancer cells remains unknown. Here, we first report that DNR can induce a high level of autophagy, which was associated with the activation of extracellular signal-regulated kinase 1/2 (ERK1/2). Moreover, cell death induced by DNR was greatly enhanced after autophagy inhibition by the pharmacological inhibitor chloroquine (CQ) and siRNAs targeting Atg5 and Atg7, the most important components for the formation of autophagosome. In conclusion, we found that DNR can induce cytoprotective autophagy by activation of ERK in myeloid leukemia cells. Autophagy inhibition thus represents a promising approach to improve the efficacy of DNR in the treatment of patients with myeloid leukemia.
C1 [Han, Weidong; Wang, KaiFeng; Li, Da; Pan, Qin; Chen, Yan; Jin, Wei; Wang, Xian; Pan, Hongming] Zhejiang Univ, Coll Med, Sir Run Run Shaw Hosp, Dept Med Oncol, Hangzhou 310003, Zhejiang, Peoples R China.
   [Sun, Jie; Feng, Lifeng; Jin, Hongchuan] Zhejiang Univ, Coll Med, Sir Run Run Shaw Hosp, Biomed Res Ctr,Canc Biol Lab, Hangzhou 310003, Zhejiang, Peoples R China.
RP Pan, HM (corresponding author), Zhejiang Univ, Coll Med, Sir Run Run Shaw Hosp, Dept Med Oncol, Hangzhou 310003, Zhejiang, Peoples R China.
EM panhongming@medmail.com.cn; jinhc@zju.edu.cn
RI Jin, Hongchuan/C-3686-2009
OI Wang, Xian/0000-0003-0041-7589; Jin, Hongchuan/0000-0002-6697-3097
FU National Natural Science Foundation of ChinaNational Natural Science
   Foundation of China (NSFC) [30901740]; China National Ministry of
   Education [20090101120124]; Zhejiang Natural Sciences FoundationNatural
   Science Foundation of Zhejiang Province [Y2090166]; Science Technology
   Department of Zhejiang Province [2010c33168]; Fundamental Research Funds
   for the Central UniversitiesFundamental Research Funds for the Central
   Universities
FX This work was supported by the National Natural Science Foundation of
   China (No.:30901740), China National Ministry of Education Grant (No.:
   20090101120124), Zhejiang Natural Sciences Foundation Grant (No.:
   Y2090166) and Research Projects of Science Technology Department of
   Zhejiang Province (No.: 2010c33168) to WH and the Fundamental Research
   Funds for the Central Universities to HJ. The funders had no role in
   study design, data collection and analysis, decision to publish, or
   preparation of the manuscript.
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NR 30
TC 87
Z9 93
U1 2
U2 22
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 1160 BATTERY STREET, STE 100, SAN FRANCISCO, CA 94111 USA
SN 1932-6203
J9 PLOS ONE
JI PLoS One
PD DEC 2
PY 2011
VL 6
IS 12
AR e28491
DI 10.1371/journal.pone.0028491
PG 7
WC Multidisciplinary Sciences
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Science & Technology - Other Topics
GA 863NO
UT WOS:000298171400101
PM 22164300
OA Green Submitted, Green Published, gold
DA 2022-04-25
ER

PT J
AU Huang, FC
AF Huang, Fu-Chen
TI The Critical Role of Membrane Cholesterol in Salmonella-Induced
   Autophagy in Intestinal Epithelial Cells
SO INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
LA English
DT Article
DE cholesterol; Salmonella; Intestine epithelia; autophagy
ID ENTERICA SEROVAR TYPHIMURIUM; COLON-CANCER CELLS; PROTEIN-KINASE-B;
   PLASMA-MEMBRANE; CROHNS-DISEASE; BECLIN 1; REGULATES AUTOPHAGY;
   INFECTION; PATHWAY; MACROAUTOPHAGY
AB It was previously observed that plasma membrane cholesterol plays a critical role in the Salmonella-induced phosphatidylinositol 3-kinase-dependent (PI3K)-dependent anti-inflammatory response in intestinal epithelial cells (IECs). The PI3K/Akt pathway is associated with autophagy which has emerged as a critical mechanism of host defense against several intracellular bacterial pathogens. Plasma membrane contributes directly to the formation of early Atg16L1-positive autophagosome precursors. Therefore, this study aimed to investigate the role of plasma membrane cholesterol on the Salmonella-induced autophagy in IECs. By using methyl-beta-cyclodextrin (MBCD), it was demonstrated that disruption of membrane cholesterol by MBCD enhanced NOD2 and Atg16L1 proteins expression in membrane, and autophagic LC3II proteins expression and LC3 punctae in Salmonella-infected Caco-2 cells, which was counteracted by Atg16L1 siRNA. Nucleotide-binding oligomerization domain-containing protein 2 (NOD2) siRNA enhanced the Salmonella-induced activation of Akt in Caco-2 cells. However, inhibitors of Akt or extracellular signal-regulated kinases (ERK) had no significant effect on Salmonella-induced autophagy Beclin 1 or LC3 proteins expression. In conclusion, our study suggests that cholesterol accumulation in the plasma membrane at the entry site of Salmonella results in the formation of Salmonella-containing vacuole (SCV) and decreased autophagy. Our results offer mechanistic insights on the critical role of membrane cholesterol in the pathogenesis of Salmonella infection in intestinal epithelial cells and the therapeutic potential of its antagonists.
C1 [Huang, Fu-Chen] Kaohsiung Chang Gung Mem Hosp, Dept Pediat, Kaohsiung 833, Taiwan.
   [Huang, Fu-Chen] Chang Gung Univ, Coll Med, Kaohsiung 833, Taiwan.
RP Huang, FC (corresponding author), Kaohsiung Chang Gung Mem Hosp, Dept Pediat, Kaohsiung 833, Taiwan.
EM huang817@cgmh.org.tw
FU National Science Council grant [NSC94-2314-B-182A-093,
   100-2314-B-182-065]; Chang Gung Memorial Hospital grantChang Gung
   Memorial Hospital [CMRPG860431]
FX Funding from National Science Council grant NSC94-2314-B-182A-093 and
   100-2314-B-182-065 and Chang Gung Memorial Hospital grant CMRPG860431 to
   F.H. is gratefully acknowledged.
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NR 42
TC 14
Z9 14
U1 0
U2 8
PU MDPI AG
PI BASEL
PA POSTFACH, CH-4005 BASEL, SWITZERLAND
SN 1422-0067
J9 INT J MOL SCI
JI Int. J. Mol. Sci.
PD JUL
PY 2014
VL 15
IS 7
BP 12558
EP 12572
DI 10.3390/ijms150712558
PG 15
WC Biochemistry & Molecular Biology; Chemistry, Multidisciplinary
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Chemistry
GA AM7ID
UT WOS:000340038500084
PM 25029544
OA Green Published, Green Submitted, gold
DA 2022-04-25
ER

PT J
AU Hongo, K
   Kazama, S
   Tsuno, NH
   Ishihara, S
   Sunami, E
   Kitayama, J
   Watanabe, T
AF Hongo, Kumiko
   Kazama, Shinsuke
   Tsuno, Nelson H.
   Ishihara, Soichiro
   Sunami, Eiji
   Kitayama, Joji
   Watanabe, Toshiaki
TI Immunohistochemical detection of high-mobility group box 1 correlates
   with resistance of preoperative chemoradiotherapy for lower rectal
   cancer: a retrospective study
SO WORLD JOURNAL OF SURGICAL ONCOLOGY
LA English
DT Article
DE High-mobility group box 1 (HMGB1); Lower rectal cancer;
   Chemoradiotherapy; Immunohistochemistry
ID END-PRODUCTS RAGE; COLORECTAL-CANCER; CHROMATIN PROTEIN; NECROTIC CELLS;
   HMGB1 RELEASE; TUMOR-GROWTH; INFLAMMATION; RECEPTOR; AUTOPHAGY;
   CARCINOMA
AB Background: High-mobility group box 1 (HMGB1) is a nucleoprotein that is related to inflammation. It has been implicated in a variety of biologically important processes, including transcription, DNA repair, differentiation, development, and extracellular signaling. Recently, its important role in the process of tumor invasion, metastasis, and resistance to anti-cancer therapies has been demonstrated. In this study, we aimed to investigate the correlation of HMGB1 expression and resistance of rectal cancer patients to chemoradiotherapy (CRT) prior to curative operation.
   Methods: We retrospectively reviewed the data of 75 lower rectal cancer patients without complete pathological response who had received preoperative CRT and had undergone curative resection at the University of Tokyo Hospital between May 2003 and June 2010. HMGB1 expression in surgically resected specimens was evaluated using immunohistochemical detection and specimens were classified into high or low HMGB1 expression groups. Clinicopathologic features, degree of tumor reduction, regression of tumor grade, and patient survival were compared between the groups using non-paired Student's t-tests and Kaplan-Meier analysis.
   Results: A total of 52 (69.3%) patients had high HMGB1 expression, and 23 (30.7%) had low expression. HMGB1 expression was significantly correlated with histologic type (P = 0.02), lymphatic invasion (P = 0.02), and venous invasion (P = 0.05). Compared to patients with low HMGB1 expression, those with high expression had a poorer response to CRT, in terms of tumor reduction ratio (42.2 versus 28.9%, respectively; P < 0.01) and post-CRT histological tumor regression grade (56.5 versus 30.8% grade 2; respectively; P = 0.03). However, no significant correlation was found between HMGB1 expression and recurrence-free and overall survival rates.
   Conclusions: HMGB1 expression may be one of the key factors regulating the response of rectal cancer to preoperative CRT in terms of tumor invasiveness and resistance to therapy.
C1 [Hongo, Kumiko; Kazama, Shinsuke; Ishihara, Soichiro; Sunami, Eiji; Kitayama, Joji; Watanabe, Toshiaki] Univ Tokyo, Grad Sch Med, Dept Surg Oncol, Bunkyo Ku, Tokyo 1138655, Japan.
   [Tsuno, Nelson H.] Univ Tokyo, Grad Sch Med, Dept Transfus Med, Bunkyo Ku, Tokyo 1138655, Japan.
RP Hongo, K (corresponding author), Univ Tokyo, Grad Sch Med, Dept Surg Oncol, Bunkyo Ku, 7-3-1 Hongo, Tokyo 1138655, Japan.
EM hongokumiko-tky@umin.ac.jp
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NR 49
TC 14
Z9 15
U1 0
U2 6
PU BIOMED CENTRAL LTD
PI LONDON
PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND
SN 1477-7819
J9 WORLD J SURG ONCOL
JI World J. Surg. Oncol.
PD JAN 27
PY 2015
VL 13
AR 7
DI 10.1186/1477-7819-13-7
PG 7
WC Oncology; Surgery
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Surgery
GA CB3YE
UT WOS:000349564600001
PM 25622595
OA Green Published, gold
DA 2022-04-25
ER

PT J
AU Lukovic, J
   Mitrovic, MM
   Popovic, S
   Milosavljevic, Z
   Stanojevic-Pirkovic, M
   Andelkovic, M
   Zelen, I
   Sorak, M
   Muskinja, J
   Ratkovic, Z
   Nikolic, IS
AF Lukovic, Jovan
   Mitrovic, Marina M.
   Popovic, Suzana
   Milosavljevic, Zoran
   Stanojevic-Pirkovic, Marijana
   Andelkovic, Marija
   Zelen, Ivanka
   Sorak, Marija
   Muskinja, Jovana
   Ratkovic, Zoran
   Nikolic, Ivana Sinisa
TI ANTITUMOR EFFECTS OF VANILLIN BASED CHALCONE ANALOGS IN VITRO
SO ACTA POLONIAE PHARMACEUTICA
LA English
DT Article
DE chalcones; colorectal cancer; cytotoxicity; apoptosis; autophagy
ID BIOLOGICAL EVALUATION; CELL-DEATH; MOLECULAR-MECHANISMS; CISPLATIN;
   FLAVOKAWAIN; DERIVATIVES; INHIBITION; ACTIVATION; APOPTOSIS; THERAPY
AB Chalcones, as a large group of organic compounds, are widely implemented in various types of anticancer therapeutics. These plant metabolites are present in fruits, vegetables, spices, and have anti-tumor, anti-inflammation, immunomodulation, antibacterial and anti-oxidative activities, as well as many other pharmacological and biological effects. The aim of the present study was to investigate cytotoxic effects, type of cell death and mechanism of action of the newly synthesized vanillin based chalcone analogs, (CH1) and (CH2) on human colon cancer HCT-116 and noncancerous (control) MRC-5 cell lines. In order to compare the effects of vanillin based chalcone analogs on investigated cell lines, as reference substances cisplatin (cisPt) and dehydrozingerone (DHZ) were used. Investigation of antitumor effect of chalcone analogs on HCT-116 cells was carried out by three methods MTT assay, flow cytometry and immunofluorescence analysis. The result of our investigation indicated that newly synthesized vanillin based chalcone analogs expressed powerful antitumor effect on cancer cells (HCT-116 cell line), while their effect on healthy cells (MRC-5 cell line) was not statistically significant. Vanillin based chalcone analogs caused overexpression and activation of mitochondrial Bax protein and caspase-3 in HCT-116 cells, indicating that their mechanism of antitumor action was mediated through activation of the inner apoptotic pathway. These results indicate possible usefulness of CH1 and CH2 in antitumor therapy whether through its direct cytotoxic effect or as adjuvant therapy. Our results indicate possible usefulness of CH1 and CH2 vanillin based chalcone analogs in antitumor therapy.
C1 [Lukovic, Jovan; Mitrovic, Marina M.; Stanojevic-Pirkovic, Marijana; Andelkovic, Marija; Zelen, Ivanka; Nikolic, Ivana Sinisa] Univ Kragujevac, Fac Med Sci, Dept Biochem, Kragujevac, Serbia.
   [Popovic, Suzana] Univ Kragujevac, Fac Med Sci, Ctr Mol Med & Stem Cell Res, Dept Microbiol & Immunol, Kragujevac, Serbia.
   [Milosavljevic, Zoran] Univ Kragujevac, Fac Med Sci, Dept Histol & Embryol, Kragujevac, Serbia.
   [Sorak, Marija] Univ Kragujevac, Fac Med Sci, Dept Gynecol & Obstet, Kragujevac, Serbia.
   [Muskinja, Jovana; Ratkovic, Zoran] Univ Kragujevac, Fac Sci, Dept Chem, Radoja Domanovica 12,POB 60, Kragujevac 34000, Serbia.
RP Zelen, I (corresponding author), Univ Kragujevac, Fac Med Sci, Dept Biochem, Kragujevac, Serbia.
EM ivanka@medf.kg.ac.rs
RI Suzana, Popovic/AGG-9720-2022
OI Nikolic, Ivana/0000-0002-1782-5506; Muskinja,
   Jovana/0000-0002-0638-3423; Sorak, Marija/0000-0002-3571-0091
FU Faculty of Medical Sciences, University of Kragujevac [JP14/17, 41010]
FX This study was financially supported by Faculty of Medical Sciences,
   University of Kragujevac (JP14/17), the project called "PrekliniEka
   ispitivanja bioaktivnih supstanci (PIBAS)ii, registry number 41010 and
   Prof. Predrag -urdjeviE for technical support.
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NR 41
TC 0
Z9 0
U1 3
U2 12
PU POLSKIE TOWARZYSTWO FARMACEUTYCZNE
PI WARSAW
PA DLUGA 16, 00-238 WARSAW, POLAND
SN 0001-6837
EI 2353-5288
J9 ACTA POL PHARM
JI ACTA POL. PHARM.
PD JAN-FEB
PY 2020
VL 77
IS 1
BP 57
EP 67
DI 10.32383/appdr/112786
PG 11
WC Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA KS3PX
UT WOS:000518225300006
DA 2022-04-25
ER

PT J
AU Kazberuk, A
   Zareba, I
   Palka, J
   Surazynski, A
AF Kazberuk, Adam
   Zareba, Ilona
   Palka, Jerzy
   Surazynski, Arkadiusz
TI A novel plausible mechanism of NSAIDs-induced apoptosis in cancer cells:
   the implication of proline oxidase and peroxisome proliferator-activated
   receptor
SO PHARMACOLOGICAL REPORTS
LA English
DT Review
DE Cancer cells; Apoptosis; Non-steroidal anti-inflammatory drugs;
   Peroxisome proliferator-activated receptor; Proline dehydrogenase;
   Proline oxidase
ID NONSTEROIDAL ANTIINFLAMMATORY DRUGS; GAMMA PPAR-GAMMA; PROLIDASE
   ACTIVITY; COLON-CANCER; TUMOR-SUPPRESSOR; COLLAGEN BIOSYNTHESIS;
   EXTRACELLULAR-MATRIX; UP-REGULATION; LUNG-CANCER; FATTY-ACIDS
AB Although pharmaco-epidemiological studies provided evidence for the anticancer potential of non-steroidal anti-inflammatory drugs (NSAIDs), the mechanism of their anti-cancer activity is not known. Several lines of evidence suggest that proline dehydrogenase/proline oxidase (PRODH/POX) may represent a target for NSAIDs-dependent anti-cancer activity. PRODH/POX catalyzes conversion of proline into Delta 1-pyrroline-5-carboxylate releasing ATP or reactive oxygen species for autophagy/apoptosis. Since NSAIDs are ligands of peroxisome proliferator-activated receptor (PPARs) and PPARs are implicated in PRODH/POX-dependent apoptosis we provided a hypothesis on the mechanism of NSAIDs-induced apoptosis in cancer cells.
C1 [Kazberuk, Adam; Zareba, Ilona; Palka, Jerzy; Surazynski, Arkadiusz] Med Univ Bialystok, Dept Med Chem, Mickiewicza 2D, PL-15222 Bialystok, Poland.
RP Surazynski, A (corresponding author), Med Univ Bialystok, Dept Med Chem, Mickiewicza 2D, PL-15222 Bialystok, Poland.
EM kadam568@gmail.com; ilona.zareba@gmail.com; pal@umb.edu.pl;
   arek@umb.edu.pl
RI Surażynski, Arkadiusz/ABG-2795-2020; Zareba, Ilona/T-6930-2018
OI Surażynski, Arkadiusz/0000-0003-4475-873X; Zareba,
   Ilona/0000-0002-7934-6973; Kazberuk, Adam/0000-0002-8485-6505
FU National Science CentreNational Science Centre, Poland
   [2017/27/N/NZ7/02370]
FX This research was supported by the National Science Centre, Grant number
   2017/27/N/NZ7/02370.
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NR 105
TC 7
Z9 7
U1 2
U2 7
PU SPRINGER HEIDELBERG
PI HEIDELBERG
PA TIERGARTENSTRASSE 17, D-69121 HEIDELBERG, GERMANY
SN 1734-1140
EI 2299-5684
J9 PHARMACOL REP
JI Pharmacol. Rep.
PD OCT
PY 2020
VL 72
IS 5
BP 1152
EP 1160
DI 10.1007/s43440-020-00140-z
EA JUL 2020
PG 9
WC Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA OI4ND
UT WOS:000556131300001
PM 32710395
OA Green Published, hybrid
DA 2022-04-25
ER

PT J
AU Wang, LH
   Huang, WD
   Zhan, JC
AF Wang, Lihua
   Huang, Weidong
   Zhan, Jicheng
TI Grape Seed Proanthocyanidins Induce Autophagy and Modulate Survivin in
   HepG2 Cells and Inhibit Xenograft Tumor Growth in Vivo
SO NUTRIENTS
LA English
DT Article
DE hepatocellular carcinoma; HepG2 cells; grape seed proanthocyanidins;
   autophagy; survivin; xenograft
ID COLON-CANCER CELLS; APOPTOSIS; EXTRACT; VITRO; GENE; GENERATION;
   PREVENTION; THERAPY; DEATH
AB Liver cancer is one of the leading causes of death worldwide. Although radiotherapy and chemotherapy are effective in general, they present various side effects, significantly limiting the curative effect. Increasing evidence has shown that the dietary intake of phytochemicals plays an essential role in the chemoprevention or chemotherapy of tumors. In this work, HepG2 cells and nude mice with HepG2-derived xenografts were treated with grape seed proanthocyanidins (GSPs). The results showed that GSPs induced autophagy, and inhibition of autophagy increased apoptosis in HepG2 cells. In addition, GSPs also reduced the expression of survivin. Moreover, survivin was involved in GSPs-induced apoptosis. GSPs at 100 mg/kg and 200 mg/kg significantly inhibited the growth of HepG2 cells in nude mice without causing observable toxicity and autophagy, while inducing the phosphorylation of mitogen-activated protein kinase (MAPK) pathway-associated proteins, p-JNK, p-ERK and p-p38 MAPK and reducing the expression of survivin. These results suggested that GSPs might be promising phytochemicals against liver cancer.
C1 [Wang, Lihua; Huang, Weidong; Zhan, Jicheng] China Agr Univ, Beijing Key Lab Viticulture & Enol, Coll Food Sci & Nutr Engn, Beijing 100083, Peoples R China.
RP Zhan, JC (corresponding author), China Agr Univ, Beijing Key Lab Viticulture & Enol, Coll Food Sci & Nutr Engn, Beijing 100083, Peoples R China.
EM lihuawang@cau.edu.cn; huanggwd@263.net; zhanjicheng@cau.edu.cn
RI Zhan, Jicheng/ABF-8501-2021
FU National Key Research and Development Program of China [2017YFD0401202]
FX This work was supported by The National Key Research and Development
   Program of China (2017YFD0401202).
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PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 2072-6643
J9 NUTRIENTS
JI Nutrients
PD DEC
PY 2019
VL 11
IS 12
AR 2983
DI 10.3390/nu11122983
PG 17
WC Nutrition & Dietetics
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Nutrition & Dietetics
GA KC0ZV
UT WOS:000506917800145
PM 31817589
OA gold, Green Published
DA 2022-04-25
ER

PT J
AU Morselli, E
   Shen, SS
   Ruckenstuhl, C
   Bauer, MA
   Marino, G
   Galluzzi, L
   Criollo, A
   Michaud, M
   Maiuri, MC
   Chano, T
   Madeo, F
   Kroemer, G
AF Morselli, Eugenia
   Shen, Shensi
   Ruckenstuhl, Christoph
   Bauer, Maria Anna
   Marino, Guillermo
   Galluzzi, Lorenzo
   Criollo, Alfredo
   Michaud, Mickael
   Maiuri, Maria Chiara
   Chano, Tokuhiro
   Madeo, Frank
   Kroemer, Guido
TI p53 inhibits autophagy by interacting with the human ortholog of yeast
   Atg17, RB1CC1/FIP200
SO CELL CYCLE
LA English
DT Article
DE aging; longevity; mTOR; rapamycin; Saccharomyces cerevisiae
ID LIFE-SPAN EXTENSION; HUMAN BREAST-CANCER; CYTOPLASMIC P53; FIP200;
   CELLS; LONGEVITY; APOPTOSIS; COMPLEX; PATHWAYS; PROTEIN
AB The tumor suppressor protein p53 tonically suppresses autophagy when it is present in the cytoplasm. This effect is phylogenetically conserved from mammals to nematodes, and human p53 can inhibit autophagy in yeast, as we show here. Bioinformatic investigations of the p53 interactome in relationship to the autophagy-relevant protein network underscored the possible relevance of a direct molecular interaction between p53 and the mammalian ortholog of the essential yeast autophagy protein Atg17, namely RB1-inducible coiled-coil protein 1 (RB1CC1), also called FAK family kinase-interacting protein of 200 KDa (FIP200). Mutational analyses revealed that a single point mutation in p53 (K382R) abolished its capacity to inhibit autophagy upon transfection into p53-deficient human colon cancer or yeast cells. In conditions in which wild type p53 co-immunoprecipitated with RB1CC1/FIP200, p53(K382R) failed to do so, underscoring the importance of the physical interaction between these proteins for the control of autophagy. In conclusion, p53 regulates autophagy through a direct molecular interaction with RB1CC1/FIP200, a protein that is essential for the very apical step of autophagy initiation.
C1 [Morselli, Eugenia; Shen, Shensi; Marino, Guillermo; Galluzzi, Lorenzo; Criollo, Alfredo; Michaud, Mickael; Maiuri, Maria Chiara; Kroemer, Guido] INSERM, U848, Paris, France.
   [Morselli, Eugenia; Shen, Shensi; Marino, Guillermo; Galluzzi, Lorenzo; Criollo, Alfredo; Michaud, Mickael; Maiuri, Maria Chiara; Kroemer, Guido] Inst Gustave Roussy, Paris, France.
   [Morselli, Eugenia; Shen, Shensi; Marino, Guillermo; Galluzzi, Lorenzo; Criollo, Alfredo; Michaud, Mickael; Maiuri, Maria Chiara] Univ Paris 11, Paris, France.
   [Ruckenstuhl, Christoph; Bauer, Maria Anna; Madeo, Frank] Graz Univ, Inst Mol Biosci, Graz, Austria.
   [Ruckenstuhl, Christoph] Med Univ Graz, Inst Pathol, Graz, Austria.
   [Chano, Tokuhiro] Shiga Univ Med Sci, Dept Clin Lab Med, Shiga, Japan.
   [Kroemer, Guido] Ctr Rech Cordeliers, Paris, France.
   [Kroemer, Guido] Univ Paris 05, Paris, France.
   [Kroemer, Guido] Hop Europeen Georges Pompidou, Paris, France.
   [Kroemer, Guido] Inst Gustave Roussy, Villejuif, France.
RP Kroemer, G (corresponding author), INSERM, U848, Paris, France.
EM kroemer@orange.fr
RI Kroemer, Guido/AAY-9859-2020; GARCÍA, GUILLERMO MARIÑO/J-1726-2012;
   KROEMER, Guido/B-4263-2013; Galluzzi, Lorenzo/AAH-3286-2021; SHEN,
   Shensi/AAW-2735-2020; Galluzzi, Lorenzo/AAG-6294-2019; Galluzzi,
   Lorenzo/K-2709-2012; GARCÍA, GUILLERMO MARIÑO/AAI-8015-2020; Chano,
   Tokuhiro/F-5816-2018; Galluzzi, Lorenzo/AAG-6432-2019
OI GARCÍA, GUILLERMO MARIÑO/0000-0003-1960-1677; KROEMER,
   Guido/0000-0002-9334-4405; SHEN, Shensi/0000-0002-5087-8220; Galluzzi,
   Lorenzo/0000-0003-2257-8500; Chano, Tokuhiro/0000-0002-9959-1183; Bauer,
   Maria A./0000-0003-3211-0434; Madeo, Frank/0000-0002-5070-1329;
   Ruckenstuhl, Christoph/0000-0002-4338-4679; Criollo,
   Alfredo/0000-0002-2737-7751
FU Ligue Nationale contre le Cancer (Equipes labelisee); Agence Nationale
   pour la Recherche (ANR)French National Research Agency (ANR); European
   CommissionEuropean CommissionEuropean Commission Joint Research Centre;
   Fondation pour la Recherche Medicale (FRM)Fondation pour la Recherche
   Medicale; Institut National du Cancer (INCa)Institut National du Cancer
   (INCA) France; Fondation Bettencourt-Schueller; Canceropole
   Ile-de-FranceRegion Ile-de-France; AXA Chair for Longevity Research;
   Austrian Science Fund FWF (Austria)Austrian Science Fund (FWF) [P23490]
FX We thank Dr. Wei Gu for providing the p53 plasmids. G.K. is supported by
   the Ligue Nationale contre le Cancer (Equipes labelisee), Agence
   Nationale pour la Recherche (ANR), European Commission (Active p53,
   Apo-Sys, ChemoRes, ApopTrain, ArtForce), Fondation pour la Recherche
   Medicale (FRM), Institut National du Cancer (INCa), Fondation
   Bettencourt-Schueller, Canceropole Ile-de-France, and the AXA Chair for
   Longevity Research. F.M. is supported by the Austrian Science Fund FWF
   (Austria, grant P23490), and the European Commission (Apo-Sys).
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NR 61
TC 100
Z9 105
U1 0
U2 21
PU LANDES BIOSCIENCE
PI AUSTIN
PA 1806 RIO GRANDE ST, AUSTIN, TX 78702 USA
SN 1538-4101
J9 CELL CYCLE
JI Cell Cycle
PD AUG 15
PY 2011
VL 10
IS 16
BP 2763
EP 2769
DI 10.4161/cc.10.16.16868
PG 7
WC Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Cell Biology
GA 810VK
UT WOS:000294155600031
PM 21775823
OA Bronze
DA 2022-04-25
ER

PT J
AU Kim, JC
   Ha, YJ
   Tak, KH
   Roh, SA
   Kwon, YH
   Kim, CW
   Yoon, YS
   Lee, JL
   Park, Y
   Kim, SK
   Kim, SY
   Cho, DH
   Kim, YS
AF Kim, Jin Cheon
   Ha, Ye Jin
   Tak, Ka Hee
   Roh, Seon Ae
   Kwon, Yi Hong
   Kim, Chan Wook
   Yoon, Yong Sik
   Lee, Jong Lyul
   Park, Yangsoon
   Kim, Seon-Kyu
   Kim, Seon-Young
   Cho, Dong-Hyung
   Kim, Yong Sung
TI Opposite functions of GSN and OAS2 on colorectal cancer metastasis,
   mediating perineural and lymphovascular invasion, respectively
SO PLOS ONE
LA English
DT Article
ID MESENCHYMAL TRANSITION; PROGNOSTIC-FACTOR; EXPRESSION; AUTOPHAGY; COLON;
   GELSOLIN; GROWTH; SYNTHETASE; ACTIVATION; SUPPRESSOR
AB The present study aimed to identify molecules associated with lymphovascular invasion (LVI) and perineural invasion (PNI) and to examine their biological behavior in colorectal cancer (CRC). LVI- and PNI-associated molecules were identified and verified using sequential processes including (1) identification of 117 recurrence-associated genes differentially expressed on RNA-seq analysis using primary cancer tissues from 130 CRC patients with and without systemic recurrence; (2) analysis of molecules associated with LVI and PNI; (3) assessment of biological properties by measuring proliferation, anoikis, invasion/migration, epithelial-mesenchymal transition and autophagy flux; and (4) verification of disease-free survival using public datasets. Gelsolin (GSN) and 2'-5'-oligoadenylate synthetase 2 (OAS2) were associated with PNI and LVI, respectively. Invasion potential was >2-fold greater in GSN-overexpressing LoVo cells than in control cells (p<0.001-0.005), whereas OAS2-overexpressing RKO cells showed reduced invasion (p<0.001-0.005). GSN downregulated E-cadherin, beta-catenin, claudin-1 and snail, and upregulated N-cadherin and ZEB1, whereas OAS2 overexpression had the opposite effects. Several autophagy-related proteins including ATG5-12, ATG6/BECN1, ATG7 and ATG101 were downregulated in GSN-overexpressing LoVo cells, whereas the opposite pattern was observed in OAS2-overexpressing RKO cells. Patients with low GSN expression had significantly higher 5-year recurrence-free survival (RFS) rates than those with GSN overexpression (73.6% vs. 64.7%, p = 0.038), whereas RFS was longer in patients with OAS2 overexpression than in those with underexpression (73.4% vs. 63.7%, p = 0.01). In conclusion, GSN and OAS2 were positively and negatively associated with recurrence, respectively, suggesting their potential value as predictors of recurrence or therapeutic targets in CRC patients.
C1 [Kim, Jin Cheon; Ha, Ye Jin; Tak, Ka Hee; Roh, Seon Ae; Kwon, Yi Hong; Kim, Chan Wook; Yoon, Yong Sik; Lee, Jong Lyul] Univ Ulsan, Dept Surg, Coll Med, Seoul, South Korea.
   [Kim, Jin Cheon; Ha, Ye Jin; Tak, Ka Hee; Roh, Seon Ae; Kwon, Yi Hong; Kim, Chan Wook; Yoon, Yong Sik; Lee, Jong Lyul; Park, Yangsoon; Kim, Seon-Kyu; Kim, Seon-Young; Cho, Dong-Hyung; Kim, Yong Sung] Asan Med Ctr, Inst Innovat Canc Res, Seoul, South Korea.
   [Park, Yangsoon] Univ Ulsan, Dept Pathol, Coll Med, Seoul, South Korea.
   [Kim, Seon-Kyu; Kim, Seon-Young; Kim, Yong Sung] Korea Res Inst Biosci & Biotechnol, Med Genom Res Ctr, Daejeon, South Korea.
   [Cho, Dong-Hyung] Kyungpook Natl Univ, Sch Life Sci, Daegu, South Korea.
RP Kim, JC (corresponding author), Univ Ulsan, Dept Surg, Coll Med, Seoul, South Korea.; Kim, JC; Cho, DH; Kim, YS (corresponding author), Asan Med Ctr, Inst Innovat Canc Res, Seoul, South Korea.; Kim, YS (corresponding author), Korea Res Inst Biosci & Biotechnol, Med Genom Res Ctr, Daejeon, South Korea.; Cho, DH (corresponding author), Kyungpook Natl Univ, Sch Life Sci, Daegu, South Korea.
EM jckim@amc.seoul.kr; chodong03@gmail.com; yongsung@kribb.re.kr
RI Lww, Jong Lyul/W-1791-2019
OI Lww, Jong Lyul/0000-0002-5878-8000; Kim, Seon-Kyu/0000-0002-4176-5187
FU Korea Research FoundationKorea Research Foundation [2016R1E1A1A02919844,
   2017R1A2B1009062]; Ministry of Science, ICT, and Future Planning,
   Republic of Korea
FX This work was supported by grants from the Korea Research Foundation
   (2016R1E1A1A02919844 to JCK and 2017R1A2B1009062 to SAR), Ministry of
   Science, ICT, and Future Planning, Republic of Korea. The funders had no
   role in study design, data collection and analysis, decision to publish,
   or preparation of the manuscript.
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NR 36
TC 14
Z9 15
U1 0
U2 1
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 1160 BATTERY STREET, STE 100, SAN FRANCISCO, CA 94111 USA
SN 1932-6203
J9 PLOS ONE
JI PLoS One
PD AUG 27
PY 2018
VL 13
IS 8
AR e0202856
DI 10.1371/journal.pone.0202856
PG 16
WC Multidisciplinary Sciences
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Science & Technology - Other Topics
GA GR6UK
UT WOS:000442804200028
PM 30148861
OA Green Published, Green Submitted, gold
DA 2022-04-25
ER

PT J
AU Chen, RJ
   Tsai, SJ
   Ho, CT
   Pan, MH
   Ho, YS
   Wu, CH
   Wang, YJ
AF Chen, Rong-Jane
   Tsai, Shang-Jie
   Ho, Chi-Tang
   Pan, Min-Hsiung
   Ho, Yuan-Soon
   Wu, Chih-Hsiung
   Wang, Ying-Jan
TI Chemopreventive Effects of Pterostilbene on Urethane-Induced Lung
   Carcinogenesis in Mice via the Inhibition of EGFR-Mediated Pathways and
   the Induction of Apoptosis and Autophagy
SO JOURNAL OF AGRICULTURAL AND FOOD CHEMISTRY
LA English
DT Article
DE chemopreventive; pterostilbene; urethane; EGFR; autophagy
ID SIGNAL-TRANSDUCTION PATHWAYS; NF-KAPPA-B; COLON CARCINOGENESIS;
   CELL-CYCLE; CANCER; MUTATIONS; ADENOCARCINOMA; PROLIFERATION;
   ANTIOXIDANT; BLUEBERRIES
AB Lung cancer is the most commonly diagnosed cancer and the leading cause of cancer deaths globally. Due to the lack of successful chemopreventive agents for lung cancer, there is an emerging need to evaluate new and effective agents for lung cancer prevention. Pterostilbene, a naturally occurring analogue of resveratrol, has been reported to be an effective chemopreventive agent against many cancers. The aim of this study is to investigate the chemopreventive effects of pterostilbene in urethane-induced murine lung tumors. Pretreatment with pterostilbene at 50 or 250 mg/kg significantly reduced tumor multiplicity by 26 and 49%, respectively. Pterostilbene also significantly inhibited tumor volume by 25 and 34% and decreased the tumor burden per mouse by 45 and 63%, respectively. The Mechanisms by which pterostilbene suppresses lung tumorigenesis have been investigated in lung tissues and homogenates. The results indicate that the pterostilbene-mediated chemopreventive effects in vivo were a result of the inhibition of epidermal growth factor receptor (EGFR) and its downstream pathways, leading to retarded cell cycle progression, and of the induction of apoptosis and autophagy during urethane-induced lung tumorigenesis.
C1 [Chen, Rong-Jane; Tsai, Shang-Jie; Wang, Ying-Jan] Natl Cheng Kung Univ, Coll Med, Dept Environm & Occupat Hlth, Tainan 70428, Taiwan.
   [Chen, Rong-Jane] Taipei Med Univ, Grad Inst Clin Med, Taipei, Taiwan.
   [Ho, Chi-Tang] Rutgers State Univ, Dept Food Sci, New Brunswick, NJ 08903 USA.
   [Pan, Min-Hsiung] Natl Kaohsiung Marine Univ, Dept Seafood Sci, Kaohsiung, Taiwan.
   [Ho, Yuan-Soon] Taipei Med Univ, Sch Med Technol & Biotechnol, Taipei, Taiwan.
   [Ho, Yuan-Soon; Wu, Chih-Hsiung] Taipei Med Univ, Ctr Excellence Canc Res, Taipei, Taiwan.
   [Wu, Chih-Hsiung] Taipei Med Univ, Shuang Ho Hosp, Sch Med, Dept Surg, Taipei, Taiwan.
RP Wu, CH (corresponding author), Taipei Med Univ, Shuang Ho Hosp, Sch Med, Dept Surg, 291 Jhongjheng Rd, Jhonghe City 23561, Taipei County, Taiwan.
EM chwu@tmu.edu.tw; yjwang@mail.ncku.edu.tw
RI Pan, Min-Hsiung/AAT-8865-2021
OI Pan, Min-Hsiung/0000-0002-5188-7030
FU National Science CouncilMinistry of Science and Technology, Taiwan [NSC
   100-2314-B-006-055]; Food and Drug Administration, Department of Health,
   Executive Yuan [DOH101-FDA-41301]; Taipei Medical University, Center of
   Excellence for Cancer Research (TMU-CECR) [DOH101-TD-C-111-008]
FX We thank the commission of this study by the National Science Council
   (NSC 100-2314-B-006-055), Food and Drug Administration, Department of
   Health, Executive Yuan (DOH101-FDA-41301), and Taipei Medical
   University, Center of Excellence for Cancer Research (TMU-CECR,
   DOH101-TD-C-111-008), for their support.
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NR 41
TC 46
Z9 48
U1 0
U2 21
PU AMER CHEMICAL SOC
PI WASHINGTON
PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA
SN 0021-8561
EI 1520-5118
J9 J AGR FOOD CHEM
JI J. Agric. Food Chem.
PD NOV 21
PY 2012
VL 60
IS 46
BP 11533
EP 11541
DI 10.1021/jf302778a
PG 9
WC Agriculture, Multidisciplinary; Chemistry, Applied; Food Science &
   Technology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Agriculture; Chemistry; Food Science & Technology
GA 040LY
UT WOS:000311325300009
PM 23113763
DA 2022-04-25
ER

PT J
AU Zorc, B
   Rajic, Z
   Perkovic, I
AF Zorc, Branka
   Rajic, Zrinka
   Perkovic, Ivana
TI Antiproliferative evaluation of various aminoquinoline derivatives
SO ACTA PHARMACEUTICA
LA English
DT Article
DE primaquine; chloroquine; mefloquine; fumardiamide; antiproliferative
   activity
ID LUNG-CANCER CELLS; PRIMAQUINE DERIVATIVES; SUBSTITUENTS SYNTHESIS;
   ANTIMALARIAL-DRUGS; CHLOROQUINE; AUTOPHAGY; UREA; ANTIMYCOBACTERIAL;
   UREIDOAMIDES; ARTEMISININ
AB Four classes of aminoquinoline derivatives were prepared: primaquine ureas 1a-f, primaquine bis-ureas 2a-f, chloroquine fumardiamides 3a-f and mefloquine fumardiamides 4a-f. Their antiproliferative activities against breast adenocarcinoma (MCF-7), lung carcinoma (H460) and colon carcinoma (HCT 116 and SW620) cell lines were evaluated in vitro, using MTT cell proliferation assay. The results revealed a low activity of primaquine urea and bis-urea derivatives and high activity of all fumardiamides, with IC50 values in low micromolar range against all tested cancer cell lines.
C1 [Zorc, Branka; Rajic, Zrinka; Perkovic, Ivana] Univ Zagreb, Fac Pharm & Biochem, Dept Med Chem, Zagreb 10000, Croatia.
RP Zorc, B (corresponding author), Univ Zagreb, Fac Pharm & Biochem, Dept Med Chem, Zagreb 10000, Croatia.
EM bzorc@pharma.hr
FU Croatian Science Foundation [IP-2014-09-1501]
FX The study was supported by the Croatian Science Foundation (research
   project IP-2014-09-1501). We thank Katja Ester, Lidija Uzelac and
   Marijeta Kralj for antiproliferative screening and Toma Keser for the
   experiments with glutathione.
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NR 40
TC 0
Z9 0
U1 0
U2 2
PU HRVATSKO FARMACEUTSKO DRUSTOV (HFD)-CROATION PHARMACEUTICAL SOC
PI ZAGREB
PA MASARYKOVA 2, 10000 ZAGREB, CROATIA
SN 1330-0075
EI 1846-9558
J9 ACTA PHARMACEUT
JI Acta Pharm.
PD DEC
PY 2019
VL 69
IS 4
BP 661
EP 672
DI 10.2478/acph-2019-0048
PG 12
WC Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA JJ1BS
UT WOS:000493896000014
PM 31639093
OA Green Published, gold
DA 2022-04-25
ER

PT J
AU Cruickshanks, N
   Roberts, JL
   Bareford, MD
   Tavallai, M
   Poklepovic, A
   Booth, L
   Spiegel, S
   Dent, P
AF Cruickshanks, Nichola
   Roberts, Jane L.
   Bareford, M. Danielle
   Tavallai, Mehrad
   Poklepovic, Andrew
   Booth, Laurence
   Spiegel, Sarah
   Dent, Paul
TI Differential regulation of autophagy and cell viability by ceramide
   species
SO CANCER BIOLOGY & THERAPY
LA English
DT Article
DE FTY720; Gilenya; Pemetrexed; Alimta; ceramide; S1P; autophagy; CerS2;
   CerS6
ID SPHINGOSINE KINASE TYPE-2; FTY720 INDUCES APOPTOSIS; CANCER-CELLS;
   CARCINOMA CELLS; IMMUNOSUPPRESSANT FTY720; GLIOBLASTOMA-MULTIFORME;
   TUMOR SUPPRESSION; DRUG FTY720; H-RAS; ACTIVATION
AB The present studies sought to determine whether the anti-folate pemetrexed (Alimta) and the sphingosine-1-phosphate receptor modulator FTY720 (Fingolimod, Gilenya) interacted to kill tumor cells. FTY720 and pemetrexed interacted in a greater than additive fashion to kill breast, brain and colorectal cancer cells. Loss of p53 function weakly enhanced the toxicity of FTY720 whereas deletion of activated RAS strongly or expression of catalytically inactive AKT facilitated killing. Combined drug exposure reduced the activity of AKT, p70 S6K and mTOR and activated JNK and p38 MAPK. Expression of activated forms of AKT, p70 S6K and mTOR or inhibition of JNK and p38 MAPK suppressed the interaction between FTY720 and pemetrexed. Treatment of cells with FTY720 and pemetrexed increased the numbers of early autophagosomes but not autolysosomes, which correlated with increased LC3II processing and increased p62 levels, suggestive of stalled autophagic flux. Knock down of ATG5 or Beclin1 suppressed autophagosome formation and cell killing. Knock down of ceramide synthase 6 suppressed autophagosome production and cell killing whereas knock down of ceramide synthase 2 enhanced vesicle formation and facilitated death. Collectively our findings argue that pemetrexed and FTY720 could be a novel adjunct modality for breast cancer treatment.
C1 [Cruickshanks, Nichola; Roberts, Jane L.; Bareford, M. Danielle; Tavallai, Mehrad; Booth, Laurence; Spiegel, Sarah; Dent, Paul] Virginia Commonwealth Univ, Dept Biochem & Mol Biol, Richmond, VA 23284 USA.
   [Poklepovic, Andrew] Virginia Commonwealth Univ, Dept Med, Richmond, VA 23298 USA.
RP Dent, P (corresponding author), Virginia Commonwealth Univ, Dept Biochem & Mol Biol, Richmond, VA 23284 USA.
EM pdent@vcu.edu
FU PHS from the National Institutes of Health [R01-CA141704, R01-CA150214,
   R01-DK52825, R01-CA61774]; NATIONAL CANCER INSTITUTEUnited States
   Department of Health & Human ServicesNational Institutes of Health (NIH)
   - USANIH National Cancer Institute (NCI) [P30CA016059] Funding Source:
   NIH RePORTER
FX Support for the present study was funded from PHS grants from the
   National Institutes of Health [R01-CA141704, R01-CA150214, R01-DK52825,
   R01-CA61774].
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NR 44
TC 16
Z9 18
U1 2
U2 22
PU TAYLOR & FRANCIS INC
PI PHILADELPHIA
PA 530 WALNUT STREET, STE 850, PHILADELPHIA, PA 19106 USA
SN 1538-4047
EI 1555-8576
J9 CANCER BIOL THER
JI Cancer Biol. Ther.
PD MAY
PY 2015
VL 16
IS 5
BP 733
EP 742
DI 10.1080/15384047.2015.1026509
PG 10
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA CI7XY
UT WOS:000354981300013
PM 25803131
OA Green Published, Bronze
DA 2022-04-25
ER

PT J
AU Chandrika, BB
   Maney, SK
   Lekshmi, SU
   Joseph, J
   Seervi, M
   Praveen, KS
   Santhoshkumar, TR
AF Chandrika, Bhavya Balan
   Maney, Sathish Kumar
   Lekshmi, Swathi U.
   Joseph, Jeena
   Seervi, Mahendra
   Praveen, K. S.
   Santhoshkumar, T. R.
TI Bax deficiency mediated drug resistance can be reversed by endoplasmic
   reticulum stress induced death signaling
SO BIOCHEMICAL PHARMACOLOGY
LA English
DT Article
DE Drug resistance; ER stress; Bax mutation; Apoptosis; Autophagy
ID MICROSATELLITE MUTATOR PHENOTYPE; PROAPOPTOTIC GENE BAX; CYTOCHROME-C
   RELEASE; MUTATIONAL INACTIVATION; APOPTOTIC RESPONSE; COLORECTAL
   CANCERS; SOLID TUMORS; MITOCHONDRIA; ACTIVATION; PROTEINS
AB Tumors often acquire drug resistance due to functional loss of pro apoptotic gene Bax, a critical and essential component of cell death rendering them insensitive to most anti-tumor agents. Compounds that can induce Bax independent apoptotic cell death are expected to overcome such drug resistance. We have employed a live cell based screening platform to identify potential compounds that can induce programmed cell death in Bax deficiency. Release of cytochrome C from mitochondria into the cytosol is a decisive initial event required for the caspase dependent cell death. We have engineered both wild type and Bax knock out colon cancer cells stably expressing cytochrome C with EGFP fusion protein to identify compounds that can trigger cytochrome C release in both cells with equal efficiency. In the fluorescent translocation assay, most of the drugs tested failed to induce cytochrome C release in Bax deficient cells validating the sensitivity of the assay. This study identified five lead compounds such as thapsigargin, tunicamycine, MG132, kaempferol and camptothecin that could induce cytochrome C release in both wild type and Bax deficient cells with equal potency. All the positive hits induced ER stress signaling as evidenced by up-regulation of Grp78. Studies with a Bak deficient cells indicate that Bak deficiency confers protection to cells from ER stress through autophagy. Further studies revealed that ER stress inducing agents are capable of triggering classical mitochondrial apoptotic cell death through the conformational activation of Bak, substantiating the potential of this pathway in designing drugs against Bax deficiency mediated drug resistance. (C) 2010 Elsevier Inc. All rights reserved.
C1 [Chandrika, Bhavya Balan; Maney, Sathish Kumar; Lekshmi, Swathi U.; Joseph, Jeena; Seervi, Mahendra; Praveen, K. S.; Santhoshkumar, T. R.] Rajiv Gandhi Ctr Biotechnol, Integrated Canc Res, Trivandrum 695014, Kerala, India.
RP Santhoshkumar, TR (corresponding author), Rajiv Gandhi Ctr Biotechnol, Integrated Canc Res, Trivandrum 695014, Kerala, India.
EM trsanthosh@rgcb.res.in
RI Seervi, Mahendra/K-8812-2019
OI Seervi, Mahendra/0000-0002-0266-2062
FU Department of Biotechnology; Department of Science and Technology,
   University Grant CommissionDepartment of Science & Technology
   (India)University Grants Commission, India; International Foundation of
   Science (Sweden)International Foundation for Science
FX This work was supported by funding from Department of Biotechnology
   (IYBA Award), Department of Science and Technology, University Grant
   Commission, and International Foundation of Science (Sweden).
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NR 40
TC 18
Z9 18
U1 0
U2 4
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0006-2952
EI 1873-2968
J9 BIOCHEM PHARMACOL
JI Biochem. Pharmacol.
PD JUN 1
PY 2010
VL 79
IS 11
BP 1589
EP 1599
DI 10.1016/j.bcp.2010.01.032
PG 11
WC Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA 581RA
UT WOS:000276540800007
PM 20138027
DA 2022-04-25
ER

PT J
AU Zhou, Y
   Yang, LP
   Xiong, L
   Wang, KP
   Hou, XY
   Li, QL
   Kong, FH
   Liu, X
   He, J
AF Zhou, Yan
   Yang, Leping
   Xiong, Li
   Wang, Kunpeng
   Hou, Xuyang
   Li, Qinglong
   Kong, Fanhua
   Liu, Xi
   He, Jun
TI KIF11 is upregulated in colorectal cancer and silencing of it impairs
   tumor growth and sensitizes colorectal cancer cells to oxaliplatin via
   p53/GSK3 beta signaling
SO JOURNAL OF CANCER
LA English
DT Article
DE KIF11; colorectal cancer; oxaliplatin; autophagy; GSK3 beta
ID CLINICAL-PRACTICE GUIDELINES; BREAST-CANCER; KINESIN SUPERFAMILY;
   RECTAL-CANCER; PHASE-I; INHIBITOR; EXPRESSION; AUTOPHAGY; TRIAL
AB Colorectal cancer (CRC) is the most frequently diagnosed cancer of the digestive tract. Chemotherapy drugs such as oxaliplatin are frequently administered to CRC patients diagnosed with advanced or metastatic disease. A deep understanding of the molecular mechanism underlying CRC tumorigenesis and identification of optimal biomarkers for estimating chemotherapy sensitivity are essential for the treatment of CRC. Numerous members of the kinesin family are dysregulated in cancers, contributing to tumorigenesis, metastasis and drug resistance. KIF11 is a key component of the bipolar spindle and is highly expressed in several cancer types. We analyzed KIF11 expression in clinical samples by Western blotting and qRT-PCR and explored its role and mechanism in CRC growth and sensitivity to oxaliplatin via detection of the phosphorylation profile of kinases and gain-and-loss-of-function assays. We found that KIF11 was upregulated in CRC tissues and was associated with advanced clinical stage and vessel invasion and that knockdown of KIF11 led to tumor growth arrest and increased sensitivity to oxaliplatin via enhanced DNA damage and apoptosis. Mechanistically, aberrantly activated p53 signaling or possibly deactivated GSK3 beta signaling was responsible for KIF11 knockdown-mediated effects in CRC cells. Thus, our data firmly demonstrated that KIF11 could serve as a potential oncogene and proper biomarker for assessing oxaliplatin sensitivity in CRC.
C1 [Zhou, Yan; Yang, Leping; Xiong, Li; Hou, Xuyang; Li, Qinglong; Kong, Fanhua; Liu, Xi; He, Jun] Cent South Univ, Xiangya Hosp2, Dept Gen Surg, Changsha 410011, Hunan, Peoples R China.
   [Wang, Kunpeng] Taizhou Univ Hosp, Taizhou Cent Hosp, Dept Gen Surg, Taizhou 318000, Zhejiang, Peoples R China.
RP He, J (corresponding author), Cent South Univ, Xiangya Hosp2, Dept Gen Surg, Changsha 410011, Hunan, Peoples R China.
EM junjunhe@csu.edu.cn
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NR 46
TC 2
Z9 2
U1 0
U2 2
PU IVYSPRING INT PUBL
PI LAKE HAVEN
PA PO BOX 4546, LAKE HAVEN, NSW 2263, AUSTRALIA
SN 1837-9664
J9 J CANCER
JI J. Cancer
PY 2021
VL 12
IS 12
BP 3741
EP 3753
DI 10.7150/jca.52103
PG 13
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA RZ4TW
UT WOS:000648591100030
PM 33995648
OA gold, Green Published
DA 2022-04-25
ER

PT J
AU See, CS
   Kitagawa, M
   Liao, PJ
   Lee, KH
   Wong, J
   Lee, SH
   Dymock, BW
AF See, Cheng Shang
   Kitagawa, Mayumi
   Liao, Pei-Ju
   Lee, Kyung Hee
   Wong, Jasmine
   Lee, Sang Hyun
   Dymock, Brian W.
TI Discovery of the cancer cell selective dual acting anti-cancer agent
   (Z)-2-(1H-indol-3-yl)-3-(isoquinolin-5-yl)acrylonitrile (A131)
SO EUROPEAN JOURNAL OF MEDICINAL CHEMISTRY
LA English
DT Article
DE Antitumor; Antimitotic; Antiproliferative; Tumor-selective
ID IN-VITRO; PAPROTRAIN; INHIBITORS; AUTOPHAGY; MODELS; VIVO; LC3
AB Selective targeting of cancer cells over normal cells is a key objective of targeted therapy. However few approaches achieve true mechanistic selectivity resulting in debilitating side effects and dose limitation. In this work we describe the discovery of A131 (4a), a new agent with an unprecedented dual mechanism of action targeting both mitosis and autophagy. Compound 4a was first identified in a phenotypic screen in which HeLa cells treated with 4a manifested mitotic arrest along with formation of multiple vesicles. Further investigations showed that 4a causes an increase in mitotic marker pH3 and autophagy marker LC3. Importantly 4a induces cell death in cancer cells while sparing normal cells which regrow after 4a is removed. Dual activities against pH3 and LC3 markers are required for cancer cell selectivity. An extensive SAR investigation confirmed 4a as the optimal dual inhibitor with potency against a panel of 30 cancer cell lines (average antiproliferative GI(50) 1.5 mu M). In a mouse model of paclitaxel-resistant colon cancer, 4a showed 74% tumor growth inhibition when administered at a dose of 20 mg/kg IP twice a day. (C) 2018 Elsevier Masson SAS. All rights reserved.
C1 [See, Cheng Shang; Dymock, Brian W.] Natl Univ Singapore, Dept Pharm, Singapore 117543, Singapore.
   [Kitagawa, Mayumi; Liao, Pei-Ju; Lee, Kyung Hee; Wong, Jasmine; Lee, Sang Hyun] Duke NUS Med Sch, Program Canc & Stem Cell Biol, Singapore 169857, Singapore.
RP Dymock, BW (corresponding author), Natl Univ Singapore, Dept Pharm, Singapore 117543, Singapore.
EM bwdnus@gmail.com
OI Dymock, Brian/0000-0002-2374-5756
FU National University of Singapore (Faculty of Science start-up
   grant)National University of Singapore [R-148-000-169-133]; NMRC
   CBRGNational Medical Research Council, Singapore [NMRC/CBRG/0091/2015];
   Duke-NUS Medical School [NUS/RECA(PILOT/2013/0006)];  [NRF-RF2010-02]
FX We gratefully acknowledge Dr Yang Shili and Professor Paul Ho for
   providing the RLM and rat PK data, and Ms Sheela David Packiaraj and
   Associate Professor Ho Han Kiat for providing the TAMH, AC10 and AMES
   data. This research was funded by generous grants from the National
   University of Singapore (Faculty of Science start-up grant
   R-148-000-169-133 to B.D.), the National Research Fellow (S.H.L.;
   NRF-RF2010-02) program, NMRC CBRG (S.H.L.; NMRC/CBRG/0091/2015) and the
   Duke-NUS Medical School [NUS/RECA(PILOT/2013/0006)].
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NR 24
TC 8
Z9 8
U1 1
U2 7
PU ELSEVIER FRANCE-EDITIONS SCIENTIFIQUES MEDICALES ELSEVIER
PI ISSY-LES-MOULINEAUX
PA 65 RUE CAMILLE DESMOULINS, CS50083, 92442 ISSY-LES-MOULINEAUX, FRANCE
SN 0223-5234
EI 1768-3254
J9 EUR J MED CHEM
JI Eur. J. Med. Chem.
PD AUG 5
PY 2018
VL 156
BP 344
EP 367
DI 10.1016/j.ejmech.2018.07.011
PG 24
WC Chemistry, Medicinal
WE Science Citation Index Expanded (SCI-EXPANDED); Index Chemicus (IC)
SC Pharmacology & Pharmacy
GA GS4YG
UT WOS:000443663200027
PM 30015072
DA 2022-04-25
ER

PT J
AU Yao, YZ
   Hu, H
   Yang, Y
   Zhou, GQ
   Shang, ZF
   Yang, XD
   Sun, K
   Zhan, SH
   Yu, ZY
   Li, PY
   Pan, GF
   Sun, L
   Zhu, XG
   He, SB
AF Yao, Yizhou
   Hu, Hao
   Yang, Yong
   Zhou, Guoqiang
   Shang, Zengfu
   Yang, Xiaodong
   Sun, Kang
   Zhan, Shenghua
   Yu, Zhengyuan
   Li, Peiyao
   Pan, Guofeng
   Sun, Liang
   Zhu, Xinguo
   He, Songbing
TI Downregulation of Enhancer of Zeste Homolog 2 (EZH2) Is Essential for
   the Induction of Autophagy and Apoptosis in Colorectal Cancer Cells
SO GENES
LA English
DT Article
DE EZH2; shRNA; DZNep; autophagy; apoptosis; colorectal cancer
ID HISTONE METHYLTRANSFERASE; EXPRESSION; PROLIFERATION; CARCINOMA;
   SENSITIVITY; INHIBITION; PATHWAYS; POLYCOMB; PROSTATE; MARKER
AB Increasing evidence indicates that elevated expression of enhancer of zeste homolog 2 gene (EZH2) in many human malignant tumors acts a significant role in the oncogenic process. However, the underlying molecular mechanism is still unclarified. It is evident that apoptosis and autophagy of tumor cells is crucial for the tumorigenesis and progression of cancer, however, the exact role of EZH2 plays in apoptosis and autophagy has not been fully elucidated in colorectal cancer (CRC). Our previous study found that the expression level of EZH2 was higher in CRC tumor tissues than in the paired normal tissues using immunohistochemical analysis. We also recently found that the autophagy-related gene-related protein Ambra1 plays an important role in the autophagy pathway in CRC cells. In this study, mRNA and protein expression of EZH2 in four CRC cell lines were tested at first and RKO and HCT116 cells showed the highest levels among them. Here we transfected with EZH2-shRNA, or added DZNep (an EZH2 inhibitor) to RKO and HCT116 cells in order to detect the effect of EZH2 on autophagy via determining the change of the protein expression of LC3 and Ambra1. The outcome indicated an obvious decrease of autophagy level in cells transfected with EZH2-shRNA or DZNep. We also found the apoptotic rate of cells was elevated significantly after downregulation of EZH2. In addition, compared to control group, CRC cells transfected with EZH2-shRNA or added DZNep revealed a significantly increased G1 cell cycle rate and an obvious decrease in the G2 cell cycle rate. Further analysis showed that knockdown of EZH2 induced cell-cycle arrest in CRC cells. Meanwhile, downregulation of EZH2 in CRC cells induces autophagy and apoptosis. Taken together, our results suggest that EZH2 plays a critical role in autophagy and apoptosis in the progression of CRC, which potentially facilitates the development of an ideal strategy for combating colorectal cancer.
C1 [Yao, Yizhou; Hu, Hao; Yang, Yong; Pan, Guofeng; Sun, Liang; Zhu, Xinguo; He, Songbing] Soochow Univ, Dept Gen Surg, Affiliated Hosp 1, Suzhou 215006, Peoples R China.
   [Zhou, Guoqiang] Changshu 2 Hosp, Dept Gastrointestinal Surg, Suzhou 215500, Peoples R China.
   [Shang, Zengfu] Soochow Univ, Dept Radiat Med, Coll Med, Suzhou 215006, Peoples R China.
   [Yang, Xiaodong] Soochow Univ, Dept Gen Surg, Affiliated Hosp 2, Suzhou 215006, Peoples R China.
   [Sun, Kang] Jiangsu Univ, Dept Gen Surg, Affiliated Hosp, Zhenjiang 212001, Peoples R China.
   [Zhan, Shenghua] Soochow Univ, Dept Pathol, Affiliated Hosp 1, Suzhou 215006, Peoples R China.
   [Yu, Zhengyuan] Soochow Univ, Dept Oncol, Affiliated Hosp 1, Suzhou 215006, Peoples R China.
   [Li, Peiyao] Chinese Peoples Liberat Army Gen Hosp, Med Engn & Maintenance Ctr, Beijing 100853, Peoples R China.
RP He, SB (corresponding author), Soochow Univ, Dept Gen Surg, Affiliated Hosp 1, Suzhou 215006, Peoples R China.
EM yaoyizhou2014@163.com; lidechun1955@163.com; magicy@126.com;
   chowgq@sina.com; zengfu.shang@suda.edu.cn; wjyxd@163.com;
   doctorsunkang@126.com; captain_hsb@163.com; strongeryy1985@163.com;
   li_peiyao@163.com; 1030705022@suda.edu.cn; 1130705026@suda.edu.cn;
   zxg45@hotmail.com; hesongbing1979@suda.edu.cn
RI yao, yizhou/ABE-8728-2020; Sun, Liang/AAY-4646-2021
OI Shang, Zeng-Fu/0000-0002-2396-1416; Yao, Yizhou/0000-0001-7976-1133; YU,
   ZHENGYUAN/0000-0002-6148-1907; Sun, Liang/0000-0002-2721-1866
FU Project of Nature Science Foundation of ChinaNational Natural Science
   Foundation of China (NSFC) [81672348]; Six Major Talent Peak Project of
   Jiangsu Province of China [2015-WSW-014]; Scientific Research Foundation
   for the Returned Overseas Chinese Scholars, State Education Ministry of
   ChinaScientific Research Foundation for the Returned Overseas Chinese
   ScholarsMinistry of Education, China; National Science Foundation of
   Jiangsu Province, China [BK2016255]; Project of Medical Science and
   Technology Development Foundation of Jiangsu Province of China
   [YG201406]; Science and Technology Research Project of Changshu City of
   China [CS201504]
FX The present study was supported by Project of Nature Science Foundation
   of China (81672348), the Six Major Talent Peak Project of Jiangsu
   Province of China (2015-WSW-014), the Scientific Research Foundation for
   the Returned Overseas Chinese Scholars, State Education Ministry of
   China (fiftieth batch, 2015), the National Science Foundation of Jiangsu
   Province, China (BK2016255), Project of Medical Science and Technology
   Development Foundation of Jiangsu Province of China (YG201406) and
   Science and Technology Research Project of Changshu City of China
   (CS201504).
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NR 49
TC 26
Z9 27
U1 1
U2 7
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 2073-4425
J9 GENES-BASEL
JI Genes
PD OCT
PY 2016
VL 7
IS 10
AR 83
DI 10.3390/genes7100083
PG 14
WC Genetics & Heredity
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Genetics & Heredity
GA EF1QI
UT WOS:000390099400013
PM 27706111
OA Green Published, gold
DA 2022-04-25
ER

PT J
AU Cosper, PF
   Leinwand, LA
AF Cosper, Pippa F.
   Leinwand, Leslie A.
TI Cancer Causes Cardiac Atrophy and Autophagy in a Sexually Dimorphic
   Manner
SO CANCER RESEARCH
LA English
DT Article
ID UBIQUITIN-PROTEASOME PATHWAY; SKELETAL-MUSCLE; MYOFIBRILLAR PROTEINS;
   MYOCARDIAL STIFFNESS; CONTRACTILE FUNCTION; HEMODYNAMIC STRESS;
   CACHEXIA; HEART; RAT; DEGRADATION
AB Approximately one-third of cancer deaths are caused by cachexia, a severe form of skeletal muscle and adipose tissue wasting that affects men more than women. The heart also undergoes atrophy in cancer patients, but the mechanisms and the basis for apparent sex differences are unclear. In a mouse colon-adenocarcinoma model, cancer causes a loss of cardiac mass due to a decrease in cardiac myocyte size that is associated with reduced levels of all sarcomeric proteins. Unlike skeletal muscle cachexia, atrophic hearts do not upregulate the ubiquitin-proteasome system or its activity but increase autophagy. Thus, cancer causes cardiac atrophy by a mechanism distinct from that in skeletal muscle. Male tumor-bearing mice have a more severe phenotype than females, including greater cardiac mass loss and mortality, a more robust pro-inflammatory response to the tumor, and greater cardiac autophagy. In females, estrogen protects against cancer-induced cardiac atrophy and body weight loss by signaling through its receptor. Sex differences in cardiac atrophy need to be considered during the treatment of patients suffering from chemotherapy-induced cardiomyopathy to prevent exacerbation of cardiac dysfunction. Cancer Res; 71( 5); 1710-20. (C)2010 AACR.
C1 [Cosper, Pippa F.; Leinwand, Leslie A.] Univ Colorado, Dept Mol Cellular & Dev Biol, Boulder, CO 80309 USA.
RP Leinwand, LA (corresponding author), Room A417,UCB 354, Boulder, CO 80309 USA.
EM Leslie.Leinwand@colorado.edu
OI Cosper, Pippa/0000-0003-3362-5587; LEINWAND, LESLIE/0000-0003-1470-4810
FU NIHUnited States Department of Health & Human ServicesNational
   Institutes of Health (NIH) - USA [2RO1HL050560]; American Heart
   AssociationAmerican Heart Association [0810037Z]; National Heart Lung
   and Blood InstituteUnited States Department of Health & Human
   ServicesNational Institutes of Health (NIH) - USANIH National Heart Lung
   & Blood Institute (NHLBI) [3T32GM008497-S1]; NATIONAL HEART, LUNG, AND
   BLOOD INSTITUTEUnited States Department of Health & Human
   ServicesNational Institutes of Health (NIH) - USANIH National Heart Lung
   & Blood Institute (NHLBI) [R01HL050560] Funding Source: NIH RePORTER;
   NATIONAL INSTITUTE OF GENERAL MEDICAL SCIENCESUnited States Department
   of Health & Human ServicesNational Institutes of Health (NIH) - USANIH
   National Institute of General Medical Sciences (NIGMS) [T32GM008497]
   Funding Source: NIH RePORTER
FX This work was supported by an NIH grant (2RO1HL050560 to L.A. Leinwand),
   a predoctoral fellowship from the American Heart Association (0810037Z
   to P.F. Cosper), and a grant from the National Heart Lung and Blood
   Institute (3T32GM008497-S1 to P.F. Cosper).
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NR 50
TC 130
Z9 133
U1 2
U2 7
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAR 1
PY 2011
VL 71
IS 5
BP 1710
EP 1720
DI 10.1158/0008-5472.CAN-10-3145
PG 11
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA 728AH
UT WOS:000287845300022
PM 21163868
OA Green Accepted, Bronze
DA 2022-04-25
ER

PT J
AU Vignot, S
   Lefebvre, C
   Frampton, GM
   Meurice, G
   Yelensky, R
   Palmer, G
   Capron, F
   Lazar, V
   Hannoun, L
   Miller, VA
   Andre, F
   Stephens, PJ
   Soria, JC
   Spano, JP
AF Vignot, Stephane
   Lefebvre, Celine
   Frampton, Garrett M.
   Meurice, Guillaume
   Yelensky, Roman
   Palmer, Gary
   Capron, Frederique
   Lazar, Vladimir
   Hannoun, Laurent
   Miller, Vincent A.
   Andre, Fabrice
   Stephens, Philip J.
   Soria, Jean-Charles
   Spano, Jean-Philippe
TI Comparative analysis of primary tumour and matched metastases in
   colorectal cancer patients: Evaluation of concordance between genomic
   and transcriptional profiles
SO EUROPEAN JOURNAL OF CANCER
LA English
DT Article
DE Colorectal cancer; Primary tumour; Metastasis; Discrepancies; Recurrent
   mutations
ID INTRATUMOR HETEROGENEITY; COLON; ADRENALINE; MUTATIONS; THERAPY
AB Purpose: Focal and temporal tumour heterogeneity can represent a major challenge for biology-guided therapies. This study proposes to investigative molecular discrepancies between primary colorectal cancer (CRC) samples and matched metastases.
   Experimental design: Surgical samples from primary and matched metastatic tissues from 13 CRC patients along with their adjacent normal tissue were evaluated. A mutational analysis was performed using a targeted Next Generation Sequencing assay (Foundation Medicine) with a focus on known recurrent somatic mutations as surrogate of key oncogenic events. Gene expression analysis was also performed to investigate transcriptional discrepancies.
   Results: Among the 26 samples, 191 mutations were identified including mutations in APC (13 pts), TP53 (11 pts), and KRAS (7 pts). Global concordance rate for mutations was 78% between primary and metastatic tumours and raised to 90% for 12 known recurrent mutations in CRC. Differential gene expression analysis revealed a low number of significantly variant transcripts between primary and metastatic tumours once the tissue effect was taken into account. Only two pathways (ST_ADRENERGIC, PID_REELINPATHWAY) were differentially up-regulated in metastases among 17 variant pathways. A common profile in primary and metastatic tumours revealed conserved pathways mostly involved in cell cycle regulation. Only two pathways were significantly down regulated compared to normal control, including regulation of autophagy (KEGG_ REGULATION_OF_AUTOPHAGY).
   Conclusion: These results suggest that profiles of primary tumour can identify key alterations present in matched CRC metastases at first metastatic progression. Gene expression analysis identified mainly conserved pathways between primary tumour and matched liver metastases. (C) 2015 Elsevier Ltd. All rights reserved.
C1 [Vignot, Stephane] Hop Chartres, Oncol Hematol, Chartres, France.
   [Vignot, Stephane; Lefebvre, Celine; Andre, Fabrice; Soria, Jean-Charles] Inst Gustave Roussy, INSERM, U981, F-94805 Villejuif Grand Paris, France.
   [Frampton, Garrett M.; Yelensky, Roman; Palmer, Gary; Miller, Vincent A.; Stephens, Philip J.] Fdn Med, Cambridge, MA USA.
   [Meurice, Guillaume; Lazar, Vladimir] Inst Gustave Roussy, Unite Genom Fonct, F-94805 Villejuif Grand Paris, France.
   [Capron, Frederique; Hannoun, Laurent; Spano, Jean-Philippe] Grp Hosp Pitie Salpetriere, F-75634 Paris, France.
RP Soria, JC (corresponding author), Inst Gustave Roussy, INSERM, U981, 114 Rue Edouard Vaillant, F-94805 Villejuif Grand Paris, France.
EM jean-charles.soria@gustaveroussy.fr
RI Lazar, Vladimir/AAV-2087-2020; ANDRE, Fabrice/AAL-2683-2020;
   Kessenbrock, Kai/B-6936-2011; Soria, Jean-Charles/F-3619-2014; Lazar,
   Vladimir/AAQ-2086-2020; Lefebvre, Celine/E-6290-2013
OI ANDRE, Fabrice/0000-0001-5795-8357; 
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NR 32
TC 64
Z9 65
U1 0
U2 15
PU ELSEVIER SCI LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND
SN 0959-8049
EI 1879-0852
J9 EUR J CANCER
JI Eur. J. Cancer
PD MAY
PY 2015
VL 51
IS 7
BP 791
EP 799
DI 10.1016/j.ejca.2015.02.012
PG 9
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA CG1LT
UT WOS:000353034800001
PM 25797355
DA 2022-04-25
ER

PT J
AU Zhang, DY
   Reyes, RM
   Osta, E
   Kari, S
   Gupta, HB
   Padron, AS
   Kornepati, AVR
   Kancharla, A
   Sun, XJ
   Deng, YL
   Wu, BG
   Vadlamudi, R
   Li, R
   Svatek, RS
   Curiel, TJ
AF Zhang, Deyi
   Reyes, Ryan M.
   Osta, Erica
   Kari, Suresh
   Gupta, Harshita B.
   Padron, Alvaro S.
   Kornepati, Anand V. R.
   Kancharla, Aravind
   Sun, Xiujie
   Deng, Yilun
   Wu, Bogang
   Vadlamudi, Ratna
   Li, Rong
   Svatek, Robert S.
   Curiel, Tyler J.
TI Bladder cancer cell-intrinsic PD-L1 signals promote mTOR and autophagy
   activation that can be inhibited to improve cytotoxic chemotherapy
SO CANCER MEDICINE
LA English
DT Article
DE autophagy; bladder cancer; chemotherapy; mTOR; PD&#8208; L1
AB Tumor cell-intrinsic programmed death-ligand 1 (PD-L1) signals mediate immunopathologic effects in breast, colon, and ovarian cancers and in melanomas, but bladder cancer (BC) effects are unreported. We show here that BC cell-intrinsic PD-L1 signals in mouse MB49 and human RT4, UM-UC3, and UM-UC-14 BC cells regulate important pathologic pathways and processes, including effects not reported in other cancers. alpha-PD-L1 antibodies reduced BC cell proliferation in vitro, demonstrating direct signaling effects. BC cell-intrinsic PD-L1 promoted mammalian target of rapamycin complex 1 (mTORC1) signals in vitro and augmented in vivo immune-independent cell growth and metastatic cancer spread, similar to effects we reported in melanoma and ovarian cancer. BC cell-intrinsic PD-L1 signals also promoted basal and stress-induced autophagy, whereas these signals inhibited autophagy in melanoma and ovarian cancer cells. BC cell-intrinsic PD-L1 also mediated chemotherapy resistance to the commonly used BC chemotherapy agents cis-platinum and gemcitabine and to the mTORC1 inhibitor, rapamycin. Thus, BC cell-intrinsic PD-L1 signals regulate important virulence and treatment resistance pathways that suggest novel, actionable treatment targets meriting additional studies. As a proof-of-concept, we showed that the autophagy inhibitor chloroquine improved cis-platinum treatment efficacy in vivo, with greater efficacy in PD-L1 null versus PD-L1-replete BC.
C1 [Zhang, Deyi; Kari, Suresh; Gupta, Harshita B.; Padron, Alvaro S.; Kancharla, Aravind; Sun, Xiujie; Deng, Yilun; Curiel, Tyler J.] Univ Texas Hlth, Dept Med, San Antonio, TX USA.
   [Reyes, Ryan M.; Osta, Erica; Kornepati, Anand V. R.; Curiel, Tyler J.] Univ Texas Hlth, Grad Sch Biomed Sci, San Antonio, TX USA.
   [Reyes, Ryan M.; Osta, Erica; Kornepati, Anand V. R.; Curiel, Tyler J.] Univ Texas Hlth, Dept Microbiol Immunol & Mol Genet, San Antonio, TX USA.
   [Reyes, Ryan M.; Vadlamudi, Ratna; Li, Rong; Svatek, Robert S.; Curiel, Tyler J.] Univ Texas Hlth, Mays Canc Ctr, San Antonio, TX USA.
   [Wu, Bogang; Li, Rong] Univ Texas Hlth, Dept Mol Med, San Antonio, TX USA.
   [Vadlamudi, Ratna] Univ Texas Hlth Sci Ctr San Antonio, Dept Obstet & Gynecol, San Antonio, TX 78229 USA.
   [Svatek, Robert S.] Univ Texas Hlth Sci Ctr San Antonio, Dept Urol, San Antonio, TX 78229 USA.
   [Zhang, Deyi] NIH, Bldg 10, Bethesda, MD 20892 USA.
   [Sun, Xiujie; Wu, Bogang; Li, Rong] George Washington Univ, Sch Med & Hlth Sci, Dept Biochem & Mol Med, Washington, DC 20052 USA.
RP Curiel, TJ (corresponding author), Univ Texas Hlth San Antonio, Dept Med, STRF MC 8252,8403 Floyd Curl Dr, San Antonio, TX 78229 USA.
EM curielt@uthscsa.edu
RI Reyes, Ryan/AAZ-9671-2021; Wu, Bogang/O-2441-2018
OI Reyes, Ryan/0000-0002-9562-5809; Wu, Bogang/0000-0003-1654-198X;
   Kancharla, Aravind/0000-0001-9095-7735
FU NIHUnited States Department of Health & Human ServicesNational
   Institutes of Health (NIH) - USA [T32GM113896, F30CA239390];
   NIH/NCATSUnited States Department of Health & Human ServicesNational
   Institutes of Health (NIH) - USANIH National Center for Advancing
   Translational Sciences (NCATS) [TL1 TR002647]; NIAUnited States
   Department of Health & Human ServicesNational Institutes of Health (NIH)
   - USANIH National Institute on Aging (NIA) [T32 AG 021890]; CPRIT
   Research Training Award [RP170345]; Roger L. And Laura D. Zeller
   Charitable Foundation Chair in Urologic Cancer [CDMRP CA170270/P1P2];
   CDMRPUnited States Department of Defense [CA054174,, CA205965]; Owens
   Foundation; Skinner endowment; Barker endowment; Clayton Medical
   Research Foundation;  [8KL2 TR000118];  [K23];  [P30 CA054174]
FX R. Reyes (NIH T32GM113896, NIH/NCATS TL1 TR002647, NIA T32 AG 021890),
   A. Kornepati (NIH F30CA239390), Y. Deng (CPRIT Research Training Award
   RP170345), R. Svatek (8KL2 TR000118, K23, P30 CA054174, Roger L. And
   Laura D. Zeller Charitable Foundation Chair in Urologic Cancer, CDMRP
   CA170270/P1P2), T. Curiel (CA054174, CA205965, CDMRP, The Owens
   Foundation, The Skinner endowment, The Barker endowment, Clayton Medical
   Research Foundation).
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NR 37
TC 4
Z9 4
U1 1
U2 5
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 2045-7634
J9 CANCER MED-US
JI Cancer Med.
PD MAR
PY 2021
VL 10
IS 6
BP 2137
EP 2152
DI 10.1002/cam4.3739
EA FEB 2021
PG 16
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA QW5WQ
UT WOS:000621118800001
PM 33626233
OA gold, Green Published
DA 2022-04-25
ER

PT J
AU De Palma, C
   Perrotta, C
AF De Palma, Clara
   Perrotta, Cristiana
TI Ceramide as a target of chemotherapy: its role in apoptosis and
   autophagy
SO CLINICAL LIPIDOLOGY
LA English
DT Review
DE apoptosis; autophagy; ceramide; chemotherapy
ID INDUCED CELL-DEATH; ACTIVATED PROTEIN-KINASE; COLON-CANCER CELLS;
   ACID-SPHINGOMYELINASE; NEUTRAL SPHINGOMYELINASE; GLUCOSYLCERAMIDE
   SYNTHASE; NANOLIPOSOMAL CERAMIDE; SPHINGOSINE KINASE-1;
   MULTIDRUG-RESISTANCE; STRESS-RESPONSE
AB Conventional chemotherapy is the elective and most effective strategy for tumor treatment. Several studies have demonstrated that a mechanism through which most chemotherapeutic agents kill tumor cells is to trigger their death through the generation of ceramide via the activation of enzymes responsible either for its de novo synthesis or for the degradation of sphingomyelin. Ceramide-induced cell death has been widely investigated, with a particular focus on apoptosis. Moreover, recently, the role of ceramide in the induction of autophagy has come to light, opening new questions on how sphingolipid messengers can act in these different but linked pathways. Cellular stress can indeed promote autophagy and apoptosis in multiple ways, including their induction sequentially, simultaneously, or in a mutually exclusive manner. This review presents some of the recent advances regarding the role of ceramide in the induction of apoptosis/autophagy, focusing on its modulation as a strategy for an effective cancer therapy.
C1 [De Palma, Clara; Perrotta, Cristiana] Univ Milan, Univ Hosp Luigi Sacco, Dept Clin Sci, Clin Pharmacol Unit, I-20157 Milan, Italy.
RP Perrotta, C (corresponding author), Univ Milan, Univ Hosp Luigi Sacco, Dept Clin Sci, Clin Pharmacol Unit, I-20157 Milan, Italy.
EM cristiana.perrotta@unimi.it
RI PERROTTA, CRISTIANA/A-9179-2010; Perrotta, Cristiana/I-2835-2016; De
   Palma, Clara/M-9842-2019
OI Perrotta, Cristiana/0000-0001-6680-4536; De Palma,
   Clara/0000-0003-0365-7414
FU Italian Association of Cancer Research (AIRC)Fondazione AIRC per la
   ricerca sul cancro
FX This work was supported by research grants from the Italian Association
   of Cancer Research (AIRC). The authors have no other relevant
   affiliations or financial involvement with any organization or entity
   with a financial interest in or financial conflict with the subject
   matter or materials discussed in the manuscript apart from those
   disclosed.
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NR 79
TC 7
Z9 7
U1 1
U2 10
PU FUTURE MEDICINE LTD
PI LONDON
PA UNITEC HOUSE, 3RD FLOOR, 2 ALBERT PLACE, FINCHLEY CENTRAL, LONDON, N3
   1QB, ENGLAND
SN 1758-4299
J9 CLIN LIPIDOL
JI Clin. Lipidol.
PD FEB
PY 2012
VL 7
IS 1
BP 111
EP 119
DI 10.2217/CLP.11.71
PG 9
WC Biochemistry & Molecular Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology
GA 896DV
UT WOS:000300546500014
DA 2022-04-25
ER

PT J
AU Liu, C
   Wang, JN
   Yang, Y
   Liu, XT
   Zhu, YB
   Zou, JJ
   Peng, SS
   Le, TH
   Chen, Y
   Zhao, SL
   He, BS
   Mi, QY
   Zhang, X
   Du, QM
AF Liu, Chao
   Wang, Jianing
   Yang, Yan
   Liu, Xiuting
   Zhu, Yubing
   Zou, Jianjun
   Peng, Sishi
   Le, Thi Ha
   Chen, Yu
   Zhao, Shuli
   He, Bangshun
   Mi, Qiongyu
   Zhang, Xu
   Du, Qianming
TI Ginsenoside Rd ameliorates colitis by inducing p62-driven
   mitophagy-mediated NLRP3 inflammasome inactivation in mice
SO BIOCHEMICAL PHARMACOLOGY
LA English
DT Article
DE Ulcerative colitis; Inflammation; Ginsenoside Rd; NLRP3 Inflammasome;
   P62
ID CROHNS-DISEASE; BOWEL-DISEASE; IFN-GAMMA; AUTOPHAGY; ACTIVATION; MOUSE;
   PHOSPHORYLATION; PANCREATITIS; IMMUNITY; INNATE
AB Previous studies reported that Ginsenoside Rd (Rd) had anti-inflammatory and anti-cancer effects. However, the molecular mechanism underlying the inhibition effect of Rd on colitis in mice hasn't been clarified clearly. Here, in our study, we detected the effects of Rd on dextran sulfate sodium (DSS)-induced murine colitis, and found that oral administration of Rd dose-dependently alleviated DSS-induced body weight loss, colon length shortening and colonic pathological damage with lower myeloperoxidase (MPO) and inducible nitric oxide synthase (iNOS) activities and higher glutathione level. In addition, the production of pro-inflammatory cytokines (IL-1 beta, TNF-a and IL-6) in both serum and colonic tissues were significantly down-regulated by Rd administration. The activation of NLRP3 inflammasome was also suppressed in Rd-treated group, resulting in reduced caspase-1 production and IL-1 beta secretion. In vitro, Rd remarkably inhibited NLRP3 inflammasome activation which was mostly dependent on the mitochondrial translocation of p62 and mitophagy. Importantly, Rd-driven inhibition of the NLRP3 inflammasome was significantly blocked by various autophagy inhibitors. Furthermore, upregulation of AMPK/ULK1 signaling pathway accounted for Rd-induced autophagy, which was also seen in vivo. In conclusion, our results demonstrated the function of Rd on the inhibition NLRP3 inflammasome and its potential application for the treatment of NLRP3-associated diseases.
C1 [Liu, Chao; Zhu, Yubing; Zou, Jianjun; Le, Thi Ha; Chen, Yu] Nanjing Med Univ, Nanjing Hosp 1, Dept Pharm, Nanjing 210006, Jiangsu, Peoples R China.
   [Liu, Chao; Liu, Xiuting; Zhu, Yubing; Zou, Jianjun; Peng, Sishi; Le, Thi Ha; Chen, Yu; Du, Qianming] China Pharmaceut Univ, Sch Basic Med & Clin Pharm, Dept Clin Pharm, Nanjing 210009, Jiangsu, Peoples R China.
   [Wang, Jianing] China Pharmaceut Univ, Jiangsu Ctr Drug Screening, Neurobiol Lab, Nanjing 210009, Jiangsu, Peoples R China.
   [Yang, Yan] Southwest Jiaotong Univ, Peoples Hosp Chengdu 3, Dept Pharm, 82 Qing Long St, Chengdu 610031, Sichuan, Peoples R China.
   [Yang, Yan] Southwest Jiaotong Univ, Affiliated Hosp, 82 Qing Long St, Chengdu 610031, Sichuan, Peoples R China.
   [Peng, Sishi; Zhao, Shuli; He, Bangshun; Mi, Qiongyu; Du, Qianming] Nanjing Med Univ, Nanjing Hosp 1, Gen Clin Res Ctr, Nanjing 210006, Jiangsu, Peoples R China.
   [Zhang, Xu] First Peoples Hosp Chengdu, Dept Med, 18 Wanxiang East Rd, Chengdu 610041, Sichuan, Peoples R China.
   [Zhang, Xu] Chengdu Med Coll, Affiliated Hosp, 18 Wanxiang East Rd, Chengdu 610041, Sichuan, Peoples R China.
RP Zhang, X; Du, QM (corresponding author), First Peoples Hosp Chengdu, Dept Med, 18 Wanxiang East Rd, Chengdu 610041, Sichuan, Peoples R China.; Zhang, X; Du, QM (corresponding author), Chengdu Med Coll, Affiliated Hosp, 18 Wanxiang East Rd, Chengdu 610041, Sichuan, Peoples R China.
EM Jason151X7@stu.cpu.edu.cn; duqianming@stu.cpu.edu.cn
OI , Qianming Du/0000-0002-1092-2899
FU Natural Science Foundation of ChinaNational Natural Science Foundation
   of China (NSFC) [81702833]; Natural Science Foundation of Jiangsu
   ProvinceNatural Science Foundation of Jiangsu Province [BK20170137,
   BK20170140]; Sichuan Science and Technology Program [2018JY0204];
   Natural Science Foundation of Chengdu Medical College [CYZ17-13];
   Science and Technology Development Fund Project of Nanjing Medical
   University [2016NJMUZD041, 2016NJMUZD043]
FX This work was supported by the Natural Science Foundation of China (No.
   81702833), the Natural Science Foundation of Jiangsu Province (No.
   BK20170137 and No. BK20170140), Sichuan Science and Technology Program
   (No. 2018JY0204), Natural Science Foundation of Chengdu Medical College
   (No. CYZ17-13) and the Science and Technology Development Fund Project
   of Nanjing Medical University (No. 2016NJMUZD041 and No. 2016NJMUZD043).
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NR 57
TC 36
Z9 40
U1 6
U2 45
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0006-2952
EI 1873-2968
J9 BIOCHEM PHARMACOL
JI Biochem. Pharmacol.
PD SEP
PY 2018
VL 155
BP 366
EP 379
DI 10.1016/j.bcp.2018.07.010
PG 14
WC Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA GU5JZ
UT WOS:000445323100035
PM 30012462
DA 2022-04-25
ER

PT J
AU Sroda-Pomianek, K
   Michalak, K
   Swiatek, P
   Pola, A
   Palko-Labuz, A
   Wesolowska, O
AF Sroda-Pomianek, Kamila
   Michalak, Krystyna
   Swiatek, Piotr
   Pola, Andrzej
   Palko-Labuz, Anna
   Wesolowska, Olga
TI Increased lipid peroxidation, apoptosis and selective cytotoxicity in
   colon cancer cell line LoVo and its doxorubicin-resistant subline
   LoVo/Dx in the presence of newly synthesized phenothiazine derivatives
SO BIOMEDICINE & PHARMACOTHERAPY
LA English
DT Article
DE Phenothiazine derivatives; Cytotoxicity; Apoptosis; Lipid peroxidation;
   Reactive oxygen species (ROS); Doxorubicin-Resistant cancer cells
ID MULTIDRUG-RESISTANCE; OXIDATIVE STRESS; P-GLYCOPROTEIN; COLLATERAL
   SENSITIVITY; COLORECTAL-CANCER; INDUCE APOPTOSIS; REVERSAL;
   CHLORPROMAZINE; ANTIOXIDANT; INHIBITION
AB Cancer cells often develop the resistance to pro-apoptotic signaling that makes them invulnerable to conventional treatment. Therapeutic strategies that make cancer cells enter the path of apoptosis are desirable due to the avoidance of inflammatory reaction that usually accompanies necrosis. In the present study phenothiazines (fluphenazine and four recently synthesized derivatives) were investigated in order to identify compounds with a potent anticancer activity. Since phenothiazines are known as multidrug resistance modulators the sensitive human colorectal adenocarcinoma cell line (LoVo) and its doxorubicin-resistant, ABCB1 overexpressing, subline (LoVo/Dx) have been employed as a model system. In studied cancer cells cytotoxic effect of the phenothiazine derivatives was accompanied by apoptosis and autophagy induction as well as by the increase of cellular lipid peroxidation and intracellular reactive oxygen species generation. Molecular modelling revealed that reactivity of phenothazines (manifested by their low energy gap) but not lipophilicity was positively correlated with their anticancer potency, pro-oxidant properties and apoptosis induction ability. Additionally, some of the studied compounds turned out to be more potent cytotoxic and pro-apoptotic agents in doxorubicin-resistant (LoVo/Dx) cells than in sensitive ones (LoVo). The hypothesis was assumed that studied phenothiazine derivatives induced apoptotic cell death by increasing the production of reactive oxygen species.
C1 [Sroda-Pomianek, Kamila; Michalak, Krystyna; Pola, Andrzej; Palko-Labuz, Anna; Wesolowska, Olga] Wroclaw Med Univ, Dept Biophys, Ul Chalubinskiego 10, PL-50368 Wroclaw, Poland.
   [Swiatek, Piotr] Wroclaw Med Univ, Dept Drug Chem, Ul Borowska 211, PL-50556 Wroclaw, Poland.
RP Sroda-Pomianek, K (corresponding author), Wroclaw Med Univ, Dept Biophys, Ul Chalubinskiego 10, PL-50368 Wroclaw, Poland.
EM kamila.sroda-pomianek@umed.wroc.pl
RI Świątek, Piotr/K-7423-2019
OI Wesolowska, Olga/0000-0003-1659-3288; Michalak,
   Krystyna/0000-0002-4018-8867; Pola, Andrzej/0000-0002-4110-299X;
   Swiatek, Piotr/0000-0003-4613-025X; Sroda-Pomianek,
   Kamila/0000-0003-3454-5044; Palko-Labuz, Anna/0000-0002-4246-5717
FU Polish Ministry of Science and Higher EducationMinistry of Science and
   Higher Education, Poland
FX This work was supported by Polish Ministry of Science and Higher
   Education (funds for Wroclaw Medical University).
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NR 72
TC 10
Z9 10
U1 0
U2 12
PU ELSEVIER FRANCE-EDITIONS SCIENTIFIQUES MEDICALES ELSEVIER
PI ISSY-LES-MOULINEAUX
PA 65 RUE CAMILLE DESMOULINS, CS50083, 92442 ISSY-LES-MOULINEAUX, FRANCE
SN 0753-3322
EI 1950-6007
J9 BIOMED PHARMACOTHER
JI Biomed. Pharmacother.
PD OCT
PY 2018
VL 106
BP 624
EP 636
DI 10.1016/j.biopha.2018.06.170
PG 13
WC Medicine, Research & Experimental; Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Research & Experimental Medicine; Pharmacology & Pharmacy
GA GR4QO
UT WOS:000442600300075
PM 29990852
DA 2022-04-25
ER

PT J
AU Weh, KM
   Clarke, J
   Kresty, LA
AF Weh, Katherine M.
   Clarke, Jennifer
   Kresty, Laura A.
TI Cranberries and Cancer: An Update of Preclinical Studies Evaluating the
   Cancer Inhibitory Potential of Cranberry and Cranberry Derived
   Constituents
SO ANTIOXIDANTS
LA English
DT Review
DE cranberry; cancer; proanthocyanidin; quercetin; ursolic acid
ID CELL-CYCLE ARREST; FIMBRIATED ESCHERICHIA-COLI; VACCINIUM-MACROCARPON;
   DOUBLE-BLIND; PROANTHOCYANIDINS INHIBIT; ANTIADHESION ACTIVITY;
   CYTOTOXIC PROPERTIES; ANTIOXIDANT STATUS; GUT MICROBIOTA; BREAST-CANCER
AB Cranberries are rich in bioactive constituents reported to influence a variety of health benefits, ranging from improved immune function and decreased infections to reduced cardiovascular disease and more recently cancer inhibition. A review of cranberry research targeting cancer revealed positive effects of cranberries or cranberry derived constituents against 17 different cancers utilizing a variety of in vitro techniques, whereas in vivo studies supported the inhibitory action of cranberries toward cancers of the esophagus, stomach, colon, bladder, prostate, glioblastoma and lymphoma. Mechanisms of cranberry-linked cancer inhibition include cellular death induction via apoptosis, necrosis and autophagy; reduction of cellular proliferation; alterations in reactive oxygen species; and modification of cytokine and signal transduction pathways. Given the emerging positive preclinical effects of cranberries, future clinical directions targeting cancer or premalignancy in high risk cohorts should be considered.
C1 [Weh, Katherine M.; Kresty, Laura A.] Med Coll Wisconsin, Div Hematol & Oncol, Dept Med, 8701 Watertown Plank Rd, Milwaukee, WI 53226 USA.
   [Clarke, Jennifer] Univ Nebraska, Dept Food Sci & Technol, 256 Food Innovat Complex, Lincoln, NE 68588 USA.
   [Clarke, Jennifer] Univ Nebraska, Dept Stat, Lincoln, NE 68583 USA.
   [Clarke, Jennifer] Univ Nebraska, Quantitat Life Sci Initiat, Lincoln, NE 68583 USA.
RP Kresty, LA (corresponding author), Med Coll Wisconsin, Div Hematol & Oncol, Dept Med, 8701 Watertown Plank Rd, Milwaukee, WI 53226 USA.
EM kweh@mcw.edu; jclarke3@unl.edu; lkresty@mcw.edu
OI Weh, Katherine/0000-0002-7745-5391; Kresty, Laura/0000-0002-4745-0522;
   Clarke, Jennifer/0000-0002-2723-7249
FU NATIONAL CANCER INSTITUTEUnited States Department of Health & Human
   ServicesNational Institutes of Health (NIH) - USANIH National Cancer
   Institute (NCI) [R01CA158319] Funding Source: NIH RePORTER; NCI NIH
   HHSUnited States Department of Health & Human ServicesNational
   Institutes of Health (NIH) - USANIH National Cancer Institute (NCI) [R01
   CA158319] Funding Source: Medline
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NR 80
TC 30
Z9 30
U1 4
U2 30
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
SN 2076-3921
J9 ANTIOXIDANTS-BASEL
JI Antioxidants
PD SEP
PY 2016
VL 5
IS 3
AR 27
DI 10.3390/antiox5030027
PG 20
WC Biochemistry & Molecular Biology; Chemistry, Medicinal; Food Science &
   Technology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Pharmacology & Pharmacy; Food Science
   & Technology
GA DU9AT
UT WOS:000382509300007
PM 27548236
OA Green Published, gold
DA 2022-04-25
ER

PT J
AU da Silva-Camargo, CCV
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AF Veloso da Silva-Camargo, Claudia Caroline
   Svoboda Baldin, Rosimeri Kuhl
   Costacurta Polli, Nayanne Louise
   Agostinho, Amanda Pereira
   Olandosk, Marcia
   de Noronha, Lucia
   Sotomaior, Vanessa Santos
TI Parkin protein expression and its impact on survival of patients with
   advanced colorectal cancer
SO CANCER BIOLOGY & MEDICINE
LA English
DT Article
DE Parkin; PARK2; advanced colorectal cancer; survival
ID RECESSIVE JUVENILE PARKINSONISM; MITOPHAGY; MITOCHONDRIA; GENE;
   CARCINOMA; LIGASE; PROLIFERATION; ACTIVATION; PROGNOSIS; AUTOPHAGY
AB Objective: Features of colorectal cancer such as natural history, molecular, chromosomal, and epigenetic alterations have been well described. However, there is still a lack of accurate prognostic markers, which is evident by the lower overall survival rates of patients with advanced cancer. Although alterations in parkin protein expression have been described in colorectal cancer, the functional significance of this protein remains unknown. The present study aimed to investigate the involvement of parkin expression in colorectal adenocarcinoma development and progression by evaluating the association between its expression, clinicopathological parameters, and expression of known proteins involved in colorectal cancer.
   Methods: Tissue microarrays consisting of 73 tumor and 64 normal tissue samples were generated to examine parkin expression and localization by immunohistochemistry.
   Results: A positive correlation of parkin and APC expression was observed in the superficial, intermediate, and profound regions of all cases (rho = 0.37; P = 0.001). Parkin expression was also significantly associated with tumors in men (P = 0.049), those of the mucinous subtype (P = 0.028), and of advanced stage (III + IV, P = 0.041). In addition, increased parkin expression was observed in the invasive front tumor region (P = 0.013). More importantly, a positive correlation was found between parkin expression and the overall survival of patients with advanced colorectal cancer (P = 0.019). Multivariate analysis showed that parkin expression was independent of any of the clinicopathological parameters evaluated in relation to patient survival.
   Conclusions: These results suggest that parkin expression status can be used as a potential independent prognostic marker of survival in advanced colorectal cancer.
C1 [Veloso da Silva-Camargo, Claudia Caroline; Costacurta Polli, Nayanne Louise; Agostinho, Amanda Pereira; Olandosk, Marcia; de Noronha, Lucia; Sotomaior, Vanessa Santos] Pontificia Univ Catolica Parana PUCPR, Sch Hlth & Biosci, Grp Adv Mol Invest NIMA, BR-80215901 Curitiba, Parana, Brazil.
   [Svoboda Baldin, Rosimeri Kuhl; de Noronha, Lucia] Univ Fed Parana UFPR, Hosp Clin, BR-80215901 Curitiba, Parana, Brazil.
RP da Silva-Camargo, CCV (corresponding author), Pontificia Univ Catolica Parana PUCPR, Sch Hlth & Biosci, Grp Adv Mol Invest NIMA, BR-80215901 Curitiba, Parana, Brazil.
EM claudia.veloso@pucpr.edu.br
RI Veloso, Claudia/AAJ-6694-2020; Sotomaior, Vanessa/AAX-4818-2020;
   noronha, lucia/F-6339-2015
OI Sotomaior, Vanessa/0000-0001-5388-6384; noronha,
   lucia/0000-0003-0310-7164
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NR 47
TC 12
Z9 12
U1 0
U2 3
PU CHINESE ANTI-CANCER ASSOC
PI TIANJIN
PA TI-YUAN-BEI, HUANHU XI LU, HEXIQU, TIANJIN, 300060, PEOPLES R CHINA
SN 2095-3941
J9 CANCER BIOL MED
JI Cancer Biol. Med.
PD FEB
PY 2018
VL 15
IS 1
BP 61
EP 69
DI 10.20892/j.issn.2095-3941.2017.0136
PG 9
WC Oncology; Medicine, Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Research & Experimental Medicine
GA FX1WD
UT WOS:000425841700007
PM 29545969
OA Green Submitted, gold, Green Published
DA 2022-04-25
ER

PT J
AU Tong, T
   Niu, YH
   Yue, Y
   Wu, SC
   Ding, H
AF Tong, Tao
   Niu, Yun-Hui
   Yue, Yuan
   Wu, Shuang-chan
   Ding, Hong
TI Beneficial effects of anthocyanins from red cabbage (Brassica oleracea
   L. var. capitata L.) administration to prevent irinotecan-induced
   mucositis
SO JOURNAL OF FUNCTIONAL FOODS
LA English
DT Article
DE Anthocyanins; Autophagy; Irinotecan; mTOR; Mucositis; Red cabbage
ID CLINICAL-PRACTICE GUIDELINES; OXIDATIVE STRESS; GASTROINTESTINAL
   MUCOSITIS; INTESTINAL MUCOSITIS; COLORECTAL-CANCER; MANAGEMENT;
   AUTOPHAGY; MICE; CHEMOTHERAPY; DIARRHEA
AB Intestinal mucositis is a common side effect of Irinotecan (CPT-11). Anthocyanins (ACs) from red cabbage against CPT-11-induced mucositis were studied. Mice were given CPT-11 (75 mg/kg, i.p. for 4 days) and treated with ACs (50, 100 mg/kg, i.g. for 7 days). On day 8, diarrhea and leukocyte count in blood were assessed. Samples of intestine were obtained for morphometric analysis, myeloperoxidase (MPO), TBARS and GSH assay. The effects of ACs on cytoprotection and intestinal permeability were studied in Caco-2 cells. ACs effectively reversed the signs of intestinal injury, including MPO activity, length of ileum and colon, leukopenia, intestinal architecture, and quantity of ileum mucus. In vitro, pretreatment with ACs enhanced transepithelial electrical resistance (TER) and the expression of ZO-1. Furthermore, the protective effects of ACs were associated to modulate autophagy through mTOR pathway. In conclusion, ACs from red cabbage are candidate for supplementary therapy of CPT-11-induced mucositis. (C) 2017 Elsevier Ltd. All rights reserved.
C1 [Niu, Yun-Hui; Yue, Yuan; Wu, Shuang-chan; Ding, Hong] Wuhan Univ, MOE Key Lab Combinatorial Biosynth & Drug Discove, Wuhan 430072, Peoples R China.
   [Tong, Tao] Yangtze Univ, Affiliated Hosp 1, Dept Oncol, Jingzhou 434000, Peoples R China.
RP Ding, H (corresponding author), Wuhan Univ, MOE Key Lab Combinatorial Biosynth & Drug Discove, Wuhan 430072, Peoples R China.
EM 2313309477@qq.com; 542010762@qq.com; 178354235@qq.com;
   1050444595@qq.com; dinghong1106@whu.edu.cn
FU National Natural Science Funds of ChinaNational Natural Science
   Foundation of China (NSFC) [81503356]
FX This work was supported by the National Natural Science Funds of China
   (81503356).
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NR 45
TC 13
Z9 14
U1 2
U2 44
PU ELSEVIER
PI AMSTERDAM
PA RADARWEG 29, 1043 NX AMSTERDAM, NETHERLANDS
SN 1756-4646
J9 J FUNCT FOODS
JI J. Funct. Food.
PD MAY
PY 2017
VL 32
BP 9
EP 17
DI 10.1016/j.jff.2017.01.051
PG 9
WC Food Science & Technology; Nutrition & Dietetics
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Food Science & Technology; Nutrition & Dietetics
GA ET4BU
UT WOS:000400224800002
DA 2022-04-25
ER

PT J
AU Areti, A
   Komirishetty, P
   Akuthota, M
   Malik, RA
   Kumar, A
AF Areti, Aparna
   Komirishetty, Prashanth
   Akuthota, Manasaveena
   Malik, Rayaz A.
   Kumar, Ashutosh
TI Melatonin prevents mitochondrial dysfunction and promotes
   neuroprotection by inducing autophagy during oxaliplatin-evoked
   peripheral neuropathy
SO JOURNAL OF PINEAL RESEARCH
LA English
DT Article
DE autophagy; melatonin; mitochondrial dysfunction; oxaliplatin;
   oxidative/nitrosative stress; peripheral neuropathy
ID ROOT GANGLION NEURONS; NF-KAPPA-B; OXIDATIVE STRESS; QUALITY-CONTROL;
   BIOENERGETIC DEFICITS; NERVOUS-SYSTEM; ANTIOXIDANT; INJURY; SKIN; RATS
AB Oxaliplatin, an organoplatinum compound, is used in the treatment of colorectal cancer, but its clinical use can be limited due to the development of peripheral neuropathy. Whilst mitochondrial dysfunction has been implicated as a major pathomechanism for oxaliplatin-induced neurotoxicity, the prevention of autophagy may also aggravate neuronal cell death. Melatonin, a well-known mitoprotectant and autophagy inducer, was used to examine its neuroprotective role in oxaliplatin-induced peripheral neuropathy (OIPN). Melatonin prevented the loss of mitochondrial membrane potential (Psi m) and promoted neuritogenesis in oxaliplatin-challenged neuro-2a cells. It did not interfere with the cytotoxic activity of oxaliplatin in human colon cancer cell line, HT-29. Melatonin treatment significantly alleviated oxaliplatin-induced pain behavior and neuropathic deficits in rats. It also ameliorated nitro-oxidative stress mediated by oxaliplatin, thus prevented nitrosylation of proteins and loss of antioxidant enzymes, and therefore, it improved mitochondrial electron transport chain function and maintained cellular bioenergetics by improving the ATP levels. The protective effects of melatonin were attributed to preventing oxaliplatin-induced neuronal apoptosis by increasing the autophagy pathway (via LC3A/3B) in peripheral nerves and dorsal root ganglion (DRG). Hence, it preserved the epidermal nerve fiber density in oxaliplatin-induced neuropathic rats. Taken together, we provide detailed molecular mechanisms for the neuroprotective effect of melatonin and suggest it has translational potential for oxaliplatin-induced neuropathy.
C1 [Areti, Aparna; Komirishetty, Prashanth; Akuthota, Manasaveena; Kumar, Ashutosh] Natl Inst Pharmaceut Educ & Res NIPER Hyderabad, Dept Pharmacol & Toxicol, Balanagar, India.
   [Komirishetty, Prashanth] Univ Alberta, Div Neurol Med Sci & Med Hlth Inst, Dept Med, Edmonton, AB, Canada.
   [Malik, Rayaz A.] Weill Cornell Med Qatar, Doha, Qatar.
   Univ Manchester, Inst Cardiovascular Med, Manchester, Lancs, England.
RP Kumar, A (corresponding author), Natl Inst Pharmaceut Educ & Res NIPER Hyderabad, Dept Pharmacol & Toxicol, Balanagar, India.
EM ashutosh.niperhyd@gov.in
RI Kumar, Ashutosh/W-2265-2019; Malik, Rayaz/H-9231-2019; Kumar,
   Ashutosh/F-2719-2018
OI Kumar, Ashutosh/0000-0001-6659-4751; Malik, Rayaz/0000-0002-7188-8903;
   Kumar, Ashutosh/0000-0001-6659-4751
FU Department of Pharmaceuticals; Ministry of chemical and fertilizers;
   NIPER-Hyderabad; Department of Science and Technology, Govt of
   IndiaDepartment of Science & Technology (India) [DST/INT/UK/P-72/2014];
   University of Manchester
FX Department of Pharmaceuticals; Ministry of chemical and fertilizers;
   NIPER-Hyderabad; Department of Science and Technology, Govt of India,
   Grant/Award Number: DST/INT/UK/P-72/2014; University of Manchester
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NR 75
TC 73
Z9 75
U1 2
U2 14
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0742-3098
EI 1600-079X
J9 J PINEAL RES
JI J. Pineal Res.
PD APR
PY 2017
VL 62
IS 3
AR e12393
DI 10.1111/jpi.12393
PG 17
WC Endocrinology & Metabolism; Neurosciences; Physiology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Endocrinology & Metabolism; Neurosciences & Neurology; Physiology
GA EP3QS
UT WOS:000397297400005
PM 28118492
DA 2022-04-25
ER

PT J
AU Panzarini, E
   Dini, L
AF Panzarini, Elisa
   Dini, Luciana
TI Nanomaterial-Induced Autophagy: A New Reversal MDR Tool in Cancer
   Therapy?
SO MOLECULAR PHARMACEUTICS
LA English
DT Review
DE autophagy; nanosized drug delivery systems (DDSs); nanomaterials (NMs);
   cancer therapies; multidrug resistance (MDR)
ID CELL LUNG-CANCER; MULTIDRUG-RESISTANCE; DRUG-RESISTANCE; P-GLYCOPROTEIN;
   COLON-CANCER; THYMIDYLATE SYNTHASE; CROSS-PRESENTATION; CO-DELIVERY;
   SHELL NANOPARTICLES; ANTICANCER DRUG
AB Most of the therapeutic strategies to counteract cancer imply killing of malignant cells. The most exploited cell death mechanism in cancer therapies is apoptosis, but recently, a lot of papers report that other mechanisms, mainly autophagy, could represent a new line of attack in the fight against cancer. One of the limitations for the effectiveness of the approved clinical treatments is the phenomenon of multidrug resistance (MDR) which enables the cancer cells to develop resistance to therapy, especially for chemotherapy. The MDR mechanisms include (a) decreased uptake of drug, (b) reduced intracellular drug concentration by efflux pumps, (c) altered cell cycle checkpoints, (d) altered drug targets, (e) increased metabolism of drugs, (f) induced emergency response genes to impair apoptotic pathway, and (g) altered drug detoxification. Great efforts have been made to reverse MDR. Currently, autophagy and nanosized drug delivery systems (DDSs) belonging to nanomaterials (NMs) provide alternative strategies to circumvent MDR. Nanosized DDSs are very promising tools to accumulate chemotherapeutics at targeting sites and control temporal and spatial drug release into tumor cells. On the other hand, autophagy could overrule drug resistance upon its activation by ensuring cell death via switching its prosurvival role to a prodeath one or by mediating the occurrence of cell death, i.e., apoptosis or necrosis. Likewise, the autophagy inhibition could counteract MDR by sensitizing the cells to anticancer molecules, i.e., Src family tyrosine kinase (SFK) inhibitors or 5-fluorouracil. Noteworthy, autophagy has been recently indicated to be a common cellular response to NMs, corroborating the fascinating idea of the exploitation of NM-induced autophagy in nanomedicine therapy. This review focuses on recently published literature about the relationship between MDR reversal and NMs or autophagy pointing to hypothesize a pivotal role of autophagy modulation induced by NMs in counteracting MDR.
C1 [Panzarini, Elisa; Dini, Luciana] Univ Salento, Dept Biol & Environm Sci & Technol DiSTeBA, I-73100 Lecce, Italy.
RP Dini, L (corresponding author), Univ Salento, Dept Biol & Environm Sci & Technol DiSTeBA, I-73100 Lecce, Italy.
EM luciana.dini@unisalento.it
OI Panzarini, Elisa/0000-0003-4219-4272
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NR 149
TC 50
Z9 52
U1 2
U2 114
PU AMER CHEMICAL SOC
PI WASHINGTON
PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA
SN 1543-8384
J9 MOL PHARMACEUT
JI Mol. Pharm.
PD AUG
PY 2014
VL 11
IS 8
BP 2527
EP 2538
DI 10.1021/mp500066v
PG 12
WC Medicine, Research & Experimental; Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Research & Experimental Medicine; Pharmacology & Pharmacy
GA AM6NW
UT WOS:000339982900004
PM 24921216
DA 2022-04-25
ER

PT J
AU Wu, DJ
   Yin, ZH
   Ji, YS
   Li, L
   Li, YX
   Meng, FQ
   Ren, XH
   Xu, M
AF Wu, Dejun
   Yin, Zhenhua
   Ji, Yisheng
   Li, Lin
   Li, Yunxin
   Meng, Fanqiang
   Ren, Xiaohan
   Xu, Ming
TI Identification of novel autophagy-related lncRNAs associated with a poor
   prognosis of colon adenocarcinoma through bioinformatics analysis
SO SCIENTIFIC REPORTS
LA English
DT Article
ID LONG NONCODING RNA; CANCER; CELLS; SUPPRESSION; EXPRESSION; PROMOTES;
   THERAPY
AB LncRNAs play a pivotal role in tumorigenesis and development. However, the potential involvement of lncRNAs in colon adenocarcinoma (COAD) needs to be further explored. All the data used in this study were obtained from The Cancer Genome Atlas database, and all analyses were conducted using R software. Basing on the seven prognosis-related lncRNAs finally selected, we developed a prognosis-predicting model with powerful effectiveness (training cohort, 1 year: AUC=0.70, 95% Cl=0.57-0.78; 3 years: AUC=0.71, 95% Cl=0.6-0.8; 5 years: AUC=0.76, 95% Cl=0.66-0.87; validation cohort, 1 year: AUC=0.70, 95% Cl=0.58-0.8; 3 years: AUC=0.73, 95% Cl=0.63-0.82; 5 years: AUC=0.68, 95% Cl=0.5-0.85). The VEGF and Notch pathway were analyzed through GSEA analysis, and low immune and stromal scores were found in high-risk patients (immune score, cor=-0.15, P<0.001; stromal score, cor=-0.18, P<0.001) , which may partially explain the poor prognosis of patients in the high-risk group. We screened lncRNAs that are significantly associated with the survival of patients with COAD and possibly participate in autophagy regulation. This study may provide direction for future research.
C1 [Wu, Dejun; Xu, Ming] Fudan Univ, Shanghai Pudong Hosp, Dept Gen Surg, Pudong Med Ctr, Shanghai 201399, Peoples R China.
   [Yin, Zhenhua] Fudan Univ, Shanghai Pudong Hosp, Dept Digest, Pudong Med Ctr, 2800 Gongwei Rd, Shanghai 201399, Peoples R China.
   [Ren, Xiaohan] Nanjing Med Univ, Affiliated Hosp 1, Dept Urol, State Key Lab Reprod, Nanjing 210029, Peoples R China.
   [Ji, Yisheng; Li, Lin; Li, Yunxin] Nanjing Med Univ, Clin Med Coll 1, Nanjing 210029, Peoples R China.
   [Meng, Fanqiang] Cent South Univ, Xiangya Med Coll, Changsha 410000, Hunan, Peoples R China.
RP Xu, M (corresponding author), Fudan Univ, Shanghai Pudong Hosp, Dept Gen Surg, Pudong Med Ctr, Shanghai 201399, Peoples R China.; Ren, XH (corresponding author), Nanjing Med Univ, Affiliated Hosp 1, Dept Urol, State Key Lab Reprod, Nanjing 210029, Peoples R China.
EM xiaohanren@njmu.edu.cn; xuming681025@sina.com
FU fund of Young Medical Talents Training Program of Pudong Health
   Committee of Shanghai [PWRq2020-67]; Discipline Construction Promoting
   Project of Shanghai Pudong Hospital [Zdxk2020-01, Zdzk2020-10]
FX This work was supported by the fund of Young Medical Talents Training
   Program of Pudong Health Committee of Shanghai (Grant No. PWRq2020-67);
   the Discipline Construction Promoting Project of Shanghai Pudong
   Hospital (Zdxk2020-01), (Zdzk2020-10).
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NR 44
TC 0
Z9 0
U1 0
U2 1
PU NATURE RESEARCH
PI BERLIN
PA HEIDELBERGER PLATZ 3, BERLIN, 14197, GERMANY
SN 2045-2322
J9 SCI REP-UK
JI Sci Rep
PD APR 13
PY 2021
VL 11
IS 1
AR 8069
DI 10.1038/s41598-021-87540-0
PG 12
WC Multidisciplinary Sciences
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Science & Technology - Other Topics
GA RN8OX
UT WOS:000640612400020
PM 33850225
OA gold, Green Published
DA 2022-04-25
ER

PT J
AU Nazim, UM
   Moon, JH
   Lee, YJ
   Seol, JW
   Park, SY
AF Nazim, Uddin Md.
   Moon, Ji-Hong
   Lee, You-Jin
   Seol, Jae-Won
   Park, Sang-Youel
TI PPAR gamma activation by troglitazone enhances human lung cancer cells
   to TRAIL-induced apoptosis via autophagy flux
SO ONCOTARGET
LA English
DT Article
DE troglitazone; PPAR gamma; autophagy; TRAIL; lung cancer cells
ID HUMAN BREAST-CANCER; DEATH RECEPTORS 4; COLON-CANCER; MEDIATED
   APOPTOSIS; SURFACE EXPRESSION; DOWN-REGULATION; UP-REGULATION; KAPPA-B;
   C-FLIP; LIGAND
AB Members of the tumor necrosis factor (TNF) transmembrane cytokine superfamily, such as TNFa and Fas ligand (FasL), play crucial roles in inflammation and immunity. TRAIL is a member of this superfamily with the ability to selectively trigger cancer cell death but does not motive cytotoxicity to most normal cells. Troglitazone are used in the cure of type II diabetes to reduce blood glucose levels and improve the sensitivity of an amount of tissues to insulin. In this study, we revealed that troglitazone could trigger TRAIL-mediated apoptotic cell death in human lung adenocarcinoma cells. Pretreatment of troglitazone induced activation of PPAR. in a dose-dependent manner. In addition conversion of LC3-I to LC3-II and PPAR. was suppressed in the presence of GW9662, a well-characterized PPAR. antagonist. Treatment with troglitazone resulted in a slight increase in conversion rate of LC3-I to LC3-II and significantly decreased p62 expression levels in a dose-dependent manner. This indicates that troglitazone induced autophagy flux activation in human lung cancer cells. Inhibition of autophagy flux applying a specific inhibitor and genetically modified ATG5 siRNA enclosed troglitazone-mediated enhancing effect of TRAIL. These data demonstrated that activation of PPAR. mediated by troglitazone enhances human lung cancer cells to TRAIL-induced apoptosis via autophagy flux and also suggest that troglitazone may be a combination therapeutic target with TRAIL protein in TRAIL-resistant cancer cells.
C1 [Nazim, Uddin Md.; Moon, Ji-Hong; Lee, You-Jin; Seol, Jae-Won; Park, Sang-Youel] Chonbuk Natl Univ, Biosafety Res Inst, Coll Vet Med, Iksan 54596, Jeonbuk, South Korea.
RP Park, SY (corresponding author), Chonbuk Natl Univ, Biosafety Res Inst, Coll Vet Med, Iksan 54596, Jeonbuk, South Korea.
EM sypark@chonbuk.ac.kr
RI Park, Sang-Youel/D-5966-2012
OI Park, Sang-Youel/0000-0003-0575-6045
FU National Research Foundation of Korea (NRF) - Korean government (MISP)
   [2013R1A4A1069486]
FX This study was supported by a grant from the National Research
   Foundation of Korea (NRF), funded by the Korean government (MISP)
   (2013R1A4A1069486).
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NR 65
TC 14
Z9 14
U1 0
U2 6
PU IMPACT JOURNALS LLC
PI ORCHARD PARK
PA 6666 E QUAKER ST, STE 1, ORCHARD PARK, NY 14127 USA
EI 1949-2553
J9 ONCOTARGET
JI Oncotarget
PD APR 18
PY 2017
VL 8
IS 16
BP 26819
EP 26831
DI 10.18632/oncotarget.15819
PG 13
WC Oncology; Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Cell Biology
GA ES8PQ
UT WOS:000399819700083
PM 28460464
OA Green Published, Green Submitted, gold
DA 2022-04-25
ER

PT J
AU Zhang, ZY
   Zhang, X
   Huang, AM
AF Zhang, Zhiyong
   Zhang, Xin
   Huang, Aimin
TI Aggresome-Autophagy Associated Gene HDAC6 Is a Potential Biomarker in
   Pan-Cancer, Especially in Colon Adenocarcinoma
SO FRONTIERS IN ONCOLOGY
LA English
DT Article
DE pan-cancer; histone deacetylase 6; immune microenvironment; DNA
   methylation; immunotherapy
ID IMMUNE CELLS; EXPRESSION; PROGNOSIS; MORTALITY; BURDEN
AB Background: Histone deacetylase 6 (HDAC6) regulates cytoplasmic signaling networks through the deacetylation of various cytoplasmic substrates. Recent studies have identified the role of HDAC6 in tumor development and immune metabolism, but its specific function remains unclear.
   Methods: The current study determined the role of HDAC6 in tumor metabolism and tumor immunity through a multi-database pan-cancer analysis. The Cancer Genome Atlas (TCGA), Genotype-Tissue Expression (GTEx), and Cancer Cell Line Encyclopedia (CCLE) datasets were used to determine the expression levels, prognosis, tumor progression, immune checkpoints, and immune metabolism of HDAC6 in 33 tumors. Pathways, immune checkpoints, immune neoantigens, immune microenvironment, tumor mutational burden (TMB), microsatellite instability (MSI), DNA mismatch repair (MMR), and the value of methyltransferases. The R package was used for quantitative analysis and panoramic description.
   Results: In the present study, we determined that HDAC6 is differentially expressed in pan carcinomas, and by survival, we found that HDAC6 was generally associated with the prognosis of pancreatic adenocarcinoma, Thymoma, and uveal melanoma, where low expression of HDAC6 had a significantly worse prognosis. Secondly, through this experiment, we confirmed that HDAC6 expression level was associated with tumor immune infiltration and tumor microenvironment, especially in PAAD. Finally, HDAC6 was associated with immune neoantigen and immune checkpoint gene expression profiles in all cancers in addition to TMB and MSI in pan-cancers.
   Conclusion: HDAC6 is differentially expressed in pan-cancers and plays an essential role in tumor metabolism and immunity. HDAC6 holds promise as a tumor potential prognostic marker, especially in colon cancer.
C1 [Zhang, Zhiyong; Zhang, Xin] Zhengzhou Univ, Dept Colorectal Surg, Affiliated Hosp 1, Zhengzhou, Peoples R China.
   [Huang, Aimin] Zhengzhou Univ, Dept Gen Surg, Med Coll, Zhengzhou, Peoples R China.
RP Zhang, ZY (corresponding author), Zhengzhou Univ, Dept Colorectal Surg, Affiliated Hosp 1, Zhengzhou, Peoples R China.; Huang, AM (corresponding author), Zhengzhou Univ, Dept Gen Surg, Med Coll, Zhengzhou, Peoples R China.
EM zazzy1973@163.com; doctorhuang518@zzu.edu.cn
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NR 46
TC 1
Z9 1
U1 6
U2 8
PU FRONTIERS MEDIA SA
PI LAUSANNE
PA AVENUE DU TRIBUNAL FEDERAL 34, LAUSANNE, CH-1015, SWITZERLAND
SN 2234-943X
J9 FRONT ONCOL
JI Front. Oncol.
PD AUG 17
PY 2021
VL 11
AR 718589
DI 10.3389/fonc.2021.718589
PG 13
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA UM6WM
UT WOS:000693470800001
PM 34485153
OA gold, Green Published
DA 2022-04-25
ER

PT J
AU Song, FL
   Li, LX
   Liang, DY
   Zhuo, YS
   Wang, XY
   Dai, HC
AF Song, Fengling
   Li, Lexing
   Liang, Danyang
   Zhuo, Yisha
   Wang, Xueyi
   Dai, Hanchuan
TI Knockdown of long noncoding RNA urothelial carcinoma associated 1
   inhibits colorectal cancer cell proliferation and promotes apoptosis via
   modulating autophagy
SO JOURNAL OF CELLULAR PHYSIOLOGY
LA English
DT Article
DE apoptosis; autophagy; cell proliferation; colorectal cancer (CRC) cell;
   long noncoding RNA (lncRNA) urothelial carcinoma associated 1 (UCA1)
ID PREDICTS POOR-PROGNOSIS; ACTIVATES AUTOPHAGY; TUMOR PROLIFERATION; UCA1;
   RESISTANCE; METASTASIS; EXPRESSION; MIGRATION; INJURY
AB Long noncoding RNA urothelial carcinoma associated 1 (UCA1) has been implicated in the growth and metastasis of colorectal cancer (CRC), and autophagy contributes to tumorigenesis and cancer cell survival. However, the regulatory role of UCA1 in CRC cell viability by modulating autophagy remains unclear. In the present study, a significant positive correlation was observed between UCA1 and microtubule-associated protein 1 light chain 3 (LC3) levels, and the elevated UCA1 was negatively correlated with the PKB/protein kinase B (AKT)/mammalian target of rapamycin (mTOR) signaling pathway in 293T cells. Downregulation of UCA1 inhibited autophagy activation and cell proliferation, whereas the apoptosis was increased and the cell cycle was arrested in G2 stage. The next results showed that UCA1 was markedly upregulated in Caco-2 cells. Knockdown of UCA1 significantly decreased the LC3-II and autophagy-related gene 5 (ATG5) protein levels and resulted in an increase in p62 expression. Conversely, the autophagy activator rapamycin (RAPA) reversed the effects. Furthermore, downregulated UCA1 decreased Caco-2 cells population in the G1 phase and increased the cells number in G2 phage. The cell proliferation was inhibited, and apoptosis rate was promoted. More important, RAPA could also abrogate the changes induced by knockdown of UCA1. Collectively, these data demonstrated that downregulated UCA1 induced autophagy inhibition, resulting in suppressing cell proliferation and promoting apoptosis, which suggested that UCA1 might serve as a potential new oncogene to regulate CRC cells viability by modulating autophagy.
C1 [Song, Fengling; Li, Lexing; Liang, Danyang; Zhuo, Yisha; Wang, Xueyi; Dai, Hanchuan] Huazhong Agr Univ, Coll Vet Med, Dept Basic Vet Med, Wuhan, Hubei, Peoples R China.
RP Dai, HC (corresponding author), Huazhong Agr Univ, Coll Vet Med, 1 Shizishan St, Wuhan 430070, Hubei, Peoples R China.
EM daihch@mail.hzau.edu.cn
FU National key RD Program [2016YFD0501210, 2017YFD0502301]; Natural
   Science Foundation of HubeiNatural Science Foundation of Hubei Province
   [2018CFB444]; Fundamental Research Funds for Central Universities of
   China [2011QC004]
FX National key R&D Program, Grant/Award Numbers: 2016YFD0501210,
   2017YFD0502301; Natural Science Foundation of Hubei, Grant/Award Number:
   2018CFB444; The Fundamental Research Funds for Central Universities of
   China, Grant/Award Number: 2011QC004
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NR 57
TC 19
Z9 19
U1 0
U2 25
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0021-9541
EI 1097-4652
J9 J CELL PHYSIOL
JI J. Cell. Physiol.
PD MAY
PY 2019
VL 234
IS 5
BP 7420
EP 7434
DI 10.1002/jcp.27500
PG 15
WC Cell Biology; Physiology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Cell Biology; Physiology
GA HK7AQ
UT WOS:000458138600180
PM 30362538
DA 2022-04-25
ER

PT J
AU Shan, TD
   Xu, JH
   Yu, T
   Li, JY
   Zhao, LN
   Ouyang, H
   Luo, S
   Lu, XJ
   Huang, CZ
   Lan, QS
   Zhong, W
   Chen, QK
AF Shan, Ti-Dong
   Xu, Ji-Hao
   Yu, Tao
   Li, Jie-Yao
   Zhao, Lin-Na
   Ouyang, Hui
   Luo, Su
   Lu, Xi-Ji
   Huang, Can-Ze
   Lan, Qiu-Shen
   Zhong, Wa
   Chen, Qi-Kui
TI Knockdown of linc-POU3F3 suppresses the proliferation, apoptosis, and
   migration resistance of colorectal cancer
SO ONCOTARGET
LA English
DT Article
DE linc-POU3F3; colorectal cancer; proliferation; apoptosis; signal pathway
ID HEPATOCELLULAR-CARCINOMA; NONCODING RNAS; AUTOPHAGY; CELLS; EPIGENETICS;
   CARCINOGENESIS; TUMORIGENESIS; DEGRADATION; INVOLVEMENT; METASTASIS
AB Long intergenic noncoding RNAs (lincRNAs) play important roles in regulating the biological functions and underlying molecular mechanisms of colorectal cancer (CRC). Here, we investigated the association of linc-POU3F3 and prognosis in CRC. We demonstrated that linc-POU3F3 was overexpressed in CRC tissues and positively correlated with tumor grade and N stage. Inhibition of linc-POU3F3 resulted in inhibition of cell proliferation and G1 cell cycle arrest, which was mediated by cyclin D1, CDK4, p18, Rb, and phosphorylated Rb. Inhibition of linc-POU3F3 induced apoptosis, and suppressed migration and invasion in LOVO and SW480 cell lines. This inhibition also increased the expressions of epithelial markers and decreased the expressions of mesenchymal markers, thus inhibiting the cancer epithelial-mesenchymal transition. The decreased migration and invasion following linc-POU3F3 knockdown were mediated by an increased BMP signal. Furthermore, autophagy was enhanced by linc-POU3F3 knockdown, suggesting the involvement of autophagy in the induced apoptosis. Collectively, linc-POU3F3 might be crucial in pro-proliferation, anti-apoptosis, and metastasis in LOVO and SW480 cells by regulating the cell cycle, intrinsic apoptosis, BMP signaling and autophagy. Thus, linc-POU3F3 is a potential therapeutic target and novel molecular biomarker for CRC.
C1 [Shan, Ti-Dong; Xu, Ji-Hao; Yu, Tao; Li, Jie-Yao; Ouyang, Hui; Luo, Su; Lu, Xi-Ji; Huang, Can-Ze; Zhong, Wa; Chen, Qi-Kui] Sun Yat Sen Univ, Sun Yat Sen Mem Hosp, Dept Gastroenterol, Guangzhou 510120, Guangdong, Peoples R China.
   [Shan, Ti-Dong; Xu, Ji-Hao; Yu, Tao; Li, Jie-Yao; Ouyang, Hui; Luo, Su; Lu, Xi-Ji; Huang, Can-Ze; Zhong, Wa; Chen, Qi-Kui] Sun Yat Sen Univ, Sun Yat Sen Mem Hosp, Guangdong Prov Key Lab Malignant Tumor Epigenet &, Guangzhou 510120, Guangdong, Peoples R China.
   [Lan, Qiu-Shen] Sun Yat Sen Univ, Sun Yat Sen Mem Hosp, Dept Gen Surg, Guangzhou 510120, Guangdong, Peoples R China.
   [Zhao, Lin-Na] Guangzhou Univ Tradit Chinese Med, Affiliated Hosp 1, Dept Gastroenterol, Guangzhou 510504, Guangdong, Peoples R China.
RP Yu, T; Chen, QK (corresponding author), Sun Yat Sen Univ, Sun Yat Sen Mem Hosp, Dept Gastroenterol, Guangzhou 510120, Guangdong, Peoples R China.; Yu, T; Chen, QK (corresponding author), Sun Yat Sen Univ, Sun Yat Sen Mem Hosp, Guangdong Prov Key Lab Malignant Tumor Epigenet &, Guangzhou 510120, Guangdong, Peoples R China.
EM yutao2014@126.com; qikuichen@yahoo.com
FU Key Laboratory of Malignant Tumor Molecular Mechanism and Translational
   Medicine of Guangzhou Bureau of Science and Information Technology
   [[2013]163]; Key Laboratory of Malignant Tumor Gene Regulation and
   Target Therapy of Guangdong Higher Education Institutes [KLB09001];
   National Natural Science Foundation of ChinaNational Natural Science
   Foundation of China (NSFC) [81270442, 81370475]
FX All authors read and approved the final manuscript. This work was
   supported by grants from the Key Laboratory of Malignant Tumor Molecular
   Mechanism and Translational Medicine of Guangzhou Bureau of Science and
   Information Technology (Grant [2013]163); the Key Laboratory of
   Malignant Tumor Gene Regulation and Target Therapy of Guangdong Higher
   Education Institutes (Grant KLB09001); and the National Natural Science
   Foundation of China (No.81270442 and No. 81370475).
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NR 48
TC 38
Z9 45
U1 0
U2 2
PU IMPACT JOURNALS LLC
PI ORCHARD PARK
PA 6666 E QUAKER ST, STE 1, ORCHARD PARK, NY 14127 USA
EI 1949-2553
J9 ONCOTARGET
JI Oncotarget
PD JAN 5
PY 2016
VL 7
IS 1
BP 961
EP 975
DI 10.18632/oncotarget.5830
PG 15
WC Oncology; Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Cell Biology
GA DD5GI
UT WOS:000369950300070
PM 26510906
OA Green Published, gold, Green Submitted
DA 2022-04-25
ER

PT J
AU Claerhout, S
   Lim, JY
   Choi, W
   Park, YY
   Kim, K
   Kim, SB
   Lee, JS
   Mills, GB
   Cho, JY
AF Claerhout, Sofie
   Lim, Jae Yun
   Choi, Woonyoung
   Park, Yun-Yong
   Kim, KyoungHyun
   Kim, Sang-Bae
   Lee, Ju-Seog
   Mills, Gordon B.
   Cho, Jae Yong
TI Gene Expression Signature Analysis Identifies Vorinostat as a Candidate
   Therapy for Gastric Cancer
SO PLOS ONE
LA English
DT Article
ID HISTONE DEACETYLASE INHIBITORS; CONNECTIVITY MAP; SERIAL ANALYSIS; HUMAN
   COLON; CELL-DEATH; PHASE-II; CARCINOMA; GROWTH; AUTOPHAGY; RISK
AB Background: Gastric cancer continues to be one of the deadliest cancers in the world and therefore identification of new drugs targeting this type of cancer is thus of significant importance. The purpose of this study was to identify and validate a therapeutic agent which might improve the outcomes for gastric cancer patients in the future.
   Methodology/Principal Findings: Using microarray technology, we generated a gene expression profile of human gastric cancer-specific genes from human gastric cancer tissue samples. We used this profile in the Broad Institute's Connectivity Map analysis to identify candidate therapeutic compounds for gastric cancer. We found the histone deacetylase inhibitor vorinostat as the lead compound and thus a potential therapeutic drug for gastric cancer. Vorinostat induced both apoptosis and autophagy in gastric cancer cell lines. Pharmacological and genetic inhibition of autophagy however, increased the therapeutic efficacy of vorinostat, indicating that a combination of vorinostat with autophagy inhibitors may therapeutically be more beneficial. Moreover, gene expression analysis of gastric cancer identified a collection of genes (ITGB5, TYMS, MYB, APOC1, CBX5, PLA2G2A, and KIF20A) whose expression was elevated in gastric tumor tissue and downregulated more than 2-fold by vorinostat treatment in gastric cancer cell lines. In contrast, SCGB2A1, TCN1, CFD, APLP1, and NQO1 manifested a reversed pattern.
   Conclusions/Significance: We showed that analysis of gene expression signature may represent an emerging approach to discover therapeutic agents for gastric cancer, such as vorinostat. The observation of altered gene expression after vorinostat treatment may provide the clue to identify the molecular mechanism of vorinostat and those patients likely to benefit from vorinostat treatment.
C1 [Claerhout, Sofie; Lim, Jae Yun; Park, Yun-Yong; Kim, Sang-Bae; Lee, Ju-Seog; Mills, Gordon B.; Cho, Jae Yong] Univ Texas MD Anderson Canc Ctr, Dept Syst Biol, Div Canc Med, Houston, TX 77030 USA.
   [Lim, Jae Yun; Cho, Jae Yong] Yonsei Univ, Coll Med, Dept Med Oncol, Gangnam Severance Hosp, Seoul, South Korea.
   [Choi, Woonyoung] Univ Texas MD Anderson Canc Ctr, Dept Canc Biol, Houston, TX 77030 USA.
   [Kim, KyoungHyun] Texas A&M Univ, Dept Vet Physiol & Pharmacol, College Stn, TX 77843 USA.
RP Claerhout, S (corresponding author), Univ Texas MD Anderson Canc Ctr, Dept Syst Biol, Div Canc Med, Houston, TX 77030 USA.
EM chojy@yuhs.ac
RI Lee, Ju-Seog/X-1786-2018
OI Lee, Ju-Seog/0000-0002-5666-9753; Kim, Kyounghyun/0000-0002-7240-2768;
   Cho, Jae Yong/0000-0002-0926-1819; Claerhout, Sofie/0000-0003-0857-0211
FU Odyssey Program; University of Texas MD Anderson Cancer Center; National
   Research Foundation of KoreaNational Research Foundation of Korea;
   Ministry of Education, Science and TechnologyMinistry of Education,
   Science and Technology, Republic of Korea [2010-0024248]; NATIONAL
   CANCER INSTITUTEUnited States Department of Health & Human
   ServicesNational Institutes of Health (NIH) - USANIH National Cancer
   Institute (NCI) [P30CA016672, P50CA098258] Funding Source: NIH RePORTER
FX Funding to SC as an Odyssey Fellow was supported by the Odyssey Program
   and the Theodore N. Law Endowment for Scientific Achievement at the
   University of Texas MD Anderson Cancer Center. This work was also
   supported by funds from the 2009 Internal Medicine Academic Research
   Fund and Basic Science Research Program through the National Research
   Foundation of Korea funded by the Ministry of Education, Science and
   Technology (No. 2010-0024248). The funders had no role in study design,
   data collection and analysis, decision to publish, or preparation of the
   manuscript.
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NR 53
TC 85
Z9 89
U1 0
U2 7
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 1160 BATTERY STREET, STE 100, SAN FRANCISCO, CA 94111 USA
SN 1932-6203
J9 PLOS ONE
JI PLoS One
PD SEP 9
PY 2011
VL 6
IS 9
AR e24662
DI 10.1371/journal.pone.0024662
PG 10
WC Multidisciplinary Sciences
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Science & Technology - Other Topics
GA 819CN
UT WOS:000294803100051
PM 21931799
OA gold, Green Published, Green Submitted
DA 2022-04-25
ER

PT J
AU Alotaibi, MR
   Asnake, B
   Di, X
   Beckman, MJ
   Durrant, D
   Simoni, D
   Baruchello, R
   Lee, RM
   Schwartz, EL
   Gewirtz, DA
AF Alotaibi, M. R.
   Asnake, B.
   Di, Xu
   Beckman, M. J.
   Durrant, D.
   Simoni, D.
   Baruchello, R.
   Lee, R. M.
   Schwartz, E. L.
   Gewirtz, D. A.
TI Stilbene 5c, a microtubule poison with vascular disrupting properties
   that induces multiple modes of growth arrest and cell death
SO BIOCHEMICAL PHARMACOLOGY
LA English
DT Article
DE Microtubules; Autophagy; Senescence; Angiogenic; Vascular disrupting
ID COMBRETASTATIN A4 PHOSPHATE; DISSEMINATED MALIGNANT-MELANOMA;
   NATIONAL-CANCER-INSTITUTE; BREAST-CANCER; PHASE-III; MITOTIC
   CATASTROPHE; DRUG-RESISTANCE; CLINICAL-TRIALS; BETA-TUBULIN; AUTOPHAGY
AB The stilbene derivative, cis-3,4',5-trimethoxy-3'-aminostilbene (stilbene 5c), is a potentially potent antitumor agent that acts via binding to the colchicine-binding site in tubulin. The current studies were designed to investigate the effectiveness of stilbene 5c against the HCT-116 human colon cancer cell line and B16/F10 melanoma cells as well as human endothelial cell tube formation and tumor perfusion. Stilbene 5c produced a time-dependent decrease in cell viability in both cell lines and the capacity of the cells to proliferate was not restored upon removal of the drug. Treatment with stilbene 5c also promoted both senescence and autophagy in both cell lines. TUNEL and annexin 5 staining indicated that apoptosis also occurs in stilbene 5c-treated HCT-116 cells, but not in B16/F10 melanoma cells. DAPI staining revealed morphological changes in the cell nuclei (binucleated and micronucleated cells) indicative of mitotic catastrophe in HCT-116 cells but not in the B16/F10 melanoma cells. p53-null HCT-116 cells demonstrated a similar growth arrest/cell death response to stilbene as p53-wild type HCT-116 cells. Stilbene 5c also completely inhibited human endothelial cell tube formation on Matrigel, consistent with potential anti-angiogenic actions. Using a new method developed for monitoring the pharmacodynamic effects of stilbene 5c in vivo, we found that a single injection of stilbene 5c reduced tumor perfusion by 65% at 4 h, returning to baseline by 24 h, while subsequent daily injections of stilbene 5c produced progressively larger reductions and smaller rebounds. This work indicates that stilbene 5c could potentially be effective against melanoma and colon cancer through the promotion of multiple modes of growth arrest and cell death coupled with anti-angiogenic and antivascular actions. (C) 2013 Elsevier Inc. All rights reserved.
C1 [Alotaibi, M. R.; Asnake, B.; Di, Xu; Beckman, M. J.; Lee, R. M.; Gewirtz, D. A.] Virginia Commonwealth Univ, Dept Pharmacol & Toxicol, Richmond, VA 23298 USA.
   [Alotaibi, M. R.; Asnake, B.; Di, Xu; Beckman, M. J.; Durrant, D.; Lee, R. M.; Gewirtz, D. A.] Virginia Commonwealth Univ, Dept Med, Richmond, VA 23298 USA.
   [Alotaibi, M. R.; Asnake, B.; Di, Xu; Beckman, M. J.; Durrant, D.; Lee, R. M.; Gewirtz, D. A.] Virginia Commonwealth Univ, Massey Canc Ctr, Richmond, VA 23298 USA.
   [Simoni, D.; Baruchello, R.] Univ Ferrara, I-44100 Ferrara, Italy.
   [Schwartz, E. L.] Albert Einstein Coll Med, Dept Med Oncol, Bronx, NY 10461 USA.
RP Gewirtz, DA (corresponding author), Virginia Commonwealth Univ, Dept Pharmacol & Toxicol, Med Coll Virginia Campus, Richmond, VA 23298 USA.
EM gewirtz@vcu.edu
FU NIH/NCIUnited States Department of Health & Human ServicesNational
   Institutes of Health (NIH) - USANIH National Cancer Institute (NCI) [RO1
   CA163907, RO1CA135043]; NATIONAL CANCER INSTITUTEUnited States
   Department of Health & Human ServicesNational Institutes of Health (NIH)
   - USANIH National Cancer Institute (NCI) [R01CA135043, P30CA016059,
   R01CA163907] Funding Source: NIH RePORTER
FX This study was supported by NIH/NCI grants RO1 CA163907 (ELS) and
   RO1CA135043 (DAG). The guidance of Dr. Fiorenza lanzini of the
   University of Iowa Carver College of Medicine relating to studies of
   mitotic catastrophe is gratefully appreciated.
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NR 58
TC 6
Z9 6
U1 0
U2 16
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0006-2952
EI 1873-2968
J9 BIOCHEM PHARMACOL
JI Biochem. Pharmacol.
PD DEC 15
PY 2013
VL 86
IS 12
BP 1688
EP 1698
DI 10.1016/j.bcp.2013.10.007
PG 11
WC Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA 275XQ
UT WOS:000328713100006
PM 24144631
OA Green Accepted
DA 2022-04-25
ER

PT J
AU Handerson, T
   Pawelek, JM
AF Handerson, T
   Pawelek, JM
TI beta 1,6-branched oligosaccharides and coarse vesicles: A common,
   pervasive phenotype in melanoma and other human cancers
SO CANCER RESEARCH
LA English
DT Article
ID N-ACETYLGLUCOSAMINYLTRANSFERASE-V; BETA-1-6 BRANCHED OLIGOSACCHARIDES;
   ASPARAGINE-LINKED OLIGOSACCHARIDES; CELL-SURFACE; HUMAN-BREAST; ABERRANT
   GLYCOSYLATION; INCREASED EXPRESSION; HORIZONTAL TRANSFER; SIGNALING
   PATHWAY; TUMOR PROGRESSION
AB We describe a new phenotype of wide occurrence in human cancer: expression of coarse vesicles rich in beta1,6-branched oligosaccharides. beta1,6-branching, catalyzed by GNT-V, is associated with metastasis and predicts poor survival in primary human breast and colon carcinomas. Yet little is known on the histopathology of this phenomenon. We studied beta1,6-branching [determined by leukocytic phytohemagglutinin (LPHA) lectin-histochemistry] in 119 archival specimens of human melanomas and other neoplasms, including carcinomas of the lung, colon, breast, ovary, prostate, kidney, and Hodgkin's lymphoma. At least portions of most tumors (96%) stained to some extent with LPHA. Staining was always, but not exclusively, associated with coarse vesicles. In melanomas, LPHA staining colocalized with CD63 and gp100. In pigmented melanomas, the vesicles were melanized and are known as "coarse melanin." LPHA-positive, coarse melanin was a feature of both tumor cells and melanophages and accounted for the well-known hypermelanotic regions of primary melanomas. LPHA-positive tumor cells varied widely in primaries (melanoma and others), ranging from 0 to 100% for a given tumor, whereas metastases were far more homogeneous (P = 0.0080), with vesicular, LPHA-positive tumor cells comprising >75% of 15 of 16 metastatic melanomas and renal cell carcinomas. In studies by others, GNT-V elicited formation of autophagy-dependent, LPHA-positive vesicles in mink lung alveolar cells (Hariri et aL, Mol. Biol. Cell, 11: 255-268, 2000), suggesting that the coarse vesicles in tumors reported here may have been induced by GNT-V. Expression of the phenotype was so common and pervasive that it appeared to be an integral component of the biology of tumor progression. The origin of this phenotype and its biological significance are as yet unclear and will require considerable further study.
C1 Yale Univ, Sch Med, Dept Dermatol, New Haven, CT 06520 USA.
RP Pawelek, JM (corresponding author), Yale Univ, Sch Med, Dept Dermatol, 333 Cedar St, New Haven, CT 06520 USA.
EM john.pawelek@yale.edu
FU NATIONAL INSTITUTE OF ARTHRITIS AND MUSCULOSKELETAL AND SKIN
   DISEASESUnited States Department of Health & Human ServicesNational
   Institutes of Health (NIH) - USANIH National Institute of Arthritis &
   Musculoskeletal & Skin Diseases (NIAMS) [P30AR041942] Funding Source:
   NIH RePORTER; NIAMS NIH HHSUnited States Department of Health & Human
   ServicesNational Institutes of Health (NIH) - USANIH National Institute
   of Arthritis & Musculoskeletal & Skin Diseases (NIAMS) [2 P30
   AR41942-06A1] Funding Source: Medline
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NR 73
TC 56
Z9 57
U1 0
U2 4
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD SEP 1
PY 2003
VL 63
IS 17
BP 5363
EP 5369
PG 7
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA 722XD
UT WOS:000185402600030
PM 14500369
DA 2022-04-25
ER

PT J
AU Mujumdar, N
   Banerjee, S
   Chen, ZY
   Sangwan, V
   Chugh, R
   Dudeja, V
   Yamamoto, M
   Vickers, SM
   Saluja, AK
AF Mujumdar, Nameeta
   Banerjee, Sulagna
   Chen, Zhiyu
   Sangwan, Veena
   Chugh, Rohit
   Dudeja, Vikas
   Yamamoto, Masato
   Vickers, Selwyn M.
   Saluja, Ashok K.
TI Triptolide activates unfolded protein response leading to chronic ER
   stress in pancreatic cancer cells
SO AMERICAN JOURNAL OF PHYSIOLOGY-GASTROINTESTINAL AND LIVER PHYSIOLOGY
LA English
DT Article
DE endoplasmic reticulum stress; apoptosis; autophagy; pancreatic cancer;
   triptolide; glucose-regulated protein 78
ID ENDOPLASMIC-RETICULUM STRESS; HEPATOCELLULAR-CARCINOMA; NEGATIVE
   REGULATOR; INDUCED APOPTOSIS; BREAST-CANCER; DEATH PROGRAM;
   COLON-CANCER; GRP78; EXPRESSION; AUTOPHAGY
AB Pancreatic cancer is a devastating disease with a survival rate of <5%. Moreover, pancreatic cancer aggressiveness is closely related to high levels of prosurvival mediators, which can ultimately lead to rapid disease progression. One of the mechanisms that enables tumor cells to evade cellular stress and promote unhindered proliferation is the endoplasmic reticulum (ER) stress response. Disturbances in the normal functions of the ER lead to an evolutionarily conserved cell stress response, the unfolded protein response (UPR). The UPR initially compensates for damage, but it eventually triggers cell death if ER dysfunction is severe or prolonged. Triptolide, a diterpene triepoxide, has been shown to be an effective compound against pancreatic cancer. Our results show that triptolide induces the UPR by activating the PKR-like ER kinase-eukaryotic initiation factor 2 alpha axis and the inositol-requiring enzyme 1 alpha-X-box-binding protein 1 axis of the UPR and leads to chronic ER stress in pancreatic cancer. Our results further show that glucose-regulated protein 78 (GRP78), one of the major regulators of ER stress, is downregulated by triptolide, leading to cell death by apoptosis in MIA PaCa-2 cells and autophagy in S2-VP10 cells.
C1 [Mujumdar, Nameeta; Banerjee, Sulagna; Chen, Zhiyu; Sangwan, Veena; Chugh, Rohit; Dudeja, Vikas; Yamamoto, Masato; Vickers, Selwyn M.; Saluja, Ashok K.] Univ Minnesota, Dept Surg, Div Basic & Translat Res, Minneapolis, MN 55455 USA.
   [Yamamoto, Masato; Vickers, Selwyn M.; Saluja, Ashok K.] Univ Minnesota, Mason Canc Ctr, Minneapolis, MN USA.
RP Saluja, AK (corresponding author), 11-214 Malcolm Moos Tower,515 Delaware St SE, Minneapolis, MN 55455 USA.
EM asaluja@umn.edu
FU University of Alabama Birmingham/University of Minnesota National Cancer
   Institute (NCI) Specialized Program of Research Excellence in Pancreatic
   Cancer Grant [P50 CA-101955]; NCIUnited States Department of Health &
   Human ServicesNational Institutes of Health (NIH) - USANIH National
   Cancer Institute (NCI) [R01 CA-170946, CA-124723, T32 CA-132715];
   NATIONAL CANCER INSTITUTEUnited States Department of Health & Human
   ServicesNational Institutes of Health (NIH) - USANIH National Cancer
   Institute (NCI) [P50CA101955, T32CA132715, R01CA124723, R01CA170946]
   Funding Source: NIH RePORTER
FX This study was supported by University of Alabama Birmingham/University
   of Minnesota National Cancer Institute (NCI) Specialized Program of
   Research Excellence in Pancreatic Cancer Grant P50 CA-101955 (to S. M.
   Vickers) and NCI Grants R01 CA-170946 and CA-124723 (to A. K. Saluja).
   R. Chugh was supported by NCI Training Grant T32 CA-132715.
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NR 40
TC 33
Z9 35
U1 1
U2 21
PU AMER PHYSIOLOGICAL SOC
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0193-1857
EI 1522-1547
J9 AM J PHYSIOL-GASTR L
JI Am. J. Physiol.-Gastroint. Liver Physiol.
PD JUN
PY 2014
VL 306
IS 11
BP G1011
EP G1020
DI 10.1152/ajpgi.00466.2013
PG 10
WC Gastroenterology & Hepatology; Physiology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology; Physiology
GA AI9FH
UT WOS:000337235900010
PM 24699326
OA Green Published
DA 2022-04-25
ER

PT J
AU Delle Cave, D
   Desiderio, V
   Mosca, L
   Ilisso, CP
   Mele, L
   Caraglia, M
   Cacciapuoti, G
   Porcelli, M
AF Delle Cave, Donatella
   Desiderio, Vincenzo
   Mosca, Laura
   Ilisso, Concetta P.
   Mele, Luigi
   Caraglia, Michele
   Cacciapuoti, Giovanna
   Porcelli, Marina
TI S-Adenosylmethionine-mediated apoptosis is potentiated by autophagy
   inhibition induced by chloroquine in human breast cancer cells
SO JOURNAL OF CELLULAR PHYSIOLOGY
LA English
DT Article
DE apoptosis; autophagy; chloroquine; drug combination; human breast cancer
   cell line MCF-7; S-Adenosylmethionine
ID IN-VITRO; HYPOMETHYLATION STATUS; OSTEOSARCOMA CELLS; LIVER-DISEASE;
   COLON-CANCER; GROWTH; METHYLATION; METHIONINE; EXPRESSION; PATHWAYS
AB The naturally occurring sulfonium compound S-adenosyl-L-methionine (AdoMet) is an ubiquitous sulfur-nucleoside that represents the main methyl donor in numerous methylation reactions. In recent years, it has been shown that AdoMet possesses antiproliferative properties in various cancer cells, but the molecular mechanisms at the basis of the effect induced by AdoMet have been only in part investigated. In the present study, we found that AdoMet strongly inhibited the proliferation of breast cancer cells MCF-7 by inducing both autophagy and apoptosis. AdoMet consistently enhanced the levels of the autophagy markers beclin-1 and LC3B-II, and caused a significant increase of pro-apoptotic Bax/Bcl-2 ratio paralleled by poly (ADP ribose) polymerase (PARP) and caspase 9, and 6 cleavage. Notably, AdoMet, already at low doses, raised the percentage of cells in G(2)/M phase of cell cycle by down-regulating the expression of cell cycle-regulatory proteins cyclin B and cyclin E with a remarkable increase of p53, p27, and p21. We also evaluated the combination of AdoMet and the autophagy inhibitor chloroquine (CLC) showing that autophagy block is synergistic in inducing both growth inhibition and apoptosis. These effects were paralleled by a strong inhibition of the activity of AKT and of the downstream effector mTOR and by an increased cleavage of caspase-6 and PARP. These data suggest, for the first time, that autophagy can act as an escape mechanism from the apoptotic activity of AdoMet, and that AdoMet could be used in combination with CLC or its analogs in the treatment of breast cancer.
C1 [Delle Cave, Donatella; Mosca, Laura; Ilisso, Concetta P.; Caraglia, Michele; Cacciapuoti, Giovanna; Porcelli, Marina] Univ Campania Luigi Vanvitelli, Dept Biochem Biophys & Gen Pathol, Via L De Crecchio 7, I-80138 Naples, Italy.
   [Desiderio, Vincenzo; Mele, Luigi] Univ Campania Luigi Vanvitelli, Dept Expt Med, Naples, Italy.
RP Caraglia, M (corresponding author), Univ Campania Luigi Vanvitelli, Dept Biochem Biophys & Gen Pathol, Via L De Crecchio 7, I-80138 Naples, Italy.
EM michele.caraglia@unina2.it
RI Mele, Luigi/AAC-9887-2019; Delle Cave, Donatella/AAM-2941-2021;
   desiderio, vincenzo/K-4244-2018; Caraglia, Michele/AAK-4569-2020
OI Mele, Luigi/0000-0002-6008-0802; Delle Cave,
   Donatella/0000-0002-4019-2778; Caraglia, Michele/0000-0003-2408-6091;
   desiderio, vincenzo/0000-0003-1819-6083; Mosca,
   Laura/0000-0001-7024-9192
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NR 59
TC 28
Z9 28
U1 1
U2 45
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0021-9541
EI 1097-4652
J9 J CELL PHYSIOL
JI J. Cell. Physiol.
PD FEB
PY 2018
VL 233
IS 2
BP 1370
EP 1383
DI 10.1002/jcp.26015
PG 14
WC Cell Biology; Physiology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Cell Biology; Physiology
GA FL9RB
UT WOS:000414593500057
PM 28518408
DA 2022-04-25
ER

PT J
AU Behl, T
   Sharma, A
   Sharma, L
   Sehgal, A
   Zengin, G
   Brata, R
   Fratila, O
   Bungau, S
AF Behl, Tapan
   Sharma, Aditi
   Sharma, Lalit
   Sehgal, Aayush
   Zengin, Gokhan
   Brata, Roxana
   Fratila, Ovidiu
   Bungau, Simona
TI Exploring the Multifaceted Therapeutic Potential of Withaferin A and Its
   Derivatives
SO BIOMEDICINES
LA English
DT Review
DE Withaferin A; anticancer; autophagy; chaperone
ID CELL-CYCLE ARREST; STEM-LIKE CELLS; BREAST-CANCER; WITHANIA-SOMNIFERA;
   MESENCHYMAL TRANSITION; COLON-CANCER; BETA-CATENIN; APOPTOSIS;
   WITHANOLIDES; AUTOPHAGY
AB Withaferin A (WA), a manifold studied, C28-steroidal lactone withanolide found in Withania somnifera. Given its unique beneficial effects, it has gathered attention in the era of modern science. Cancer, being considered a "hopeless case and the leading cause of death worldwide, and the available conventional therapies have many lacunae in the form of side effects. The poly pharmaceutical natural compound, WA treatment, displayed attenuation of various cancer hallmarks by altering oxidative stress, promoting apoptosis, and autophagy, inhibiting cell proliferation, reducing angiogenesis, and metastasis progression. The cellular proteins associated with antitumor pathways were also discussed. WA structural modifications attack multiple signal transduction pathways and enhance the therapeutic outcomes in various diseases. Moreover, it has shown validated pharmacological effects against multiple neurodegenerative diseases by inhibiting acetylcholesterinases and butyrylcholinesterases enzyme activity, antidiabetic activity by upregulating adiponectin and preventing the phosphorylation of peroxisome proliferator-activated receptors (PPAR gamma), cardioprotective activity by AMP-activated protein kinase (AMPK) activation and suppressing mitochondrial apoptosis. The current review is an extensive survey of various WA associated disease targets, its pharmacokinetics, synergistic combination, modifications, and biological activities.
C1 [Behl, Tapan; Sehgal, Aayush] Chitkara Univ, Chitkara Coll Pharm, Chandigarh 140401, Punjab, India.
   [Sharma, Aditi; Sharma, Lalit] Shoolini Univ, Sch Pharmaceut Sci, Solan 173229, Himachal Prades, India.
   [Zengin, Gokhan] Selcuk Univ Campus, Dept Biol, Fac Sci, TR-42250 Konya, Turkey.
   [Brata, Roxana; Fratila, Ovidiu] Univ Oradea, Fac Med & Pharm, Dept Med Disciplines, Oradea 410073, Romania.
   [Bungau, Simona] Univ Oradea, Fac Med & Pharm, Dept Pharm, Oradea 410028, Romania.
RP Behl, T (corresponding author), Chitkara Univ, Chitkara Coll Pharm, Chandigarh 140401, Punjab, India.; Bungau, S (corresponding author), Univ Oradea, Fac Med & Pharm, Dept Pharm, Oradea 410028, Romania.
EM tapanbehl31@gmail.com; aditisharma31790@gmail.com;
   lalitluckysharma88@gmail.com; aayushsehgal00@gmail.com;
   biyologzengin@gmail.com; roxana.gavrila@yahoo.com; ovidiufr@yahoo.co.uk;
   sbungau@uoradea.ro
RI Fratila, Ovidiu Cristian/AAD-3419-2022; Bungau, Simona
   Gabriela/C-1831-2015; Brata, Roxana Daniela/AAD-4661-2022
OI Bungau, Simona Gabriela/0000-0003-3236-1292; Sharma, Dr.
   Lalit/0000-0001-9855-704X
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NR 166
TC 15
Z9 15
U1 0
U2 3
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 2227-9059
J9 BIOMEDICINES
JI Biomedicines
PD DEC
PY 2020
VL 8
IS 12
AR 571
DI 10.3390/biomedicines8120571
PG 24
WC Biochemistry & Molecular Biology; Medicine, Research & Experimental;
   Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Research & Experimental Medicine;
   Pharmacology & Pharmacy
GA PJ5KE
UT WOS:000601805600001
PM 33291236
OA Green Published, gold
DA 2022-04-25
ER

PT J
AU Liu, J
   Xie, YL
   Wu, SS
   Lv, D
   Wei, XM
   Chen, F
   Wang, ZL
AF Liu, Jun
   Xie, Yaliu
   Wu, Sisi
   Lv, Dan
   Wei, Xuemei
   Chen, Fei
   Wang, Zhenling
TI Combined effects of EGFR and hedgehog signaling blockade on inhibition
   of head and neck squamous cell carcinoma
SO INTERNATIONAL JOURNAL OF CLINICAL AND EXPERIMENTAL PATHOLOGY
LA English
DT Article
DE Malignant sinonasal tumors; EGFR; Hedgehog; apoptosis; autophagy
ID GROWTH-FACTOR RECEPTOR; TARGETED THERAPY; TUMOR-GROWTH; COPY NUMBER;
   HUMAN COLON; CANCER; SURVIVAL; BEHAVIOR; AUTOPHAGY; PATHWAYS
AB Head and neck cancer, the sixth most common cancer, has poor prognosis and short survival. Antiepidermal growth factor receptor ( EGFR) therapies have been recently developed for the treatment of multiple cancer types. JK184, an inhibitor of Hedgehog pathway, prevents the growth of many tumor cell lines in several studies. Whether it enhances chemosensitivity to block EGFR expression by shEGFR plasmid and blocks the Hedgehog pathway by JK184 remains unclear in sinonasal tumors. The changes in cell apoptosis and proteins have been detected by flow cytometry and Western blotting, respectively. In vivo, the maxillary sinus model was established to detect the inhibition of tumor growth and tumor weight. A synergistic effect has been observed with JK184 combined with shEGFR, which is positively correlated with increased autophagy. The maxillary sinus model results demonstrated that the inhibitory rate of the combined therapy was higher than that of JK184 or shEGFR alone. Our findings suggest that JK184 in combination with shEGFR might have potential as a new therapeutic regimen against sinonasal tumors.
C1 [Liu, Jun; Lv, Dan; Chen, Fei] Sichuan Univ, West China Hosp, Dept Otorhinolaryngol Head & Neck Surg, Chengdu 610041, Sichuan, Peoples R China.
   [Xie, Yaliu] 7th Hosp Chengdu City, Dept Otorhinolaryngol, Chengdu, Sichuan, Peoples R China.
   [Wu, Sisi] Sichuan Univ, Core Facil, West China Hosp, Chengdu, Sichuan, Peoples R China.
   [Wu, Sisi; Wang, Zhenling] Sichuan Univ, Canc Ctr, West China Hosp, Chengdu 610041, Sichuan, Peoples R China.
   [Wu, Sisi; Wang, Zhenling] Collaborat Innovat Ctr Biotherapy, Chengdu 610041, Sichuan, Peoples R China.
   [Wei, Xuemei] Chengdu 363 Hosp, Dept Otorhinolaryngol Head & Neck Surg, Chengdu, Sichuan, Peoples R China.
RP Chen, F (corresponding author), Sichuan Univ, West China Hosp, Dept Otorhinolaryngol Head & Neck Surg, Chengdu 610041, Sichuan, Peoples R China.; Wang, ZL (corresponding author), Sichuan Univ, Canc Ctr, West China Hosp, Chengdu 610041, Sichuan, Peoples R China.; Wang, ZL (corresponding author), Collaborat Innovat Ctr Biotherapy, Chengdu 610041, Sichuan, Peoples R China.
EM 375572059@qq.com; wangzhenling@scu.edu
RI , 刀客/ABG-3664-2020
OI Liu, Jun/0000-0003-4800-7749
FU Science and Technology department of Sichuan Pro-vince [2012SZ0024];
   National Natural Science Foundation of ChinaNational Natural Science
   Foundation of China (NSFC) [81000056]
FX The authors thank Shuang Zhang, State Key Laboratory of Biotherapy and
   Cancer Center, West China Hospital, Sichuan University, and
   Collaborative Innovation Center for Biotherapy, Chengdu, China, for
   providing the ShEGFR plasmid. This work was supported by the Science and
   Technology department of Sichuan Pro-vince (No. 2012SZ0024) and by a
   grant from the National Natural Science Foundation of China (No.
   81000056).
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NR 45
TC 1
Z9 1
U1 1
U2 5
PU E-CENTURY PUBLISHING CORP
PI MADISON
PA 40 WHITE OAKS LN, MADISON, WI 53711 USA
SN 1936-2625
J9 INT J CLIN EXP PATHO
JI Int. J. Clin. Exp. Pathol.
PY 2017
VL 10
IS 9
BP 9816
EP 9828
PG 13
WC Oncology; Pathology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Pathology
GA FI7AU
UT WOS:000412148800086
PM 31966869
DA 2022-04-25
ER

PT J
AU Boland, CR
AF Boland, C. Richard
TI Chronic Inflammation, Colorectal Cancer and Gene Polymorphisms
SO DIGESTIVE DISEASES
LA English
DT Article; Proceedings Paper
CT 173rd Falk Symposium From Chronic Inflammation to Cancer
CY JUN 04-05, 2010
CL Brno, CZECH REPUBLIC
DE Chronic inflammation; Colorectal cancer; Gene polymorphisms
ID GENOME-WIDE ASSOCIATION; AGE-OF-ONSET; CROHNS-DISEASE; SUSCEPTIBILITY
   LOCI; ULCERATIVE-COLITIS; BOWEL-DISEASE; COLON-CANCER; RISK LOCI;
   HEREDITARY; VARIANTS
AB Chronic inflammation is commonly present in gastrointestinal mucosal sites at increased risk for cancer, such as in inflammatory bowel disease (IBD) or chronic gastritis caused by Helicobacter pylori infection. Why some patients have more mucosal inflammation than others, and why certain individuals with chronic inflammation develop cancer, are problems that have not been solved. Unlike the case for the syndromic forms of familial colorectal cancer (CRC), the risks for IBD and other forms of chronic inflammation have not been linked to highly penetrant single gene mutations. Single nucleotide polymorphisms (SNP) are variations in DNA sequence that can be linked to any phenotype (cancer, chronic inflammation, etc.) in genome-wide association studies (GWAS). CRC has been linked to several highly penetrant single gene loci, as well as multiple SNP. The propensity to develop IBD has not been linked to single gene mutations in most instances, but has been linked to SNP in the NOD2 locus (which appear to create hypomorphic alleles for this bacterial response gene), the IL23R locus, the autophagy gene ATG16L1 and a wide range of other loci including the Toll-like receptors, JAK2 and STAT3, and perhaps 70 more. At present, the problem in predicting risk for chronic inflammation is that there are many genetic polymorphisms with relatively modest individual effects. Our challenge is to understand how the SNPs that are linked to variations in the inflammatory response interact with one another (i.e. to understand the 'epistasis' involved), and to integrate this with the variety of individual environmental exposures. This represents an opportunity for informatics science to help personalize our approach to chronic inflammatory diseases of the gut and identify those at greatest risk for cancer. Copyright (C) 2010 S. Karger AG, Basel
C1 [Boland, C. Richard] Baylor Univ, Med Ctr, Div Gastroenterol, GI Canc Res Lab, Dallas, TX 75246 USA.
RP Boland, CR (corresponding author), Baylor Univ, Med Ctr, Div Gastroenterol, GI Canc Res Lab Hoblitzelle 250, 3500 Gaston Ave, Dallas, TX 75246 USA.
EM rickbo@baylorhealth.edu
FU Baylor Foundation; Baylor Research Institute; Sammons Cancer Center of
   Baylor University Medical Center; NIHUnited States Department of Health
   & Human ServicesNational Institutes of Health (NIH) - USA [R-01
   CA72851]; NATIONAL CANCER INSTITUTEUnited States Department of Health &
   Human ServicesNational Institutes of Health (NIH) - USANIH National
   Cancer Institute (NCI) [R01CA072851] Funding Source: NIH RePORTER
FX This work was supported by the Baylor Foundation, the Baylor Research
   Institute and the Sammons Cancer Center of Baylor University Medical
   Center. C.R.B. is the recipient of NIH Grant R-01 CA72851.
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NR 35
TC 13
Z9 15
U1 3
U2 9
PU KARGER
PI BASEL
PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND
SN 0257-2753
EI 1421-9875
J9 DIGEST DIS
JI Dig. Dis.
PY 2010
VL 28
IS 4-5
BP 590
EP 595
DI 10.1159/000320053
PG 6
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED); Conference Proceedings Citation Index - Science (CPCI-S)
SC Gastroenterology & Hepatology
GA 684LK
UT WOS:000284551200005
PM 21088407
OA Green Published, Bronze
DA 2022-04-25
ER

PT J
AU Park, SJ
   Jo, DS
   Jo, SY
   Shin, DW
   Shim, S
   Jo, YK
   Shin, JH
   Ha, YJ
   Jeong, SY
   Hwang, JJ
   Kim, YS
   Suh, YA
   Chang, JW
   Kim, JC
   Cho, DH
AF Park, So Jung
   Jo, Doo Sin
   Jo, Se-Young
   Shin, Dong Woon
   Shim, Sangmi
   Jo, Yoon Kyung
   Shin, Ji Hyun
   Ha, Ye Jin
   Jeong, Seong-Yun
   Hwang, Jung Jin
   Kim, Young Sam
   Suh, Young-Ah
   Chang, Jong Wook
   Kim, Jin Cheon
   Cho, Dong-Hyung
TI Inhibition of never in mitosis A (NIMA)-related kinase-4 reduces
   survivin expression and sensitizes cancer cells to TRAIL-induced cell
   death
SO ONCOTARGET
LA English
DT Article
DE NEK4; survivin; cancer; TRAIL
ID APOPTOSIS; QUERCETIN; RESISTANCE; AUTOPHAGY; NECROPTOSIS; PROGRESSION;
   COMPLEXITY; PATHWAYS; FAMILY
AB The tumor necrosis factor-related apoptosis inducing ligand (TRAIL) preferentially induces apoptosis in cancer cells. However, many tumors are resistant to TRAIL-induced apoptosis, and resistance mechanisms are not fully understood. To identify novel regulatory molecules of TRAIL resistance, we screened a siRNA library targeting the human kinome, and NEK4 (NIMA-related kinase-4) was identified. Knockdown of NEK4 sensitized TRAIL-resistant cancer cells and in vivo xenografts to cell death. In contrast, over expression of NEK4 suppressed TRAIL-induced cell death in TRAIL-sensitive cancer cells. In addition, loss of NEK4 resulted in decrease of the antiapoptotic protein survivin, but an increase in apoptotic cell death. Interestingly, NEK4 was highly upregulated in tumor tissues derived from patients with lung cancer and colon cancer. These results suggest that inhibition of NEK4 sensitizes cancer cells to TRAIL-induced apoptosis by regulation of survivin expression.
C1 [Park, So Jung; Jo, Doo Sin; Shin, Dong Woon; Jo, Yoon Kyung; Shin, Ji Hyun; Cho, Dong-Hyung] Kyung Hee Univ, Grad Sch East West Med Sci, Gyeonggi Do 17104, South Korea.
   [Jo, Se-Young; Ha, Ye Jin; Jeong, Seong-Yun; Hwang, Jung Jin; Suh, Young-Ah; Kim, Jin Cheon] Univ Ulsan, Coll Med, Asan Med Ctr, Asan Inst Med Res, Seoul 05505, South Korea.
   [Shim, Sangmi] Seoul Natl Univ, Coll Med, Dept Biomed Sci, Seoul 03080, South Korea.
   [Kim, Young Sam] Yonsei Univ, Coll Med, Dept Internal Med, Seoul 03722, South Korea.
   [Chang, Jong Wook] Samsung Med Ctr, Res Inst Future Med, Stem Cell & Regenerat Med Inst, Seoul 06351, South Korea.
   [Chang, Jong Wook] Sungkyunkwan Univ, SAIHST, Dept Hlth Sci & Technol, Seoul 06351, South Korea.
   [Kim, Jin Cheon] Univ Ulsan, Coll Med, Asan Med Ctr, Dept Surg, Seoul 05505, South Korea.
RP Chang, JW (corresponding author), Samsung Med Ctr, Res Inst Future Med, Stem Cell & Regenerat Med Inst, Seoul 06351, South Korea.; Chang, JW (corresponding author), Sungkyunkwan Univ, SAIHST, Dept Hlth Sci & Technol, Seoul 06351, South Korea.; Kim, JC (corresponding author), Univ Ulsan, Coll Med, Asan Med Ctr, Dept Surg, Seoul 05505, South Korea.
EM jongwook.chang@samsung.com; jckim@amc.seoul.kr
RI Hwang, Jung Jin/F-3424-2014
FU National Research Foundation [NRF-2013R1A2A1A03070986,
   2013R1A1A1058361]; Ministry of Science, ICT, and Future Planning,
   Republic of Korea; Korean Health Technology R&D Project, Ministry of
   Health and Welfare, Republic of Korea [HI14C3484]
FX This study was supported by grants from the National Research Foundation
   (NRF-2013R1A2A1A03070986 and 2013R1A1A1058361), Ministry of Science,
   ICT, and Future Planning, Republic of Korea, funded by the Korean Health
   Technology R&D Project, Ministry of Health and Welfare, Republic of
   Korea (HI14C3484).
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NR 40
TC 8
Z9 8
U1 0
U2 5
PU IMPACT JOURNALS LLC
PI ORCHARD PARK
PA 6666 E QUAKER ST, STE 1, ORCHARD PARK, NY 14127 USA
EI 1949-2553
J9 ONCOTARGET
JI Oncotarget
PD OCT 4
PY 2016
VL 7
IS 40
BP 65957
EP 65967
DI 10.18632/oncotarget.11781
PG 11
WC Oncology; Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Cell Biology
GA EB3QQ
UT WOS:000387281000110
PM 27602754
OA Green Published, Green Submitted, gold
DA 2022-04-25
ER

PT J
AU Cosin-Roger, J
   Simmen, S
   Melhem, H
   Atrott, K
   Frey-Wagner, I
   Hausmann, M
   de Valliere, C
   Spalinger, MR
   Spielmann, P
   Wenger, RH
   Zeitz, J
   Vavricka, SR
   Rogler, G
   Ruiz, PA
AF Cosin-Roger, Jesus
   Simmen, Simona
   Melhem, Hassan
   Atrott, Kirstin
   Frey-Wagner, Isabelle
   Hausmann, Martin
   de Valliere, Cheryl
   Spalinger, Marianne R.
   Spielmann, Patrick
   Wenger, Roland H.
   Zeitz, Jonas
   Vavricka, Stephan R.
   Rogler, Gerhard
   Ruiz, Pedro A.
TI Hypoxia ameliorates intestinal inflammation through NLRP3/mTOR
   downregulation and autophagy activation
SO NATURE COMMUNICATIONS
LA English
DT Article
ID GENOME-WIDE ASSOCIATION; HIGH-ALTITUDE JOURNEYS; INDUCIBLE FACTOR-I;
   BOWEL-DISEASE; CROHNS-DISEASE; HIF HYDROXYLASES; GENE-EXPRESSION; CANCER
   CELLS; KAPPA-B; COLITIS
AB Hypoxia regulates autophagy and nucleotide-binding oligomerization domain receptor, pyrin domain containing (NLRP)3, two innate immune mechanisms linked by mutual regulation and associated to IBD. Here we show that hypoxia ameliorates inflammation during the development of colitis by modulating autophagy and mammalian target of rapamycin (mTOR)/NLRP3 pathway. Hypoxia significantly reduces tumor necrosis factor a, interleukin (IL)-6 and NLRP3 expression, and increases the turnover of the autophagy protein p62 in colon biopsies of Crohn's disease patients, and in samples from dextran sulfate sodium-treated mice and Il-10(-/-) mice. In vitro, NF-.kappa signaling and NLRP3 expression are reduced through hypoxia-induced autophagy. We also identify NLRP3 as a novel binding partner of mTOR. Dimethyloxalylglycine-mediated hydroxylase inhibition ameliorates colitis in mice, downregulates NLRP3 and promotes autophagy. We suggest that hypoxia counteracts inflammation through the downregulation of the binding of mTOR and NLRP3 and activation of autophagy.
C1 [Cosin-Roger, Jesus; Simmen, Simona; Melhem, Hassan; Atrott, Kirstin; Frey-Wagner, Isabelle; Hausmann, Martin; de Valliere, Cheryl; Spalinger, Marianne R.; Zeitz, Jonas; Vavricka, Stephan R.; Rogler, Gerhard; Ruiz, Pedro A.] Univ Zurich, Univ Hosp Zurich, Dept Gastroenterol & Hepatol, Ramistr 100, CH-8091 Zurich, Switzerland.
   [Spielmann, Patrick; Wenger, Roland H.] Univ Zurich, Inst Physiol, Winterthurerstr 190, CH-8057 Zurich, Switzerland.
   [Spielmann, Patrick; Wenger, Roland H.; Rogler, Gerhard] Univ Zurich, Zurich Ctr Integrat Human Physiol ZIHP, CH-8057 Zurich, Switzerland.
RP Ruiz, PA (corresponding author), Univ Zurich, Univ Hosp Zurich, Dept Gastroenterol & Hepatol, Ramistr 100, CH-8091 Zurich, Switzerland.
EM PedroAntonio.Ruiz-Castro@usz.ch
RI Wenger, Roland/B-7953-2009
OI Wenger, Roland/0000-0001-7592-4839; Hausmann,
   Martin/0000-0002-0696-0251; Cosin roger, Jesus/0000-0002-2468-4908;
   Spielmann, Patrick/0000-0001-7056-0351; Ruiz-Castro, Pedro
   Antonio/0000-0001-7528-1474
FU Swiss Philanthropy Foundation; Swiss National Science FoundationSwiss
   National Science Foundation (SNSF)European Commission [324730_138291,
   314730_153380]; Swiss IBD Cohort [314730_153380]; European Crohn's and
   Colitis Organisation (ECCO) Fellowship
FX We thank Mirjam Blattmann and Sylvie Scharl for their organizing and
   collecting the human colon biopsies. Mehdi Madanchi is gratefully
   acknowledged for his help in collecting the human subject data. We
   extend our special appreciation to Silvia Lang for her technical
   support, and the Zurich Integrative Rodent Physiology (ZIRP) core
   facility of the University of Zurich for their support in the animal
   experiments. This research was supported by a grant from the Swiss
   Philanthropy Foundation to GR and research grants from the Swiss
   National Science Foundation to GR (Grant No. 324730_138291 and
   314730_153380), and the Swiss IBD Cohort (Grant No. 314730_153380).
   J.C.-R. was supported by the European Crohn's and Colitis Organisation
   (ECCO) Fellowship.
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NR 69
TC 119
Z9 134
U1 7
U2 36
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 2041-1723
J9 NAT COMMUN
JI Nat. Commun.
PD JUL 24
PY 2017
VL 8
AR 98
DI 10.1038/s41467-017-00213-3
PG 13
WC Multidisciplinary Sciences
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Science & Technology - Other Topics
GA FB5AN
UT WOS:000406153800001
PM 28740109
OA Green Accepted, Green Published, gold
DA 2022-04-25
ER

PT J
AU Patel, S
   Hurez, V
   Nawrocki, ST
   Goros, M
   Michalek, J
   Sarantopoulos, J
   Curiel, T
   Mahalingam, D
AF Patel, Sukeshi
   Hurez, Vincent
   Nawrocki, Steffan T.
   Goros, Martin
   Michalek, Joel
   Sarantopoulos, John
   Curiel, Tyler
   Mahalingam, Devalingam
TI Vorinostat and hydroxychloroquine improve immunity and inhibit autophagy
   in metastatic colorectal cancer
SO ONCOTARGET
LA English
DT Article
DE vorinostat; hydroxychloroquine; colorectal cancer; autophagy; immunity
ID REGULATORY T-CELLS; IN-VIVO; MICROSATELLITE INSTABILITY; TARGETING
   AUTOPHAGY; SOLID TUMORS; IMMUNOTHERAPY; COMBINATION; EXPRESSION;
   CARCINOMA; APOPTOSIS
AB Hydroxychloroquine (HCQ) enhances the anti-cancer activity of the histone deacetylase inhibitor, vorinostat (VOR), in pre-clinical models and early phase clinical studies of metastatic colorectal cancer (mCRC). Mechanisms could include autophagy inhibition, accumulation of ubiquitinated proteins, and subsequent tumor cell apoptosis. There is growing evidence that autophagy inhibition could lead to improved anticancer immunity. To date, effects of autophagy on immunity have not been reported in cancer patients. To address this, we expanded an ongoing clinical study to include patients with advanced, refractory mCRC to evaluate further the clinical efficacy and immune effects of VOR plus HCQ. Refractory mCRC patients received VOR 400 milligrams orally with HCQ 600 milligrams orally daily, in a 3-week cycle. The primary endpoint was median progression-free survival (mPFS). Secondary endpoints include median overall survival (mOS), adverse events (AE), pharmacodynamic of inhibition of autophagy in primary tumors, immune cell analyses, and cytokine levels. Twenty patients were enrolled (19 evaluable for survival) with a mPFS of 2.8 months and mOS of 6.7 months. Treatment-related grade 3-4 AEs occurred in 8 patients (40%), with fatigue, nausea/vomiting, and anemia being the most common. Treatment significantly reduced CD4(+)CD25(hi)Foxp3(+) regulatory and PD-1(+) (exhausted) CD4(+) and CD8(+) T cells and decreased CD45RO-CD62L(+) (naive) T cells, consistent with improved anti-tumor immunity. On-study tumor biopsies showed increases in lysosomal protease cathepsin D and p62 accumulation, consistent with autophagy inhibition. Taken together, VOR plus HCQ is active, safe and well tolerated in refractory CRC patients, resulting in potentially improved anti-tumor immunity and inhibition of autophagy.
C1 [Patel, Sukeshi; Hurez, Vincent; Nawrocki, Steffan T.; Goros, Martin; Michalek, Joel; Sarantopoulos, John; Curiel, Tyler; Mahalingam, Devalingam] Univ Texas Hlth Sci Ctr San Antonio, Cancer Therapy & Res Ctr, San Antonio, TX 78229 USA.
RP Mahalingam, D (corresponding author), Univ Texas Hlth Sci Ctr San Antonio, Cancer Therapy & Res Ctr, San Antonio, TX 78229 USA.
EM mahalingam@uthscsa.edu
RI Hurez, Vincent/AAF-6765-2019
OI Patel, Sukeshi/0000-0002-1176-0713; Hurez, Vincent/0000-0003-0271-4157
FU Cancer Therapy and Research Center (CTRC) Pilot Funding; Holly Beach
   Public Library Association; William and Ella Owens Foundation; NIHUnited
   States Department of Health & Human ServicesNational Institutes of
   Health (NIH) - USA [P30CA054174]; NATIONAL CANCER INSTITUTEUnited States
   Department of Health & Human ServicesNational Institutes of Health (NIH)
   - USANIH National Cancer Institute (NCI) [P30CA054174] Funding Source:
   NIH RePORTER
FX Cancer Therapy and Research Center (CTRC) Pilot Funding (Devalingam
   Mahalingam); The Holly Beach Public Library Association (Tyler Curiel);
   The William and Ella Owens Foundation (Tyler Curiel); NIH grant
   P30CA054174 (All authors).
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NR 38
TC 40
Z9 41
U1 2
U2 10
PU IMPACT JOURNALS LLC
PI ORCHARD PARK
PA 6666 E QUAKER ST, STE 1, ORCHARD PARK, NY 14127 USA
EI 1949-2553
J9 ONCOTARGET
JI Oncotarget
PD SEP 13
PY 2016
VL 7
IS 37
BP 59087
EP 59097
DI 10.18632/oncotarget.10824
PG 11
WC Oncology; Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Cell Biology
GA EB1YW
UT WOS:000387153900028
PM 27463016
OA Green Published, Green Submitted, gold
DA 2022-04-25
ER

PT J
AU Lv, Q
   Wang, W
   Xue, JF
   Hua, F
   Mu, R
   Lin, H
   Yan, J
   Lv, XX
   Chen, XG
   Hu, ZW
AF Lv, Qi
   Wang, Wei
   Xue, Jianfei
   Hua, Fang
   Mu, Rong
   Lin, Heng
   Yan, Jun
   Lv, Xiaoxi
   Chen, Xiaoguang
   Hu, Zhuo-Wei
TI DEDD Interacts with PI3KC3 to Activate Autophagy and Attenuate
   Epithelial-Mesenchymal Transition in Human Breast Cancer
SO CANCER RESEARCH
LA English
DT Article
ID DOMAIN-CONTAINING PROTEIN; TUMOR-METASTASIS; STEM-CELLS; DEATH; GROWTH;
   SNAIL; TWIST; PROGRESSION; COMPLEX; FAMILY
AB Epithelial-to-mesenchymal transition (EMT), a crucial developmental program, contributes to cancer invasion and metastasis. In this study, we show that death-effector domain-containing DNA-binding protein (DEDD) attenuates EMT and acts as an endogenous suppressor of tumor growth and metastasis. We found that expression levels of DEDD were conversely correlated with poor prognosis in patients with breast and colon cancer. Both in vitro and in vivo, overexpression of DEDD attenuated the invasive phenotype of highly metastatic cells, whereas silencing of DEDD promoted the invasion of nonmetastatic cells. Via direct interaction with the class III PI-3-kinase (PI3KC3)/Beclin1, DEDD activated autophagy and induced the degradation of Snail and Twist, two master regulators of EMT. The DEDD-PI3KC3 interaction led to stabilization of PI3KC3, which further contributed to autophagy and the degradation of Snail and Twist. Together, our findings highlight a novel mechanism in which the intracellular signaling protein DEDD functions as an endogenous tumor suppressor. DEDD expression therefore may represent a prognostic marker and potential therapeutic target for the prevention and treatment of cancer metastasis. Cancer Res; 72(13); 3238-50. (c) 2012 AACR.
C1 [Lv, Qi; Wang, Wei; Xue, Jianfei; Hua, Fang; Mu, Rong; Lin, Heng; Yan, Jun; Lv, Xiaoxi; Chen, Xiaoguang; Hu, Zhuo-Wei] Chinese Acad Med Sci, Inst Mat Med, State Key Lab Bioact Subst & Funct Nat Med, Mol Immunol Grp, Beijing 100050, Peoples R China.
   [Lv, Qi; Wang, Wei; Xue, Jianfei; Hua, Fang; Mu, Rong; Lin, Heng; Yan, Jun; Lv, Xiaoxi; Chen, Xiaoguang; Hu, Zhuo-Wei] Chinese Acad Med Sci, Inst Mat Med, State Key Lab Bioact Subst & Funct Nat Med, Canc Pharmacol Grp, Beijing 100050, Peoples R China.
   [Lv, Qi; Wang, Wei; Xue, Jianfei; Hua, Fang; Mu, Rong; Lin, Heng; Yan, Jun; Lv, Xiaoxi; Chen, Xiaoguang; Hu, Zhuo-Wei] Peking Union Med Coll, Beijing 100050, Peoples R China.
RP Hu, ZW (corresponding author), Chinese Acad Med Sci, Inst Mat Med, State Key Lab Bioact Subst & Funct Nat Med, Mol Immunol Grp, Beijing 100050, Peoples R China.
EM huzhuowei@imm.ac.cn
OI Lv, Qi/0000-0001-9076-7042
FU National Major Basic Research Program of China (973)National Basic
   Research Program of China [2006CB503808]; National Natural Science
   Foundation of ChinaNational Natural Science Foundation of China (NSFC)
   [81030056, 30973557, 81101595]; Creation of Major New Drugs
   [2009ZX09301-003-13, 2009ZX09301-003-9-1]
FX This work was supported by grants from National Major Basic Research
   Program of China (973: #2006CB503808), National Natural Science
   Foundation of China (81030056, 30973557, 81101595), and Creation of
   Major New Drugs (2009ZX09301-003-13, 2009ZX09301-003-9-1).
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NR 48
TC 120
Z9 125
U1 2
U2 20
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD JUL 1
PY 2012
VL 72
IS 13
BP 3238
EP 3250
DI 10.1158/0008-5472.CAN-11-3832
PG 13
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA 986OB
UT WOS:000307350700014
PM 22719072
OA Bronze
DA 2022-04-25
ER

PT J
AU Won, SJ
   Yen, CH
   Lin, TY
   Jiang-Shieh, YF
   Lin, CN
   Chen, JT
   Su, CL
AF Won, Shen-Jeu
   Yen, Cheng-Hsin
   Lin, Ting-Yu
   Jiang-Shieh, Ya-Fen
   Lin, Chun-Nan
   Chen, Jyun-Ti
   Su, Chun-Li
TI Autophagy mediates cytotoxicity of human colorectal cancer cells treated
   with garcinielliptone FC
SO JOURNAL OF CELLULAR PHYSIOLOGY
LA English
DT Article
DE apoptosis; autophagy; garcinielliptone FC; human colorectal cancer
ID NF-KAPPA-B; GARCINIA-SUBELLIPTICA; APOPTOSIS; THERAPY; DEATH;
   INFLAMMATION; EXPRESSION; SURVIVAL; PATHWAY; SYSTEM
AB The tautomeric pair of garcinielliptone FC (GFC) is a novel tautomeric pair of polyprenyl benzophenonoid isolated from the pericarps of Garcinia subelliptica Merr. (G. subelliptica, Clusiaceae), a tree with abundant sources of polyphenols. Our previous report demonstrated that GFC induced apoptosis on various types of human cancer cell lines including chemoresistant human colorectal cancer HT-29 cells. In the present study, we observed that many autophagy-related genes in GFC-treated HT-29 cells were up- and down-regulated using a cDNA microarray containing oncogenes and kinase genes. GFC-induced autophagy of HT-29 cells was confirmed by observing the formation of acidic vesicular organelles, LC3 puncta, and double-membrane autophagic vesicles using flow cytometry, confocal microscopy, and transmission electron microscopy, respectively. Inhibition of AKT/mTOR/P70S6K signaling as well as formation of Atg5-Atg12 and PI3K/Beclin-1 complexes were observed using Western blot. Administration of autophagy inhibitor (3-methyladenine and shRNA Atg5) and apoptosis inhibitor Z-VAD showed that the GFC-induced autophagy was cytotoxic form and GFC-induced apoptosis enhanced GFC-induced autophagy. Our data suggest the involvement of autophagy and apoptosis in GFC-induced anticancer mechanisms of human colorectal cancer.
C1 [Won, Shen-Jeu; Lin, Ting-Yu] Natl Cheng Kung Univ, Dept Microbiol & Immunol, Coll Med, Tainan, Taiwan.
   [Yen, Cheng-Hsin; Chen, Jyun-Ti; Su, Chun-Li] Natl Taiwan Normal Univ, Dept Human Dev & Family Studies, 162,Sec 1,He Ping East Rd, Taipei 106, Taiwan.
   [Jiang-Shieh, Ya-Fen] Natl Cheng Kung Univ, Dept Anat, Coll Med, Tainan, Taiwan.
   [Lin, Chun-Nan] Kaohsiung Med Univ, Sch Pharm, Kaohsiung, Taiwan.
RP Su, CL (corresponding author), Natl Taiwan Normal Univ, Dept Human Dev & Family Studies, 162,Sec 1,He Ping East Rd, Taipei 106, Taiwan.
EM chunlisu@ntnu.edu.tw
FU National Science CouncilMinistry of Science and Technology, Taiwan
   [98-2313-B-003-002-MY3, 101-2313-B-003-002MY3]; National Taiwan Normal
   University, Taiwan [103-07-C105T0700]; Ministry of Science and
   Technology, Taiwan MOST [104-2320-B-003-007]
FX National Science Council, Grant numbers: 98-2313-B-003-002-MY3,
   101-2313-B-003-002MY3; National Taiwan Normal University, Taiwan, Grant
   number: 103-07-C105T0700; Ministry of Science and Technology, Taiwan
   MOST, Grant number: 104-2320-B-003-007
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NR 29
TC 3
Z9 3
U1 0
U2 54
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0021-9541
EI 1097-4652
J9 J CELL PHYSIOL
JI J. Cell. Physiol.
PD JAN
PY 2018
VL 233
IS 1
BP 497
EP 505
DI 10.1002/jcp.25910
PG 9
WC Cell Biology; Physiology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Cell Biology; Physiology
GA FI3BF
UT WOS:000411829600043
PM 28294332
DA 2022-04-25
ER

PT J
AU Liu, J
   Hu, XJ
   Jin, B
   Qu, XJ
   Hou, KZ
   Liu, YP
AF Liu, Jing
   Hu, Xue-Jun
   Jin, Bo
   Qu, Xiu-Juan
   Hou, Ke-Zuo
   Liu, Yun-Peng
TI ss-Elemene induces apoptosis as well as protective autophagy in human
   non-small-cell lung cancer A549 cells
SO JOURNAL OF PHARMACY AND PHARMACOLOGY
LA English
DT Article
DE apoptosis; autophagy; ss-elemene; lung cancer; mTOR
ID BETA-ELEMENE; GLIOBLASTOMA CELLS; MTOR PATHWAY; COLON-CANCER; ARREST;
   CYCLE; INHIBITION; THERAPY
AB Objectives beta-Elemene, a novel traditional Chinese medicine, has been shown to be effective against a wide range of tumours. In this study, the antitumour effect of beta-elemene on human non-small-cell lung cancer (NSCLC) A549 cells and the mechanism involved have been investigated.
   Methods Cell viability and apoptosis were measured by the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay and flow cytometry, respectively. Protein expression was assayed by Western blotting. Autophagy was evaluated under fluorescence microscopy and transmission electron microscopy.
   Key findings beta-Elemene inhibited the viability of A549 cells in a dose-dependent manner. This suppression of cell viability was due to the induction of apoptosis. Further study showed that beta-elemene inhibited the activity of the PI3K/Akt/mTOR/p70S6K1 signalling pathway, and at the same time it triggered a robust autophagy. The autophagy was characterized by the accumulation of punctate LC3 dots in the cytoplasm, morphological changes, and the increased levels of LC3-II as well as Atg5-Atg12 conjugated proteins. Inhibition of autophagy with chlorochine significantly enhanced the antitumour effect of beta-elemene.
   Conclusions Our data indicated that beta-elemene inhibited the activity of the PI3K/Akt/mTOR/p70S6K1 signalling pathway in human NSCLC A549 cells, which resulted in apoptosis as well as protective autophagy. A combination of beta-elemene with autophagy inhibitor might be an effective therapeutic option for advanced NSCLC.
C1 [Liu, Jing; Jin, Bo; Qu, Xiu-Juan; Hou, Ke-Zuo; Liu, Yun-Peng] China Med Univ, Hosp 1, Dept Med Oncol, Shenyang 110001, Peoples R China.
   [Hu, Xue-Jun] China Med Univ, Hosp 1, Dept Resp Med, Shenyang 110001, Peoples R China.
RP Liu, YP (corresponding author), China Med Univ, Hosp 1, Dept Med Oncol, Shenyang 110001, Peoples R China.
EM cmuliuyunpeng@yahoo.cn
FU First Hospital of China Medical University [fsfh1002]; Education
   Department of Liaoning Province [2008S246, 2008RC55, 20060945, 20060992]
FX This work was supported by the Fund for Scientific Research of The First
   Hospital of China Medical University, fsfh1002; Fund of The Education
   Department of Liaoning Province (NO. 2008S246, NO. 2008RC55, NO.
   20060945, NO. 20060992).
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NR 30
TC 45
Z9 53
U1 1
U2 14
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0022-3573
EI 2042-7158
J9 J PHARM PHARMACOL
JI J. Pharm. Pharmacol.
PD JAN
PY 2012
VL 64
IS 1
BP 146
EP 153
DI 10.1111/j.2042-7158.2011.01371.x
PG 8
WC Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA 861ID
UT WOS:000298011700017
PM 22150682
DA 2022-04-25
ER

PT J
AU Yoshie, T
   Nishiumi, S
   Izumi, Y
   Sakai, A
   Inoue, J
   Azuma, T
   Yoshida, M
AF Yoshie, Tomoo
   Nishiumi, Shin
   Izumi, Yoshihiro
   Sakai, Aya
   Inoue, Jun
   Azuma, Takeshi
   Yoshida, Masaru
TI Regulation of the metabolite profile by an APC gene mutation in
   colorectal cancer
SO CANCER SCIENCE
LA English
DT Article
ID ADENOMATOUS POLYPOSIS; COLON; AUTOPHAGY; SERUM; METABOLOMICS;
   EXPRESSION; SARCOSINE; SURVIVAL; IDENTIFY; PROTEIN
AB Mutation of the APC gene occurs during the early stages of colorectal cancer development. To obtain new insights into the mechanisms underlying the aberrant activation of the Wnt pathway that accompanies APC mutation, we carried out a gas chromatographymass spectrometry-based semiquantitative metabolome analysis. In vitro experiments comparing SW480 cells expressing normal APC and truncated APC indicated that the levels of metabolites involved in the latter stages of the intracellular tricarboxylic acid cycle, including succinic acid, fumaric acid, and malic acid, were significantly higher in the SW480 cells expressing the truncated APC. In an in vivo study, we found that the levels of most amino acids were higher in the non-polyp tissues of APCmin/+ mice than in the normal tissues of the control mice and the polyp tissues of APCmin/+ mice. Ribitol, the levels of which were decreased in the polyp lesions of the APCmin/+ mice and the SW480 cells expressing the truncated APC, reduced the growth of SW480 cells with the APC mutation, but did not affect the growth of SW480 transfectants expressing full-length APC. The level of sarcosine was found to be significantly higher in the polyp tissues of APCmin/+ mice than in their non-polyp tissues and the normal tissues of the control mice, and the treatment of SW480 cells with 50 mu M sarcosine resulted in a significant increase in their growth rate. These findings suggest that APC mutation causes changes in energetic metabolite pathways and that these alterations might be involved in the development of colorectal cancer. (Cancer Sci 2012; 103: 10101021)
C1 [Yoshie, Tomoo; Nishiumi, Shin; Izumi, Yoshihiro; Sakai, Aya; Inoue, Jun; Azuma, Takeshi; Yoshida, Masaru] Kobe Univ, Grad Sch Med, Dept Internal Med, Div Gastroenterol, Kobe, Hyogo 657, Japan.
   [Yoshida, Masaru] Kobe Univ, Grad Sch Med, Integrated Ctr Mass Spectrometry, Kobe, Hyogo 657, Japan.
   [Yoshida, Masaru] Kobe Univ, Grad Sch Med, Div Metabol Res, Kobe, Hyogo 657, Japan.
RP Yoshida, M (corresponding author), Kobe Univ, Grad Sch Med, Dept Internal Med, Div Gastroenterol, Kobe, Hyogo 657, Japan.
EM myoshida@med.kobe-u.ac.jp
RI Nishiumi, Shin/ABD-5775-2020
OI Nishiumi, Shin/0000-0003-2126-3013
FU Global COE (Global Center of Excellence for Education and Research on
   Signal Transduction Medicine in the Coming Generation) from the Ministry
   of Education, Culture, Sports, Science, and Technology of JapanMinistry
   of Education, Culture, Sports, Science and Technology, Japan (MEXT);
   Ministry of Agriculture, Forestry and Fisheries of JapanMinistry of
   Agriculture Forestry & Fisheries - Japan
FX This study was supported by grants from the Research Fellows of the
   Global COE Program (Global Center of Excellence for Education and
   Research on Signal Transduction Medicine in the Coming Generation) from
   the Ministry of Education, Culture, Sports, Science, and Technology of
   Japan (to T.Y., M.Y., and T. A.), and from the Ministry of Agriculture,
   Forestry and Fisheries of Japan (Development of fundamental technology
   for analysis and evaluation of functional agricultural products and
   functional foods) (to M.Y.).
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NR 34
TC 27
Z9 27
U1 1
U2 16
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1347-9032
EI 1349-7006
J9 CANCER SCI
JI Cancer Sci.
PD JUN
PY 2012
VL 103
IS 6
BP 1010
EP 1021
DI 10.1111/j.1349-7006.2012.02262.x
PG 12
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA 951ZA
UT WOS:000304758200006
PM 22380946
OA Bronze, Green Published
DA 2022-04-25
ER

PT J
AU Hu, YF
   Li, X
   Lin, L
   Liang, ST
   Yan, J
AF Hu, Yefang
   Li, Xi
   Lin, Ling
   Liang, Siting
   Yan, Jian
TI Puerarin inhibits non-small cell lung cancer cell growth via the
   induction of apoptosis
SO ONCOLOGY REPORTS
LA English
DT Article
DE puerarin; non-small cell lung cancer; cell growth; apoptosis; autophagy
ID COLON-CANCER; PRESSURE-OVERLOAD; NATURAL COMPOUNDS; IN-VIVO; ACTIVATION;
   ISOFLAVONES; PATHWAYS; HOMOLOG; BAX
AB Puerarin, an isoflavone isolated from Kudzu roots, has been demonstrated to have beneficial effect on cardiovascular and cerebral vascular diseases. Recently research has revealed that puerarin exerts an anticancer role in many different types of cancer. The aim of the present study was to investigate the antitumor effects of puerarin on non-small cell lung cancer (NSCLC). Treatment of puerarin significantly inhibited the growth of NSCLC cell lines as determined by CCK-8 kit in vitro. Flow cytometry results indicated that puerarin treatments promoted NSCLC cell apoptosis. This result was further confirmed by western blot analysis of expression levels of proteins involved in the mitochondrial-mediated apoptosis pathway. Moreover, puerarin slightly induced cell autophagy through the PI3K/Akt and MAPK/Erk1/2 signaling pathways. In addition, a tumor xenograft model was established using nude mice, and the inhibitory effects on tumor growth by puerarin treatment were also detected. Taken together, these findings demonstrated that puerarin has anticancer activities and puerarin is a potential therapeutic agent for lung cancer.
C1 [Hu, Yefang; Lin, Ling; Liang, Siting; Yan, Jian] Guilin Tradit Chinese Med Hosp, Pharm Dept, Guilin 541002, Guangxi, Peoples R China.
   [Li, Xi] Guangxi Normal Univ, Key Lab Chem & Mol Engn Med Resources, 2 Lingui Rd, Guilin 541004, Guangxi, Peoples R China.
RP Li, X (corresponding author), Guangxi Normal Univ, Key Lab Chem & Mol Engn Med Resources, 2 Lingui Rd, Guilin 541004, Guangxi, Peoples R China.
EM xi_li_china@hotmail.com
FU Key Laboratory for Chemistry and Molecular Engineering of Medicinal
   Resources (Guangxi Normal University) [CMEMR2016-B01]
FX This study was supported by the Key Laboratory for Chemistry and
   Molecular Engineering of Medicinal Resources (Guangxi Normal University)
   (CMEMR2016-B01).
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NR 34
TC 16
Z9 19
U1 5
U2 33
PU SPANDIDOS PUBL LTD
PI ATHENS
PA POB 18179, ATHENS, 116 10, GREECE
SN 1021-335X
EI 1791-2431
J9 ONCOL REP
JI Oncol. Rep.
PD APR
PY 2018
VL 39
IS 4
BP 1731
EP 1738
DI 10.3892/or.2018.6234
PG 8
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA GA2ZB
UT WOS:000428195300020
PM 29393465
OA Bronze
DA 2022-04-25
ER

PT J
AU Ropolo, A
   Catrinacio, C
   Renna, FJ
   Boggio, V
   Orquera, T
   Gonzalez, CD
   Vaccaro, MI
AF Ropolo, Alejandro
   Catrinacio, Cintia
   Renna, Felipe Javier
   Boggio, Veronica
   Orquera, Tamara
   Gonzalez, Claudio D.
   Vaccaro, Maria, I
TI A Novel E2F1-EP300-VMP1 Pathway Mediates Gemcitabine-Induced Autophagy
   in Pancreatic Cancer Cells Carrying Oncogenic KRAS
SO FRONTIERS IN ENDOCRINOLOGY
LA English
DT Article
DE pancreatic cancer; gemcitabine; autophagy; VMP1
ID VMP1 EXPRESSION; RESISTANCE; E2F1; ADENOCARCINOMA; APOPTOSIS;
   TRANSCRIPTION; CHEMOTHERAPY; PROGRESSION; MACHINERY; OVERCOME
AB Autophagy is an evolutionarily preserved degradation process of cytoplasmic cellular constituents, which participates in cell response to disease. We previously characterized VMP1 (Vacuole Membrane Protein 1) as an essential autophagy related protein that mediates autophagy in pancreatic diseases. We also demonstrated that VMP1-mediated autophagy is induced by HIF-1A (hypoxia inducible factor 1 subunit alpha) in colon-cancer tumor cell lines, conferring resistance to photodynamic treatment. Here we identify a new molecular pathway, mediated by VMP1, by which gemcitabine is able to trigger autophagy in human pancreatic tumor cell lines. We demonstrated that gemcitabine requires the VMP1 expression to induce autophagy in the highly resistant pancreatic cancer cells PANC-1 and MIAPaCa-2 that carry activatedKRAS. E2F1 is a transcription factor that is regulated by the retinoblastoma pathway. We found that E2F1 is an effector of gemcitabine-induced autophagy and regulates the expression and promoter activity of VMP1. Chromatin immunoprecipitation assays demonstrated that E2F1 binds to theVMP1promoter in PANC-1 cells. We have also identified the histone acetyltransferase EP300 as a modulator of VMP1 promoter activity. Our data showed that the E2F1-EP300 activator/co-activator complex is part of the regulatory pathway controlling the expression and promoter activity of VMP1 triggered by gemcitabine in PANC-1 cells. Finally, we found that neither VMP1 nor E2F1 are induced by gemcitabine treatment in BxPC-3 cells, which do not carry oncogenic KRAS and are sensitive to chemotherapy. In conclusion, we have identified the E2F1-EP300-VMP1 pathway that mediates gemcitabine-induced autophagy in pancreatic cancer cells. These results strongly support that VMP1-mediated autophagy may integrate the complex network of events involved in pancreatic ductal adenocarcinoma chemo-resistance. Our experimental findings point at E2F1 and VMP1 as novel potential therapeutic targets in precise treatment strategies for pancreatic cancer.
C1 [Ropolo, Alejandro; Catrinacio, Cintia; Renna, Felipe Javier; Boggio, Veronica; Orquera, Tamara; Gonzalez, Claudio D.; Vaccaro, Maria, I] Univ Buenos Aires, Sch Pharm & Biochem, Inst Biochem & Mol Med, Dept Pathophysiol,UBA CONICET, Buenos Aires, DF, Argentina.
   [Gonzalez, Claudio D.] CEMIC Univ Inst, Buenos Aires, DF, Argentina.
RP Ropolo, A (corresponding author), Univ Buenos Aires, Sch Pharm & Biochem, Inst Biochem & Mol Med, Dept Pathophysiol,UBA CONICET, Buenos Aires, DF, Argentina.
EM aropolo@ffyb.uba.ar
OI Gonzalez, Claudio/0000-0002-3772-8850
FU Consejo Nacional de Investigaciones Cientificas y Tecnicas
   (CONICET)Consejo Nacional de Investigaciones Cientificas y Tecnicas
   (CONICET) [PIP 2015-2017 GI-11220150100160CO]; Agencia Nacional de
   Promocion Cientifica y Tecnologica (ANPCyT)ANPCyT [PICT20132048,
   PICT2016-1032]; Universidad de Buenos AiresUniversity of Buenos Aires
   [UBACYT 2014-2017 GC-20020130100764BA, UBACyT
   2018-2020-20020170100082BA]
FX This work was supported by grants from: Consejo Nacional de
   Investigaciones Cientificas y Tecnicas (CONICET) [PIP 2015-2017
   GI-11220150100160CO]; Agencia Nacional de Promocion Cientifica y
   Tecnologica (ANPCyT) [PICT20132048; PICT2016-1032] and Universidad de
   Buenos Aires [UBACYT 2014-2017 GC-20020130100764BA; UBACyT
   2018-2020-20020170100082BA].
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NR 68
TC 4
Z9 4
U1 1
U2 5
PU FRONTIERS MEDIA SA
PI LAUSANNE
PA AVENUE DU TRIBUNAL FEDERAL 34, LAUSANNE, CH-1015, SWITZERLAND
SN 1664-2392
J9 FRONT ENDOCRINOL
JI Front. Endocrinol.
PD JUN 23
PY 2020
VL 11
AR 411
DI 10.3389/fendo.2020.00411
PG 14
WC Endocrinology & Metabolism
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Endocrinology & Metabolism
GA MK3DM
UT WOS:000548664100001
PM 32655498
OA Green Published, gold
DA 2022-04-25
ER

PT J
AU Chu, CA
   Lee, CT
   Lee, JC
   Wang, YW
   Huang, CT
   Lan, SH
   Lin, PC
   Lin, BW
   Tian, YF
   Liu, HS
   Chow, NH
AF Chu, Chien-An
   Lee, Chung-Ta
   Lee, Jenq-Chang
   Wang, Yi-Wen
   Huang, Ching-Tang
   Lan, Sheng-Hui
   Lin, Peng-Chan
   Lin, Bo-Wen
   Tian, Yu-Feng
   Liu, Hsiao-Sheng
   Chow, Nan-Haw
TI MiR-338-5p promotes metastasis of colorectal cancer by inhibition of
   phosphatidylinositol 3-kinase, catalytic subunit type 3-mediated
   autophagy pathway
SO EBIOMEDICINE
LA English
DT Article
DE miR-338-5p; PIK3C3; Autophagy and colorectal cancer
ID SUPPRESSES TUMORIGENESIS; SIGNALING PATHWAY; CELL-MIGRATION; EXPRESSION;
   MICRORNA; IDENTIFICATION; PROLIFERATION; PROGNOSIS; CARCINOMA; INVASION
AB Background: In our preliminary screening, expression of miR-338-5p was found to be higher in primary colorectal cancer (CRC) with metastasis. The autophagy related gene- phosphatidylinositol 3-kinase, catalytic subunit type 3 (PIK3C3) appeared to be targeted by miR-338-5p. Here, we provide solid evidence in support of PIK3C3 involved in miR-338-5p related metastasis of CRC in vitro and in vivo.
   Methods: The potential clinical relevance of miR-338-5p and its target gene was analysed on benign colorectal polyps and primary CRCs by QPCR Mouse spleen xenograft experiment was performed to examine the importance of miR-338-5p for metastasis.
   Findings: PIK3C3 was one of target genes of miR-338-5p. In primary CRCs, expression of miR-338-5p is positively related to tumour staging, distant metastasis and poor patient survival. Patients with higher ratios of miR-338-5p/PIK3C3 also had significantly poor overall survival, supporting their significance in the progression of CRC. Over-expression of miR-338-5p promotes CRC metastasis to the liver and lung in vivo, in which PIK3C3 was down-regulated in the metastatic tumours. In contrast, overexpression of PIK3C3 in miR-338-5p stable cells inhibited the growth of metastatic tumours. Both migration and invasion of CRC in vitro induced by miR-338-5p are mediated by suppression of PIK3C3. Using forward and reverse approaches, autophagy was proved to involve in CRC migration and invasion induced by miR-338-5p.
   Interpretation: MiR-338-5p induces migration, invasion and metastasis of CRC in part through PIK3C3-related autophagy pathway. The miR-338-5p/PIK3C3 ratio may become a prognostic biomarker for CRC patients. (C) 2019 Published by Elsevier B.V.
C1 [Chu, Chien-An; Huang, Ching-Tang; Lan, Sheng-Hui; Liu, Hsiao-Sheng; Chow, Nan-Haw] Natl Cheng Kung Univ, Coll Med, Inst Basic Med Sci, Tainan, Taiwan.
   [Lee, Chung-Ta; Wang, Yi-Wen; Chow, Nan-Haw] Natl Cheng Kung Univ Hosp, Dept Pathol, Tainan, Taiwan.
   [Lee, Chung-Ta; Wang, Yi-Wen; Chow, Nan-Haw] Natl Cheng Kung Univ, Coll Med, Tainan, Taiwan.
   [Lee, Chung-Ta] Natl Cheng Kung Univ Hosp, Dept Pathol, Dou Liou Branch, Douliou City, Yunlin, Taiwan.
   [Lee, Jenq-Chang; Lin, Bo-Wen] Natl Cheng Kung Univ Hosp, Coll Med, Dept Surg, Tainan, Taiwan.
   [Lan, Sheng-Hui] Natl Yang Ming Univ, Dept Life Sci, Taipei, Taiwan.
   [Lan, Sheng-Hui] Natl Yang Ming Univ, Inst Genome Sci, Taipei, Taiwan.
   [Liu, Hsiao-Sheng] Natl Cheng Kung Univ, Coll Med, Dept Microbiol & Immunol, 1 Univ Rd, Tainan 701, Taiwan.
   [Lin, Peng-Chan] Natl Cheng Kung Univ, Coll Med, Dept Internal Med, Tainan, Taiwan.
   [Tian, Yu-Feng] Chia Nan Univ Pharm & Sci, Dept Hlth & Nutr, Tainan, Taiwan.
   [Tian, Yu-Feng] Chi Mei Med Ctr, Dept Surg, Div Colorectal Surg, Tainan, Taiwan.
RP Liu, HS (corresponding author), Natl Cheng Kung Univ, Coll Med, Dept Microbiol & Immunol, 1 Univ Rd, Tainan 701, Taiwan.; Chow, NH (corresponding author), Natl Cheng Kung Univ, Coll Med, Dept Pathol, 1 Univ Rd, Tainan 701, Taiwan.
EM a713@mail.ncku.edu.tw; chownh@mail.ncku.edu.tw
RI Lan, Sheng-Hui/AAV-1662-2021
OI Liu, Hsiao-Sheng/0000-0003-0576-7203
FU National Cheng Kung University Hospital, Tainan, TAIWAN
   [NCKUH-10704015]; Ministry of Science and Technology, TAIWANMinistry of
   Science and Technology, Taiwan [MOST-105-2320-B-006 -029 -MY3]
FX This work was supported by research grant NCKUH-10704015 from the
   National Cheng Kung University Hospital, Tainan, TAIWAN and grant
   MOST-105-2320-B-006 -029 -MY3 from the Ministry of Science and
   Technology, TAIWAN. The funders have no role in the study design, data
   collection, data analysis, interpretation, and writing of the report.U
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NR 52
TC 27
Z9 28
U1 2
U2 4
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 2352-3964
J9 EBIOMEDICINE
JI EBioMedicine
PD MAY
PY 2019
VL 43
BP 270
EP 281
DI 10.1016/j.ebiom.2019.04.010
PG 12
WC Medicine, General & Internal; Medicine, Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC General & Internal Medicine; Research & Experimental Medicine
GA IB2HZ
UT WOS:000470091600039
PM 30982765
OA Green Published, gold
DA 2022-04-25
ER

PT J
AU Mellor, HR
   Harris, AL
AF Mellor, Howard R.
   Harris, Adrian L.
TI The role of the hypoxia-inducible BH3-only proteins BNIP3 and BNIP3L in
   cancer
SO CANCER AND METASTASIS REVIEWS
LA English
DT Review
DE hypoxia; tumor; cell death; BH3; apoptosis; autophagy
ID AUTOPHAGIC CELL-DEATH; TRANSMEMBRANE DOMAIN; BREAST-CANCER;
   UP-REGULATION; GENE-EXPRESSION; GXXXG MOTIF; BH3 DOMAIN; IN-SITU;
   MITOCHONDRIAL; APOPTOSIS
AB In this review, we summarize current knowledge of the biological functions of the atypical BH3-only proteins BNIP3 and BNIP3L, focusing on the role of these proteins in cancer. Hypoxia increases the expression of BNIP3 through the transcription factor HIF-1, but despite a considerable number of investigations, it has proven difficult to establish a clear role for BNIP3 in the cellular hypoxic response. BNIP3 can induce a form of cell death that shows features of both necrosis and apoptosis, but unusually for a BH3-only protein, death occurs independently of the BH3 domain and is critically dependent on a C-terminal transmembrane domain, which also localizes the protein to the mitochondria. BNIP3 expression does not always result in cell death, suggesting that additional factors may suppress BNIP3 or cooperate with it to induce death. BNIP3 is highly expressed in some tumors, including those of the breast, lung and cervix. However, in colorectal and pancreatic cancers BNIP3 is frequently epigenetically silenced, possibly reflecting different functions for BNIP3 in different tissues. Recent reports have shown that BNIP3 can induce autophagy and there is some evidence to suggest this may represent an emerging role for BH3-only proteins in general. However, the mechanism through which BNIP3 induces autophagy and the cellular consequences of this are yet to be established.
C1 Univ Oxford, John Radcliffe Hosp, Canc Res UK Mol Oncol Labs, Growth Factor Grp, Oxford OX3 9DS, England.
RP Harris, AL (corresponding author), Univ Oxford, John Radcliffe Hosp, Canc Res UK Mol Oncol Labs, Growth Factor Grp, Oxford OX3 9DS, England.
EM howard.mellor@imm.ox.ac.uk; aharris.lab@cancer.org.uk
RI Harris, Adrian/ABA-3343-2020
OI Harris, Adrian/0000-0003-1376-8409
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NR 68
TC 90
Z9 96
U1 1
U2 17
PU SPRINGER
PI DORDRECHT
PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS
SN 0167-7659
EI 1573-7233
J9 CANCER METAST REV
JI Cancer Metastasis Rev.
PD DEC
PY 2007
VL 26
IS 3-4
BP 553
EP 566
DI 10.1007/s10555-007-9080-0
PG 14
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA 230MC
UT WOS:000250879600016
PM 17805942
DA 2022-04-25
ER

PT J
AU Matrone, A
   Grossi, V
   Chiacchiera, F
   Fina, E
   Cappellari, M
   Caringella, AM
   Di Naro, E
   Loverro, G
   Simone, C
AF Matrone, Antonio
   Grossi, Valentina
   Chiacchiera, Fulvio
   Fina, Emanuela
   Cappellari, Marianna
   Caringella, Anna Maria
   Di Naro, Edoardo
   Loverro, Giuseppe
   Simone, Cristiano
TI p38 alpha Is Required for Ovarian Cancer Cell Metabolism and Survival
SO INTERNATIONAL JOURNAL OF GYNECOLOGICAL CANCER
LA English
DT Article
DE Ovarian cancer; p38 alpha; HIF1 alpha; AMPK; FoxO3A; Autophagy
ID POSITRON-EMISSION-TOMOGRAPHY; HYPOXIA; TUMOR; DEATH; AUTOPHAGY; FOXO;
   PHOSPHORYLATION; TRANSCRIPTION; EXPRESSION; APOPTOSIS
AB Introduction: Ovarian cancer is highly sensitive to chemotherapy but also shows a high rate of recurrence and drug resistance. These negative outcomes mostly depend on altered apoptotic pathways, making the design of new therapeutic strategies based on the induction of other types of cell death highly desirable. Several lines of research are now addressing cancer-specific features to specifically target tumor cells, thus reducing adverse effects. In this light, a great deal of attention has been devoted to the metabolic reprogramming occurring in cancer cells, which display increased levels of glycolysis compared with their normal counterparts. We recently showed that inhibition of p38 alpha impairs key metabolic functions of colorectal cancer cells, inducing growth arrest, autophagy, and cell death both in vivo and in vitro. These effects are mediated by a switch from hypoxia-inducible factor 1 alpha (HIF1 alpha) to forkhead transcription factor O (Fox)-dependent transcription.
   Methods: We first characterized p38 expression in OVCAR-3, A2780, and SKOV-3 ovarian cancer cell lines. Then, we treated these cells with the p38 alpha/p38A-specific inhibitor SB202190 and performed a morphological, proliferation, and survival analyses. Finally, we studied HIF1 alpha and FoxO3A expressions and signaling pathways to evaluate their role in SB202190-induced effects.
   Results: p38 alpha blockade induces the formation of intracellular autophagic vacuoles and reduces growth and viability of ovarian cancer cells. As in colorectal cancer, the underlying molecular mechanism seems to rely on a shift from HIF1 alpha- to FoxO3A-dependent transcription, which is promoted by the activation of the adenosine monophosphate-activated protein kinase pathway.
   Conclusions: These data corroborate the hypothesis that pharmacological modulation of genes involved in cancer-specific homeostasis, such as p38 alpha, might be exploited to design new therapeutic approaches to cancer treatment.
C1 [Matrone, Antonio; Grossi, Valentina; Chiacchiera, Fulvio; Fina, Emanuela; Cappellari, Marianna; Simone, Cristiano] Ist Ric Farmacol Mario Negri, Consorzio Mario Negri Sud, Dept Translat Pharmacol, Lab Signal Dependent Transcript, I-66030 Santa Maria Imbaro, Italy.
   [Caringella, Anna Maria; Di Naro, Edoardo; Loverro, Giuseppe] Univ Bari, Sch Med, Dept Obstet & Gynecol, Bari, Italy.
RP Simone, C (corresponding author), Ist Ric Farmacol Mario Negri, Consorzio Mario Negri Sud, Dept Translat Pharmacol, Lab Signal Dependent Transcript, I-66030 Santa Maria Imbaro, Italy.
EM simone@negrisud.it
RI GROSSI, Valentina/O-6546-2019; Chiacchiera, Fulvio/ABD-6137-2020;
   Chiacchiera, Fulvio/K-6740-2016; Grossi, Valentina/K-9821-2016; Simone,
   Cristiano/K-3452-2018; Fina, Emanuela/E-2828-2017
OI GROSSI, Valentina/0000-0003-3843-1618; Chiacchiera,
   Fulvio/0000-0003-3830-2090; Grossi, Valentina/0000-0003-3843-1618;
   Simone, Cristiano/0000-0002-2628-7658; Fina,
   Emanuela/0000-0002-9837-4320; di naro, edoardo/0000-0001-7675-7171;
   loverro, giuseppe/0000-0002-8192-9959
FU Italian Association for Cancer ResearchFondazione AIRC per la ricerca
   sul cancro; Progetti di Ricerca Scientifica di Ateneo-es. fin. 2009,
   Universita degli Studi di Bari
FX This work was partially supported by a My First Grant (to C. S.) from
   the Italian Association for Cancer Research and the Progetti di Ricerca
   Scientifica di Ateneo-es. fin. 2009, Universita degli Studi di Bari (to
   G. L.).
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U1 0
U2 8
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA TWO COMMERCE SQ, 2001 MARKET ST, PHILADELPHIA, PA 19103 USA
SN 1048-891X
EI 1525-1438
J9 INT J GYNECOL CANCER
JI Int. J. Gynecol. Cancer
PD FEB
PY 2010
VL 20
IS 2
BP 203
EP 211
DI 10.1111/IGC.0b013e3181c8ca12
PG 9
WC Oncology; Obstetrics & Gynecology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Obstetrics & Gynecology
GA 562NT
UT WOS:000275059300003
PM 20169663
DA 2022-04-25
ER

PT S
AU Vegliante, R
   Ciriolo, MR
AF Vegliante, Rolando
   Ciriolo, Maria R.
BE Litwack, G
TI Autophagy and Autophagic Cell Death: Uncovering New Mechanisms Whereby
   Dehydroepiandrosterone Promotes Beneficial Effects on Human Health
SO DEHYDROEPIANDROSTERONE
SE Vitamins and Hormones
LA English
DT Review; Book Chapter
ID COLONIC ADENOCARCINOMA CELLS; PREVENTS OXIDATIVE INJURY;
   GENE-EXPRESSION; SIGNALING PATHWAY; DHEA TREATMENT; CANCER CELLS;
   BONE-MARROW; AGING BRAIN; APOPTOSIS; PROLIFERATION
AB Dehydroepiandrosterone (DHEA) is the most abundant steroid hormone in human serum and a precursor of sexual hormones. Its levels, which are maximum between the age of 20 and 30, dramatically decline with aging thus raising the question that many pathological conditions typical of the elderly might be associated with the decrement of circulating DHEA. Moreover, since its very early discovery, DHEA and its metabolites have been shown to be active in many pathophysiological contexts, including cardiovascular disease, brain disorders, and cancer. Indeed, treatment with DHEA has beneficial effects for the cure of these and many other pathologies in vitro, in vivo, and in patient studies. However, the molecular mechanisms underlying DHEA effects have been only partially elucidated.
   Autophagy is a self-digestive process, by which cell homeostasis is maintained, damaged organelles removed, and cell survival assured upon stress stimuli. However, high rate of autophagy is detrimental and leads to a form of programmed cell death known as autophagic cell death (ACD).
   In this chapter, we describe the process of autophagy and the morphological and biochemical features of ACD. Moreover, we analyze the beneficial effects of DHEA in several pathologies and the molecular mechanisms with particular emphasis on its regulation of cell death processes. Finally, we review data indicating DHEA and structurally related steroid hormones as modulators of both autophagy and ACD, a research field that opens new avenues in the therapeutic use of these compounds.
C1 [Vegliante, Rolando] Hop Civil, Inst Hematol & Immunol, Microenvironm Niche Tumorigenesis & Targeted Ther, MN3T, Strasbourg, France.
   [Ciriolo, Maria R.] Univ Roma Tor Vergata, Rome, Italy.
   [Ciriolo, Maria R.] IRCCS San Raffaele La Pisana, Rome, Italy.
RP Ciriolo, MR (corresponding author), Univ Roma Tor Vergata, Rome, Italy.; Ciriolo, MR (corresponding author), IRCCS San Raffaele La Pisana, Rome, Italy.
EM ciriolo@bio.uniroma2.it
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NR 131
TC 10
Z9 10
U1 0
U2 2
PU ELSEVIER ACADEMIC PRESS INC
PI SAN DIEGO
PA 525 B STREET, SUITE 1900, SAN DIEGO, CA 92101-4495 USA
SN 0083-6729
BN 978-0-12-814361-2
J9 VITAM HORM
JI Vitam. Horm.
PY 2018
VL 108
BP 273
EP 307
DI 10.1016/bs.vh.2018.01.006
PG 35
WC Biochemistry & Molecular Biology; Endocrinology & Metabolism
WE Book Citation Index – Science (BKCI-S); Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Endocrinology & Metabolism
GA BL5NS
UT WOS:000452381500011
PM 30029730
DA 2022-04-25
ER

PT J
AU Song, XX
   Lee, DH
   Dilly, AK
   Lee, YS
   Choudry, HA
   Kwon, YT
   Bartlett, DL
   Lee, YJ
AF Song, Xinxin
   Lee, Dae-Hee
   Dilly, Ashok-Kumar
   Lee, Young-Sun
   Choudry, Haroon Asif
   Kwon, Yong Tae
   Bartlett, David L.
   Lee, Yong J.
TI Crosstalk Between Apoptosis and Autophagy Is Regulated by the
   Arginylated BiP/Beclin-1/p62 Complex
SO MOLECULAR CANCER RESEARCH
LA English
DT Article
ID UNFOLDED PROTEIN RESPONSE; BECLIN 1; PERITONEAL CARCINOMATOSIS;
   CELL-DEATH; ER STRESS; PROTEASOME INHIBITION; SELECTIVE AUTOPHAGY;
   COLORECTAL-CANCER; MULTIPLE-MYELOMA; MITOMYCIN-C
AB Emerging evidence demonstrates that autophagy and apoptosis are interconnected and their interplay greatly affects cell death. However, the key regulators in this crosstalk remain elusive. Therefore, the role of N-terminal arginylated BiP (R-BiP)/Beclin-1/p62 complex was examined in the crosstalk between apoptosis and autophagy during combination chemotherapy with mitomycin C and bortezomib using immunoblot, immunoprecipitation, and cellular imaging assays in wild-type (WT) and genetically engineered colorectal cancer cells. In addition, the tumoricidal efficacy of the combinatorial treatment in a nude mouse tumor xenograft model of colorectal cancer was assessed. Bortezomib combined with mitomycin C synergistically induced cytotoxicity and apoptosis rather than autophagy. Mechanistically, this combination inactivated Akt and subsequently induced Beclin-1 (BECN1) dephosphorylation at Ser 234/295. Dephos-phorylation of Beclin-1 resulted in increased cleavage of Beclin-1 and disruption of the R-BiP/Beclin-1/p62 complex, which led to switching autophagy to the synergistic induction of apoptosis. Importantly, the combination significantly suppressed LS174T intraperitoneal xenograft tumor growth, induced Akt inactivation and Beclin-1 cleavage, and decreased autophagy in vivo. Moreover, the tumoricidal efficacy of the combinatorial treatment was less effective, in vitro and in vivo, in HCT116 tumors harboring a Beclin-1 caspase 8 cleavage site mutant knock-in.
   Implications: This study uncovers that the R-BiP/Beclin-1/p62 complex has an important role in the crosstalk between apoptosis and autophagy. The results also propose how mono-drug resistance can be overcome using potent combinations to improve anticancer therapy.
C1 [Song, Xinxin; Dilly, Ashok-Kumar; Lee, Young-Sun; Choudry, Haroon Asif; Bartlett, David L.; Lee, Yong J.] Univ Pittsburgh, Sch Med, Dept Surg, Pittsburgh, PA USA.
   [Lee, Dae-Hee] Korea Univ, Coll Med, Dept Internal Med, Div Med Oncol, Seoul, South Korea.
   [Lee, Dae-Hee] Korea Univ, Coll Med, Brain Korea Program Biomed Sci 21, Seoul, South Korea.
   [Kwon, Yong Tae] Seoul Natl Univ, Prot Metab Med Res Ctr, Seoul, South Korea.
   [Lee, Dae-Hee] Seoul Natl Univ, Dept Biomed Sci, Coll Med, Seoul, South Korea.
RP Lee, YJ (corresponding author), Univ Pittsburgh, Dept Surg, Hillman Canc Ctr, 5117 Ctr Ave,Room 1-46C, Pittsburgh, PA 15213 USA.
EM leeyj@upmc.edu
FU NCIUnited States Department of Health & Human ServicesNational
   Institutes of Health (NIH) - USANIH National Cancer Institute (NCI)
   [CA205267, CA212125]; National Research Foundation of KoreaNational
   Research Foundation of Korea [NRF-2013R1A2A2A01014170,
   NRF-2016R1A2B3011389]; Nobel Laureates Invitation Program of Seoul
   National University;  [P30CA047904]; NATIONAL CANCER INSTITUTEUnited
   States Department of Health & Human ServicesNational Institutes of
   Health (NIH) - USANIH National Cancer Institute (NCI) [R03CA205267,
   P30CA047904, R03CA212125] Funding Source: NIH RePORTER
FX This work was supported by the following grants: NCI grants CA205267 and
   CA212125 to Y.J. Lee; National Research Foundation of Korea Program
   grants NRF-2013R1A2A2A01014170 and NRF-2016R1A2B3011389 to Y.T. Kwon;
   and Nobel Laureates Invitation Program of Seoul National University to
   Y.T. Kwon. This project used the UPCI Core Facility and was supported in
   part by award P30CA047904 to the University of Pittsburgh Cancer
   Institute.
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NR 58
TC 24
Z9 27
U1 1
U2 5
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 1541-7786
EI 1557-3125
J9 MOL CANCER RES
JI Mol. Cancer Res.
PD JUL
PY 2018
VL 16
IS 7
BP 1077
EP 1091
DI 10.1158/1541-7786.MCR-17-0685
PG 15
WC Oncology; Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Cell Biology
GA GL6EC
UT WOS:000437272500002
PM 29669822
OA Green Accepted, Bronze
DA 2022-04-25
ER

PT J
AU Koyuncu, I
   Gonel, A
   Temiz, E
   Karaogul, E
   Uyar, Z
AF Koyuncu, Ismail
   Gonel, Ataman
   Temiz, Ebru
   Karaogul, Eyyup
   Uyar, Zafer
TI Pistachio Green Hull Extract Induces Apoptosis through Multiple
   Signaling Pathways by Causing Oxidative Stress on Colon Cancer Cells
SO ANTI-CANCER AGENTS IN MEDICINAL CHEMISTRY
LA English
DT Article
DE Apoptosis; cytotoxicity; colorectal cancer; anti-cancer agent; oxidative
   stress; phenolic compounds
AB Background: Pistachio is considered to be one of the fifty foods with the highest antioxidant effect. However, the anticancer effect mechanisms of this plant extracts are unknown.
   Objective: The aim of this study was to investigate the anticancer effect of different extracts from the green hull of pistachio.
   Methods: The cytotoxic effects of different solvent extracts on cancer and normal cells were examined by cell viability assay and flow cytometric analysis. The levels of the apoptotic gene and protein were investigated by Western Blot and ELISA, and qPCR. The intracellular free radical exchange was determined by oxidative and nitric oxide analyses. DNA damage level was measured by the 8-OHdG test. Phenolic and free fatty acid components were examined by LC-MS/MS and GC-MS, respectively.
   Results: It was determined that the n-hexane fraction showed a higher cytotoxic effect on cancer cells. Oxidative and cell cycle analyses indicated that the n-hexane fraction arrested cell cycle of HT-29 at the sub-G(1) phase by increasing DNA damage through oxidative stress. In addition, gene expression analysis of the HT-29 treated with the n-hexane fraction indicated that apoptotic and autophagic gene expressions were significantly upregulated. LC-MS/MS analysis of the n-hexane fraction revealed the presence of 15 phenolic compounds, containing mainly gallic acid and catechin hydrate, and GC-MS analysis determined the presence of the following fatty acids: 9-octadecenoic acid, 9,12-octadecadienoic acid and hexadecenoic acid.
   Conclusion: Based on these grounds, we suggest that the n-hexane fraction of pistachio green hull damages DNA, arrests the cell cycle at the G(1) subphase, and induces apoptosis through oxidative pathways in colon cancer.
C1 [Koyuncu, Ismail; Gonel, Ataman; Temiz, Ebru] Harran Univ, Med Fac, Dept Med Biochem, Sanliurfa, Turkey.
   [Karaogul, Eyyup] Harran Univ, Engn Fac, Food Sci & Technol, Sanliurfa, Turkey.
   [Uyar, Zafer] Harran Univ, Sci Fac, Dept Chem, Sanliurfa, Turkey.
RP Koyuncu, I (corresponding author), Harran Univ, Med Fac, Dept Med Biochem, Sanliurfa, Turkey.
EM ismailkoyuncu1@gmail.com
RI Uyar, Zafer/AAF-5391-2021; Temiz, Ebru/ABF-6573-2021
OI Uyar, Zafer/0000-0002-6310-8823; 
FU HUBAK department of Harran University [15057]; GAP institution, Turkey
   [19001]
FX This research was supported by the HUBAK department of Harran University
   (Project number: 15057) and GAP institution (Grand number: 19001) ,
   Turkey.
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NR 59
TC 1
Z9 1
U1 2
U2 2
PU BENTHAM SCIENCE PUBL LTD
PI SHARJAH
PA EXECUTIVE STE Y-2, PO BOX 7917, SAIF ZONE, 1200 BR SHARJAH, U ARAB
   EMIRATES
SN 1871-5206
EI 1875-5992
J9 ANTI-CANCER AGENT ME
JI Anti-Cancer Agents Med. Chem.
PY 2021
VL 21
IS 6
BP 725
EP 737
DI 10.2174/1871520620999200730155524
PG 13
WC Oncology; Chemistry, Medicinal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Pharmacology & Pharmacy
GA RB0XJ
UT WOS:000631840600006
PM 32748756
DA 2022-04-25
ER

PT J
AU Liao, D
   Li, T
   Ye, CG
   Zeng, LY
   Li, HH
   Pu, XX
   Ding, CC
   He, ZW
   Huang, GL
AF Liao, Dan
   Li, Tong
   Ye, Caiguo
   Zeng, Liuyan
   Li, Huahui
   Pu, Xingxiang
   Ding, Congcong
   He, Zhiwei
   Huang, Guo-Liang
TI miR-221 inhibits autophagy and targets TP53INP1 in colorectal cancer
   cells
SO EXPERIMENTAL AND THERAPEUTIC MEDICINE
LA English
DT Article
DE autophagy; colorectal cancer; miR-221; tumor protein 53-induced nuclear
   protein 1
ID HEPATOCELLULAR-CARCINOMA; PROMOTES AUTOPHAGY; MICRORNA; DEATH;
   RADIOSENSITIVITY; MARKER; LC3
AB Colorectal cancer (CRC) is the third most common cancer and the fourth leading cause of cancer-associated mortalities worldwide. MicroRNAs (miRNAs/miRs) serve important roles in tumor development, progression and metastasis. miR-221 has been reported to modulate proliferation, apoptosis, cell cycle distribution and cell migration in a variety of cancers. However, the function of miR-221 in the autophagy of cancer is unclear. In the present study, the role of miR-221 in the autophagy of CRC cells was investigated and its associated target was identified. Survival analysis using The Cancer Genome Atlas data suggested that a higher expression of miR-221 was associated with poor survival in patients with CRC. A Cell Counting kit-8 assay revealed that miR-221 promoted CRC cell proliferation. Autophagy flux analyzed by microtubule-associated protein 1 light chain 3 (LC3) turnover indicated that miR-221 reduced autophagy in CRC cells using different protease inhibitors (E64d and pepstatin A; Bafilomycin A1) in nutrient-rich medium or under starvation conditions. Tumor protein 53-induced nuclear protein 1 (TP53INP1) was identified as a potential novel target of miR-221 by bioinformative prediction. The protein expression of TP53INP1 was inversely regulated by miR-221 in CRC cells. Furthermore, luciferase activity assays were performed and indicated that miR-221 may regulate the luciferase activity of wild-type TP53INP1 without interfering with the activity of mutant TP53INP1. These data suggested that miR-221 may promote the cell proliferation of CRC via the inhibition of autophagy and targeted TP53INP1.
C1 [Liao, Dan; Li, Tong; Ye, Caiguo; Li, Huahui; Ding, Congcong; He, Zhiwei; Huang, Guo-Liang] Guangdong Med Univ, Guangdong Prov Key Lab Med Mol Diagnost, Key Lab Epigenet Dongguan City, China Amer Canc Res Inst,Dongguan Sci Res Ctr, Dongguan 523808, Guangdong, Peoples R China.
   [Liao, Dan] Southern Med Univ, Dept Gynaecol & Obstet, Dongguan Peoples Hosp 3, Affiliated Dongguan Shilong Peoples Hosp, Dongguan 523326, Guangdong, Peoples R China.
   [Zeng, Liuyan] Guangdong Med Univ, Affiliated Hosp, Dept Hlth Management Ctr, Zhanjiang 524001, Guangdong, Peoples R China.
   [Pu, Xingxiang] Cent South Univ, Dept Chest Internal Med 2, Hunan Canc Hosp, Affiliated Canc Hosp,Xiangya Sch Med, Changsha 410013, Hunan, Peoples R China.
RP He, ZW; Huang, GL (corresponding author), Guangdong Med Univ, China Amer Canc Res Inst, Dongguan Sci Res Ctr, 1 Xincheng Rd, Dongguan 523808, Guangdong, Peoples R China.
EM zhiweihe688@yahoo.com; huangguoliang@gdmu.edu.cn
RI Huang, Guoliang/H-1625-2011
OI Huang, Guoliang/0000-0002-8902-8100
FU Science and Technology Planning Project of Guangdong Province
   [2013B021800070]; Training Plan for Outstanding Young Teachers in Higher
   Education Institutions of Guangdong Province [YQ201403/YQ2014086]; Hunan
   Provincial Natural Science Foundation of ChinaNatural Science Foundation
   of Hunan Province [2015jj6066]; Project of Hunan Provincial Department
   of Health [B2012-095]
FX This study was supported by the Science and Technology Planning Project
   of Guangdong Province (grant no. 2013B021800070), the Training Plan for
   Outstanding Young Teachers in Higher Education Institutions of Guangdong
   Province (grant no. YQ201403/YQ2014086), the Hunan Provincial Natural
   Science Foundation of China (grant no. 2015jj6066), and the Project of
   Hunan Provincial Department of Health (grant no. B2012-095).
CR An Y, 2015, CELL DEATH DIS, V6, DOI 10.1038/cddis.2015.123
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NR 35
TC 25
Z9 25
U1 0
U2 7
PU SPANDIDOS PUBL LTD
PI ATHENS
PA POB 18179, ATHENS, 116 10, GREECE
SN 1792-0981
EI 1792-1015
J9 EXP THER MED
JI Exp. Ther. Med.
PD FEB
PY 2018
VL 15
IS 2
BP 1712
EP 1717
DI 10.3892/etm.2017.5522
PG 6
WC Medicine, Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Research & Experimental Medicine
GA FT5VP
UT WOS:000423221600076
PM 29434757
OA Green Published, gold
DA 2022-04-25
ER

PT J
AU Wang, JG
   Zhang, CJ
   Zhang, JB
   He, YK
   Lee, YM
   Chen, SB
   Lim, TK
   Ng, SK
   Shen, HM
   Lin, QS
AF Wang, Jigang
   Zhang, Chong-Jing
   Zhang, Jianbin
   He, Yingke
   Lee, Yew Mun
   Chen, Songbi
   Lim, Teck Kwang
   Ng, Shukie
   Shen, Han-Ming
   Lin, Qingsong
TI Mapping sites of aspirin-induced acetylations in live cells by
   quantitative acid-cleavable activity-based protein profiling (QA-ABPP)
SO SCIENTIFIC REPORTS
LA English
DT Article
ID CHEMICAL PROTEOMICS APPROACH; MULTIPLE CELLULAR-PROTEINS; ACTIVITY-BASED
   PROBES; COLON-CANCER CELLS; COLORECTAL-CANCER; TARGET IDENTIFICATION;
   AUTOPHAGY; MTOR; MOLECULES; STRATEGY
AB Target-identification and understanding of mechanism-of-action (MOA) are challenging for development of small-molecule probes and their application in biology and drug discovery. For example, although aspirin has been widely used for more than 100 years, its molecular targets have not been fully characterized. To cope with this challenge, we developed a novel technique called quantitative acid-cleavable activity-based protein profiling (QA-ABPP) with combination of the following two parts: (i) activity-based protein profiling (ABPP) and iTRAQ (TM) quantitative proteomics for identification of target proteins and (ii) acid-cleavable linker-based ABPP for identification of peptides with specific binding sites. It is known that reaction of aspirin with its target proteins leads to acetylation. We thus applied the above technique using aspirin-based probes in human cancer HCT116 cells. We identified 1110 target proteins and 2775 peptides with exact acetylation sites. By correlating these two sets of data, 523 proteins were identified as targets of aspirin. We used various biological assays to validate the effects of aspirin on inhibition of protein synthesis and induction of autophagy which were elicited from the pathway analysis of Aspirin target profile. This technique is widely applicable for target identification in the field of drug discovery and biology, especially for the covalent drugs.
C1 [Wang, Jigang; Lee, Yew Mun; Lim, Teck Kwang; Lin, Qingsong] Natl Univ Singapore, Dept Biol Sci, Singapore 117543, Singapore.
   [Zhang, Chong-Jing; Chen, Songbi] Chinese Acad Trop Agr Sci, Trop Crops Genet Resources Inst, Danzhou, Hainan, Peoples R China.
   [Zhang, Jianbin; Ng, Shukie; Shen, Han-Ming] Natl Univ Singapore, Yong Loo Lin Sch Med, Dept Physiol, Singapore 117597, Singapore.
   [He, Yingke] Singapore Gen Hosp, Dept Anaesthesiol, Singapore 169608, Singapore.
RP Shen, HM (corresponding author), Natl Univ Singapore, Yong Loo Lin Sch Med, Dept Physiol, Block MD9,2 Med Dr, Singapore 117597, Singapore.
EM han-ming_shen@nuhs.edu.sg; dbslinqs@nus.edu.sg
RI SHEN, Han-Ming/B-5942-2011; Lin, Qingsong/H-9794-2012; Zhang,
   Chong-Jing/AAO-5782-2021; Lee, Yew Mun/G-8891-2017
OI SHEN, Han-Ming/0000-0001-7369-5227; Lin, Qingsong/0000-0001-9117-8514;
   Lee, Yew Mun/0000-0002-8360-7689; Zhang, Chong-Jing/0000-0002-3396-9999
FU NUS research scholarshipNational University of Singapore; Initial Fund
   of High-level Creative Talents in Hainan Province
FX J.W. and J.Z. were supported by NUS research scholarship. We would like
   to thank Prof. Kim Chu-Young for helpful discussions and proofreading of
   this manuscript. We acknowledge the financial support from the Initial
   Fund of High-level Creative Talents in Hainan Province (Chen Songbi).
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NR 51
TC 48
Z9 49
U1 3
U2 52
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 2045-2322
J9 SCI REP-UK
JI Sci Rep
PD JAN 20
PY 2015
VL 5
AR 7896
DI 10.1038/srep07896
PG 12
WC Multidisciplinary Sciences
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Science & Technology - Other Topics
GA AZ1XL
UT WOS:000348028300015
PM 25600173
OA gold, Green Published
DA 2022-04-25
ER

PT J
AU Maioli, E
   Torricelli, C
   Valacchi, G
AF Maioli, E.
   Torricelli, C.
   Valacchi, G.
TI Rottlerin and Cancer: Novel Evidence and Mechanisms
SO SCIENTIFIC WORLD JOURNAL
LA English
DT Review
ID PROTEIN-KINASE-C; NF-KAPPA-B; ENDOPLASMIC-RETICULUM STRESS;
   DELTA-INDEPENDENT PATHWAY; MALIGNANT GLIOMA-CELLS; COLON-CARCINOMA
   CELLS; NECROSIS-FACTOR-ALPHA; PKC-DELTA; INDUCED APOPTOSIS;
   BREAST-CANCER
AB Because cancers are caused by deregulation of hundreds of genes, an ideal anticancer agent should target multiple gene products or signaling pathways simultaneously. Recently, extensive research has addressed the chemotherapeutic potential of plant-derived compounds. Among the ever-increasing list of naturally occurring anticancer agents, Rottlerin appears to have great potentiality for being used in chemotherapy because it affects several cell machineries involved in survival, apoptosis, autophagy, and invasion. The underlying mechanisms that have been described are diverse, and the final, cell-specific, Rottlerin outcome appears to result from a combination of signaling pathways at multiple levels. This paper seeks to summarize the multifocal signal modulatory properties of Rottlerin, which merit to be further exploited for successful prevention and treatment of cancer.
C1 [Maioli, E.; Torricelli, C.] Univ Siena, Dept Physiol, I-53100 Siena, Italy.
   [Valacchi, G.] Univ Ferrara, Dept Biol & Evolut, I-44100 Ferrara, Italy.
   [Valacchi, G.] Kyung Hee Univ, Dept Food & Nutr, Seoul 130701, South Korea.
RP Maioli, E (corresponding author), Univ Siena, Dept Physiol, Aldo Moro St, I-53100 Siena, Italy.
EM maioli@unisi.it
OI MAIOLI, Emanuela/0000-0002-0701-1445
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NR 95
TC 44
Z9 46
U1 0
U2 4
PU HINDAWI PUBLISHING CORPORATION
PI NEW YORK
PA 410 PARK AVENUE, 15TH FLOOR, #287 PMB, NEW YORK, NY 10022 USA
SN 1537-744X
J9 SCI WORLD J
JI Sci. World J.
PY 2012
AR 350826
DI 10.1100/2012/350826
PG 11
WC Multidisciplinary Sciences
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Science & Technology - Other Topics
GA 916FT
UT WOS:000302085700001
PM 22272173
OA Green Published, gold, Green Submitted
DA 2022-04-25
ER

PT J
AU Lin, BW
   Gong, CC
   Song, HF
   Cui, YY
AF Lin, Bo-Wen
   Gong, Cheng-Chen
   Song, Hai-Fei
   Cui, Ying-Yu
TI Effects of anthocyanins on the prevention and treatment of cancer
SO BRITISH JOURNAL OF PHARMACOLOGY
LA English
DT Review
ID MASSONIANA BARK EXTRACT; NF-KAPPA-B; RECEPTOR TYROSINE KINASES;
   OXIDATIVE STRESS MARKERS; BLACK RICE ANTHOCYANINS; SUPPRESS
   TUMOR-GROWTH; CELLS IN-VITRO; CONCISE GUIDE; COLON-CANCER; BLUEBERRY
   ANTHOCYANINS
AB Anthocyanins are a class of water-soluble flavonoids, which show a range of pharmacological effects, such as prevention of cardiovascular disease, obesity control and antitumour activity. Their potential antitumour effects are reported to be based on a wide variety of biological activities including antioxidant; anti-inflammation; anti-mutagenesis; induction of differentiation; inhibiting proliferation by modulating signal transduction pathways, inducing cell cycle arrest and stimulating apoptosis or autophagy of cancer cells; anti-invasion; anti-metastasis; reversing drug resistance of cancer cells and increasing their sensitivity to chemotherapy. In this review, the latest progress on the anticancer activities of anthocyanins and the underlying molecular mechanisms is summarized using data from basic research in vitro and in vivo, from clinical trials and taking into account theory and practice.
C1 [Cui, Ying-Yu] Tongji Univ, Minist Educ, Key Lab Arrhythmias, Shanghai, Peoples R China.
   [Cui, Ying-Yu] Tongji Univ, Inst Med Genet, Sch Med, Shanghai, Peoples R China.
RP Cui, YY (corresponding author), Tongji Univ, Sch Med, Dept Regenerat Med, Shanghai 200092, Peoples R China.
EM yycui@tongji.edu.cn
RI Andrew, Ruth/C-2727-2008; Cui, Ying-Yu/G-6386-2011
OI Andrew, Ruth/0000-0002-6916-2994; Cui, Ying-Yu/0000-0002-6324-0795
FU University Students Innovation Training Program of Shanghai Municipal
   Government [201610247134]; Yangfan Project of Tongji University School
   of Medicine [2012YF05]
FX This work was supported by the University Students Innovation Training
   Program of Shanghai Municipal Government [grant number 201610247134 to
   HF Song] and the Yangfan Project of Tongji University School of Medicine
   [grant number 2012YF05 to YY Cui]. The authors thank the staff of the
   Key Laboratory of Arrhythmias, Ministry of Education (Tongji University)
   for their technical assistance. We also thank the editor and reviewers
   for their comments and suggestions, which have improved this review
   considerably.
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NR 137
TC 136
Z9 143
U1 13
U2 163
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0007-1188
EI 1476-5381
J9 BRIT J PHARMACOL
JI Br. J. Pharmacol.
PD JUN
PY 2017
VL 174
IS 11
BP 1226
EP 1243
DI 10.1111/bph.13627
PG 18
WC Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA EU7SY
UT WOS:000401236200004
PM 27646173
OA Green Published, Bronze
HC Y
HP N
DA 2022-04-25
ER

PT J
AU Lee, M
   Choi, H
   Kim, KS
   Kim, DH
   Kim, CH
   Lee, YC
AF Lee, Miri
   Choi, Hyunju
   Kim, Kyoung-Sook
   Kim, Dong-Hyun
   Kim, Cheorl-Ho
   Lee, Young-Choon
TI Curcumin Downregulates Human GM3 Synthase (hST3Gal V) Gene Expression
   with Autophagy Induction in Human Colon Carcinoma HCT116 Cells
SO EVIDENCE-BASED COMPLEMENTARY AND ALTERNATIVE MEDICINE
LA English
DT Article
ID TRANSCRIPTIONAL REGULATION; VALPROIC ACID; DIFFERENTIATION;
   GANGLIOSIDES; GLYCOSPHINGOLIPIDS; INVOLVEMENT; CANCER; ORGANIZATION;
   ACTIVATION; DEATH
AB Our recent report showed that curcumin, polyphenolic compound isolated from the herb Curcuma longa, upregulated the gene expression of human GD3 synthase (hST8Sia I) responsible for ganglioside GD3 synthesis with autophagy induction in human lung adenocarcinoma A549 cells. In this study, on the contrary to this finding, we demonstrated that curcumin downregulated the gene expression of human GM3 synthase (hST3Gal V) catalyzing ganglioside GM3 synthesis with autophagy induction in human colon carcinoma HCT116 cells. To clarify the mechanism leading to the downregulation of hST3Gal V gene expression in curcumin-treated HCT116 cells, we analyzed the curcumin-inducible promoter of the hST3Gal V gene by luciferase reporter assays. Promoter deletion analysis demonstrated that the -177 to -83 region, which includes putative binding sites for transcription factors NFY, CREB/ATF, SP1, EGR3, and MZF1, acts as the curcumin-responsive promoter of the hST3Gal V gene. Site-directed mutagenesis and chromatin immunoprecipitation analysis demonstrated that the CREB/ATF binding site at -143 is pivotal for curcumin-induced downregulation of hST3Gal V gene in HCT116 cells. The transcriptional activation of hST3Gal V in HCT116 cells was significantly repressed by an inhibitor of AMP-activated protein kinase (AMPK). These results suggest that AMPK signal pathway mediates hST3Gal V gene expression in HCT116 cells.
C1 [Lee, Miri; Kim, Kyoung-Sook; Kim, Dong-Hyun; Lee, Young-Choon] Dong A Univ, Coll Hlth Sci, Dept Med Biotechnol, Busan 49315, South Korea.
   [Choi, Hyunju; Kim, Cheorl-Ho] Sungkyunkwan Univ, Dept Biol Sci, Mol & Cellular Glycobiol Unit, Kyunggi Do 16419, South Korea.
RP Lee, YC (corresponding author), Dong A Univ, Coll Hlth Sci, Dept Med Biotechnol, Busan 49315, South Korea.; Kim, CH (corresponding author), Sungkyunkwan Univ, Dept Biol Sci, Mol & Cellular Glycobiol Unit, Kyunggi Do 16419, South Korea.
EM chkimbio@skku.edu; yclee@dau.ac.kr
RI Kim, Cheorl-Ho/T-6753-2019
OI Kim, Cheorl-Ho/0000-0002-6323-0714
FU Dong-A University
FX This work was supported by the Dong-A University research fund.
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NR 25
TC 2
Z9 2
U1 0
U2 0
PU HINDAWI LTD
PI LONDON
PA ADAM HOUSE, 3RD FLR, 1 FITZROY SQ, LONDON, W1T 5HF, ENGLAND
SN 1741-427X
EI 1741-4288
J9 EVID-BASED COMPL ALT
JI Evid.-based Complement Altern. Med.
PY 2018
VL 2018
AR 6746412
DI 10.1155/2018/6746412
PG 7
WC Integrative & Complementary Medicine
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Integrative & Complementary Medicine
GA HB5XC
UT WOS:000451135900001
PM 30534177
OA Green Published, Green Submitted, gold
DA 2022-04-25
ER

PT J
AU Tan, H
   Li, X
   Yang, WH
   Kang, Y
AF Tan, Hao
   Li, Xiang
   Yang, Wei-Han
   Kang, Yong
TI A flavone, Wogonin from Scutellaria baicalensis inhibits the
   proliferation of human colorectal cancer cells by inducing of autophagy,
   apoptosis and G2/M cell cycle arrest via modulating the PI3K/AKT and
   STAT3 signalling pathways
SO JOURNAL OF BUON
LA English
DT Article
DE wogonin; colorectal cancer; autophagy; apoptosis
ID NATURAL-PRODUCTS; ACTIVATION
AB Purpose: The purpose of this study was to examine the anticancer effects of a flavone from Scutellaria baicalensis wogonin against a panel of colorectal cancer cells.
   Methods: The SW1417, SW48, DLD-1, HCT-I5, LS-180 and CCD-18Co cell lines were used for the evaluation of the anticancer effects of wogonin. WST-1 and colony formation assays were used for cell viability assessment. Cell cycle analysis was assessed by flow cytometry. Autophagy was detected by electron microscopy. Apoptosis was detected by acridine orange (AO)/ethidium bromide (EB) staining. Cell protein expression was checked by western blotting.
   Results: The cytotoxic effects of wogonin were comparatively negligible against the normal CCD-18Co cells with an IC50 of >100 mu M. Investigation of the mechanism of action revealed that wogonin exerts growth inhibitory effects on the SW48 colorectal cancer cells by autophagic and apoptotic cell death. This was also accompanied with upregulation of autophagic proteins such as LC3II and Beclin 1 as well as the apoptotic proteins such as caspase 3, 8 and 9 and Bax expressions. Wogonin also induced arrest of the SW48 cells at the G2/M check point of the cell cycle. In addition, wogonin could also inhibit the PI3K/AKT and STAT3 signal transduction pathways.
   Conclusion: These results suggest that wogonin exerts potent anticancer effects on colorectal cancer cells and may prove essential in the management of colorectal cancer.
C1 [Tan, Hao; Li, Xiang; Yang, Wei-Han; Kang, Yong] Shanxi Prov Acad Tradit Chinese Med, Bing Zhouxi St 46, Taiyuan 030012, Shanxi, Peoples R China.
RP Kang, Y (corresponding author), Shanxi Prov Acad Tradit Chinese Med, Bing Zhouxi St 46, Taiyuan 030012, Shanxi, Peoples R China.
EM KNanceylse@yahoo.com
CR Aran V, 2016, CLIN COLORECTAL CANC, V15, P195, DOI 10.1016/j.clcc.2016.02.008
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NR 23
TC 19
Z9 21
U1 1
U2 3
PU IMPRIMATUR PUBLICATIONS
PI ATHENS
PA 30 DEM POLIORKETES ST, ATHENS, 136 76, GREECE
SN 1107-0625
EI 2241-6293
J9 J BUON
JI J. BUON
PD MAY-JUN
PY 2019
VL 24
IS 3
BP 1143
EP 1149
PG 7
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA ID6CK
UT WOS:000471764000038
PM 31424673
DA 2022-04-25
ER

PT J
AU Zhang, JX
   Tan, P
   Guo, L
   Gong, J
   Ma, JJ
   Li, J
   Lee, M
   Fang, SH
   Jing, J
   Johnson, G
   Sun, DQ
   Cao, WM
   Dashwood, R
   Han, L
   Zhou, YB
   Dong, WG
   Huang, Y
AF Zhang, Jixiang
   Tan, Peng
   Guo, Lei
   Gong, Jing
   Ma, Jingjing
   Li, Jia
   Lee, Minjung
   Fang, Shaohai
   Jing, Ji
   Johnson, Gavin
   Sun, Deqiang
   Cao, Wen-ming
   Dashwood, Roderick
   Han, Leng
   Zhou, Yubin
   Dong, Wei-Guo
   Huang, Yun
TI p53-dependent autophagic degradation of TET2 modulates cancer
   therapeutic resistance
SO ONCOGENE
LA English
DT Article
ID DNA-DAMAGE; STEM-CELLS; P53; 5-HYDROXYMETHYLCYTOSINE; 5-METHYLCYTOSINE;
   ANTICANCER; MUTATIONS; MOUSE; REPLICATION; METHYLATION
AB Tumor cells with p53 inactivation frequently exhibit chemotherapy resistance, which poses a long-standing challenge to cancer treatment. Here we unveiled a previously unrecognized role of TET2 in mediating p53-loss induced chemotherapy resistance in colon cancer. Deletion of TET2 in p53-null colon cancer cells enhanced DNA damage and restored chemotherapy sensitivity. By taking a two-pronged approach that combined pharmacological inhibition with genetic depletion, we discovered that p53 destabilized TET2 at the protein level by promoting its autophagic degradation. At the molecular level, we further revealed a physical association between TET2 and p53 that facilitated the nucleoplasmic shuttling of TET2, as well as its recruitment to the autophagosome for degradation. Our study has unveiled a functional interplay between TET2 and p53 during anti-cancer therapy. Our findings establish the rationale for targeting TET2 to overcome chemotherapy resistance associated with mutant p53 tumors.
C1 [Zhang, Jixiang; Guo, Lei; Li, Jia; Lee, Minjung; Fang, Shaohai; Johnson, Gavin; Sun, Deqiang; Dashwood, Roderick; Huang, Yun] Texas A&M Univ, Ctr Epigenet & Dis Prevent, Inst Biosci & Technol, Houston, TX 77030 USA.
   [Zhang, Jixiang; Ma, Jingjing; Dong, Wei-Guo] Wuhan Univ, Dept Gastroenterol, Renmin Hosp, Wuhan 430060, Hubei, Peoples R China.
   [Tan, Peng; Guo, Lei; Jing, Ji; Zhou, Yubin] Texas A&M Univ, Inst Biosci & Technol, Ctr Translat Canc Res, Houston, TX 77030 USA.
   [Gong, Jing; Han, Leng] Univ Texas Hlth Sci Ctr Houston, McGovern Med Sch, Dept Biochem & Mol Biol, Houston, TX 77030 USA.
   [Cao, Wen-ming] Zhejiang Canc Hosp, Dept Breast Med Oncol, Hangzhou 310022, Zhejiang, Peoples R China.
   [Dashwood, Roderick; Huang, Yun] Texas A&M Univ, Coll Med, Dept Mol & Cellular Med, College Stn, TX 77843 USA.
   [Zhou, Yubin] Texas A&M Univ, Coll Med, Dept Med Physiol, Temple, TX 76504 USA.
RP Huang, Y (corresponding author), Texas A&M Univ, Ctr Epigenet & Dis Prevent, Inst Biosci & Technol, Houston, TX 77030 USA.; Dong, WG (corresponding author), Wuhan Univ, Dept Gastroenterol, Renmin Hosp, Wuhan 430060, Hubei, Peoples R China.; Zhou, YB (corresponding author), Texas A&M Univ, Inst Biosci & Technol, Ctr Translat Canc Res, Houston, TX 77030 USA.; Huang, Y (corresponding author), Texas A&M Univ, Coll Med, Dept Mol & Cellular Med, College Stn, TX 77843 USA.; Zhou, YB (corresponding author), Texas A&M Univ, Coll Med, Dept Med Physiol, Temple, TX 76504 USA.
EM yzhou@ibt.tamhsc.edu; dwg@whu.edu.cn; yun.huang@ibt.tamhsc.edu
RI Zhou, Yubin/D-4748-2011; Dashwood, Roderick/AAF-2025-2020; Tan,
   Peng/ABD-8190-2020
OI Zhou, Yubin/0000-0001-7962-0517; Cao, Wen-Ming/0000-0002-5644-3156; Tan,
   Peng/0000-0001-6992-9000; sun, deqiang/0000-0002-5806-7289; Fang,
   Shaohai/0000-0003-3940-9586
FU Cancer Prevention and Research Institute of Texas [RR140053, RP170660,
   RR150085]; American Heart AssociationAmerican Heart Association
   [16IRG27250155]; John S. Dunn Foundation; Center for Translational
   Environmental Health Research (CTEHR); National Institute of
   HealthUnited States Department of Health & Human ServicesNational
   Institutes of Health (NIH) - USA [R01HL134780, R01GM112003]; Welch
   FoundationThe Welch Foundation [BE-1913]; American Cancer
   SocietyAmerican Cancer Society [RSG-18-043-01-LIB, RSG-16-215-01-TBE];
   Texas AM University; NATIONAL HEART, LUNG, AND BLOOD INSTITUTEUnited
   States Department of Health & Human ServicesNational Institutes of
   Health (NIH) - USANIH National Heart Lung & Blood Institute (NHLBI)
   [R01HL134780] Funding Source: NIH RePORTER; NATIONAL INSTITUTE OF
   GENERAL MEDICAL SCIENCESUnited States Department of Health & Human
   ServicesNational Institutes of Health (NIH) - USANIH National Institute
   of General Medical Sciences (NIGMS) [R01GM112003] Funding Source: NIH
   RePORTER
FX This work was supported by grants from Cancer Prevention and Research
   Institute of Texas (RR140053 to YH, to RP170660 to YZ, RR150085 to LH),
   the Innovation Award from American Heart Association (16IRG27250155 to
   YH), the John S. Dunn Foundation Collaborative Research Award (to YH),
   the Center for Translational Environmental Health Research (CTEHR) Seed
   Grant to YH, the National Institute of Health grants (R01HL134780 to YH,
   R01GM112003 to YZ), the Welch Foundation (BE-1913 to YZ), the American
   Cancer Society (RSG-18-043-01-LIB to YH, RSG-16-215-01-TBE to YZ), and
   by an allocation from the Texas A&M University start-up funds (YH).
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NR 44
TC 10
Z9 11
U1 1
U2 10
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0950-9232
EI 1476-5594
J9 ONCOGENE
JI Oncogene
PD MAR 14
PY 2019
VL 38
IS 11
BP 1905
EP 1919
DI 10.1038/s41388-018-0524-5
PG 15
WC Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics &
   Heredity
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics &
   Heredity
GA HO7XX
UT WOS:000461164400009
PM 30390073
OA Green Accepted
DA 2022-04-25
ER

PT J
AU Li, TY
   Liu, DN
   Lei, X
   Jiang, QG
AF Li, Taiyuan
   Liu, Dongning
   Lei, Xiong
   Jiang, Qunguang
TI Par3L enhances colorectal cancer cell survival by inhibiting Lkb1/AMPK
   signaling pathway
SO BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
LA English
DT Article
DE Par3L; CRISPR/Cas; Colorectal cancer; AMPIC pathway; Lkb1
ID HEPATOCELLULAR-CARCINOMA; POOR-PROGNOSIS; LKB1; EXPRESSION; AMPK;
   METASTASIS; METABOLISM; AUTOPHAGY; PAR-3
AB Partitioning defective 3-like protein (Par3L) is a recently identified cell polarity protein that plays an important role in mammary stem cell maintenance. Previously, we showed that high expression of Par3L is associated with poor survival in malignant colorectal cancer (CRC), but the underlying mechanism remained unknown. To this end, we established a Par3L knockout colorectal cancer cell line using the CRISPR/Cas system. Interestingly, reduced proliferation, enhanced cell death and caspase-3 activation were observed in Par3L knockout (KO) cells as compared with wildtype (WT) cells. Consistent with previous studies, we showed that Par3L interacts with a tumor suppressor protein liver kinase B1 (Lkb1). Moreover, Par3L depletion resulted in abnormal activation of Lkb1 /AMPKsignaling cascade. Knockdown of Lkb1 in these cells could significantly reduce AMPK activity and partially rescue cell death caused by Par3L knockdown. Furthermore, we showed that Par3L KO cells were more sensitive to chemotherapies and irradiation. Together, these results suggest that Par3L is essential for colorectal cancer cell survival by inhibiting Lkb1/AMPK signaling pathway, and is a putative therapeutic target for CRC. (C) 2016 Elsevier Inc. All rights reserved.
C1 [Li, Taiyuan; Liu, Dongning; Lei, Xiong; Jiang, Qunguang] Nanchang Univ, Affiliated Hosp 1, Dept Gastrointestinal Surg, Nanchang, Jiangxi, Peoples R China.
RP Jiang, QG (corresponding author), Nanchang Univ, Hosp Nanchang 1, 17 Yongwai St, Nanchang 330006, Jiangxi, Peoples R China.
EM JiangQG168@gmail.com
FU National Natural Science Foundation of ChinaNational Natural Science
   Foundation of China (NSFC) [81560397]
FX This work was supported by the National Natural Science Foundation of
   China (81560397).
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NR 18
TC 10
Z9 11
U1 1
U2 15
PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 0006-291X
EI 1090-2104
J9 BIOCHEM BIOPH RES CO
JI Biochem. Biophys. Res. Commun.
PD JAN 22
PY 2017
VL 482
IS 4
BP 1037
EP 1041
DI 10.1016/j.bbrc.2016.11.154
PG 5
WC Biochemistry & Molecular Biology; Biophysics
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Biophysics
GA EK1XB
UT WOS:000393720000079
PM 27908725
DA 2022-04-25
ER

PT J
AU Chen, MC
   Lin, YC
   Liao, YH
   Liou, JP
   Chen, CH
AF Chen, Mei-Chuan
   Lin, Yu-Chen
   Liao, Yu-Hsuan
   Liou, Jing-Ping
   Chen, Chun-Han
TI MPT0G612, a Novel HDAC6 Inhibitor, Induces Apoptosis and Suppresses
   IFN-gamma-Induced Programmed Death-Ligand 1 in Human Colorectal
   Carcinoma Cells
SO CANCERS
LA English
DT Article
DE HDAC6; apoptosis; autophagy; PD-L1; colorectal cancer
ID HISTONE DEACETYLASE INHIBITORS; CANCER; GROWTH; IDENTIFICATION;
   DEXAMETHASONE; RICOLINOSTAT; ACETYLATION; COMBINATION; EXPRESSION;
   BORTEZOMIB
AB Colorectal cancer (CRC) is the third most common cancer and the leading cause of cancer-associated death worldwide. Histone deacetylases (HDACs) have been implicated in regulating complex cellular mechanisms to influence tumor biology and immunogenicity in various types of cancer. The potential of selective inhibition of HDAC6 has been widely discussed for the treatment of hematologic malignancies. We previously identified that MPT0G612 is a novel HDAC6 inhibitor exhibiting a promising antitumor activity against several solid tumors. The purpose of the present study was to evaluate the feasibility and pharmacological mechanisms of MPT0G612 as a potential therapy for CRC patients. Results revealed that MPT0G612 significantly suppresses the proliferation and viability, as well as induces apoptosis in CRC cells. Autophagy activation with LC3B-II formation and p62 degradation was observed, and the inhibition of autophagy by pharmacological inhibitor or Atg5 knockdown enhances MPT0G612-induced cell death. In addition, HDAC6 knockdown reduces MPT0G612-mediated autophagy and further potentiates apoptotic cell death. Furthermore, MPT0G612 downregulates the expression of PD-L1 induced by IFN-gamma in CRC cells. These results suggest that MPT0G612 is a potent cell death inducer through inhibiting HDAC6-associated pathway, and a potential agent for combination strategy with immune checkpoint inhibitors for the treatment of CRC.
C1 [Chen, Mei-Chuan; Liao, Yu-Hsuan] Taipei Med Univ, Coll Pharm, PhD Program Clin Drug Dev Herbal Med, Taipei 110, Taiwan.
   [Chen, Mei-Chuan] Taipei Med Univ Hosp, Tradit Herbal Med Res Ctr, Taipei 110, Taiwan.
   [Lin, Yu-Chen; Chen, Chun-Han] Taipei Med Univ, Coll Med, Sch Med, Dept Pharmacol, Taipei 110, Taiwan.
   [Liou, Jing-Ping] Taipei Med Univ, Coll Pharm, Sch Pharm, Taipei 110, Taiwan.
   [Chen, Chun-Han] Taipei Med Univ, Wan Fang Hosp, Cell Physiol & Mol Image Res Ctr, Taipei 110, Taiwan.
RP Chen, CH (corresponding author), Taipei Med Univ, Coll Med, Sch Med, Dept Pharmacol, Taipei 110, Taiwan.; Chen, CH (corresponding author), Taipei Med Univ, Wan Fang Hosp, Cell Physiol & Mol Image Res Ctr, Taipei 110, Taiwan.
EM mcchen1250@tmu.edu.tw; amylin0083@tmu.edu.tw; a0916143813@gmail.com;
   jpl@tmu.edu.tw; brianchc@tmu.edu.tw
FU Ministry of Science and Technology of the Republic of ChinaMinistry of
   Science and Technology, China [MOST 107-2320-B-038-039]; Taipei Medical
   University [TMU104-AE1-B32]
FX This research was funded by the Ministry of Science and Technology of
   the Republic of China, grant number MOST 107-2320-B-038-039, and by
   Taipei Medical University, grand number TMU104-AE1-B32.
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NR 72
TC 12
Z9 13
U1 0
U2 6
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 2072-6694
J9 CANCERS
JI Cancers
PD OCT
PY 2019
VL 11
IS 10
AR 1617
DI 10.3390/cancers11101617
PG 15
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA JQ3CF
UT WOS:000498826000214
PM 31652644
OA Green Published, gold
DA 2022-04-25
ER

PT J
AU Zhidkov, ME
   Smirnova, PA
   Tryapkin, OA
   Kantemirov, AV
   Khudyakova, YV
   Malyarenko, OS
   Ermakova, SP
   Grigorchuk, VP
   Kaune, M
   von Amsberg, G
   Dyshlovoy, SA
AF Zhidkov, Maxim E.
   Smirnova, Polina A.
   Tryapkin, Oleg A.
   Kantemirov, Alexey V.
   Khudyakova, Yuliya V.
   Malyarenko, Olesya S.
   Ermakova, Svetlana P.
   Grigorchuk, Valeria P.
   Kaune, Moritz
   von Amsberg, Gunhild
   Dyshlovoy, Sergey A.
TI Total Syntheses and Preliminary Biological Evaluation of Brominated
   Fascaplysin and Reticulatine Alkaloids and Their Analogues
SO MARINE DRUGS
LA English
DT Article
DE total synthesis; 14-bromoreticulatine; 3; 10-dibromofascaplysin;
   bioactivity
ID 1ST SYNTHESES; MARINE; PIGMENT; APOPTOSIS; SESTERTERPENE; ANGIOGENESIS;
   INHIBITION; AUTOPHAGY; CARBOLINE; PRODUCTS
AB A simple approach toward the synthesis of the marine sponge derived pigment fascaplysin was used to obtain the marine alkaloids 3-bromofascaplysin and 3,10-dibromofascaplysin. These compounds were used for first syntheses of the alkaloids 14-bromoreticulatate and 14-bromoreticulatine. Preliminary bioassays showed that 14-bromoreticulatine has a selective antibiotic (to Pseudomonas aeruginosa) activity and reveals cytotoxicity toward human melanoma, colon, and prostate cancer cells. 3,10-Dibromofascaplysin was able to target metabolic activity of the prostate cancer cells, without disrupting cell membrane's integrity and had a wide therapeutic window amongst the fascaplysin alkaloids.
C1 [Zhidkov, Maxim E.; Smirnova, Polina A.; Tryapkin, Oleg A.; Kantemirov, Alexey V.; Dyshlovoy, Sergey A.] Far Eastern Fed Univ, Sch Nat Sci, Dept Organ Chem, 8 Sukhanov Str, Vladivostok 690950, Russia.
   [Zhidkov, Maxim E.; Smirnova, Polina A.; Tryapkin, Oleg A.; Kantemirov, Alexey V.; Dyshlovoy, Sergey A.] Far Eastern Fed Univ, Sch Nat Sci, Lab Biol Act Cpds, 8 Sukhanov Str, Vladivostok 690950, Russia.
   [Khudyakova, Yuliya V.; Malyarenko, Olesya S.; Ermakova, Svetlana P.; Dyshlovoy, Sergey A.] GB Elyakov Pacific Inst Bioorgan Chem, 159 Prospekt 100 Let Vladivostoku, Vladivostok 690022, Russia.
   [Grigorchuk, Valeria P.] Russian Acad Sci, Inst Biol & Soil Sci, Fed Sci Ctr East Asia Terr Biodivers, Far Eastern Branch, 159 Prospect 100 Let Vladivostoku, Vladivostok 690022, Russia.
   [Kaune, Moritz; von Amsberg, Gunhild; Dyshlovoy, Sergey A.] Univ Med Ctr Hamburg Eppendorf, Hubertus Wald Tumorzentrum, Dept Oncol Hematol & Bone Marrow Transplantat, Sect Pneumol, D-20246 Hamburg, Germany.
   [von Amsberg, Gunhild; Dyshlovoy, Sergey A.] Univ Hosp Hamburg Eppendorf, Martini Klin, Prostate Canc Ctr, D-20246 Hamburg, Germany.
RP Zhidkov, ME (corresponding author), Far Eastern Fed Univ, Sch Nat Sci, Dept Organ Chem, 8 Sukhanov Str, Vladivostok 690950, Russia.; Zhidkov, ME (corresponding author), Far Eastern Fed Univ, Sch Nat Sci, Lab Biol Act Cpds, 8 Sukhanov Str, Vladivostok 690950, Russia.
EM mzhidkov@rambler.ru
RI Grigorchuk, Valeria/T-3780-2018; Tryapkin, Oleg/AAP-7891-2021; Ermakova,
   Svetlana P/G-2766-2013; Malyarenko, Olesya/AAQ-6336-2021; Dyshlovoy,
   Sergey A./B-3586-2013; , Maxim/F-1272-2014
OI Malyarenko, Olesya/0000-0002-3262-0373; Dyshlovoy, Sergey
   A./0000-0002-7155-9245; Tryapkin, Oleg/0000-0001-8732-0055; ,
   Maxim/0000-0001-5754-2554
FU FEFU Endowment Foundation [D-349-17]
FX This research was funded by the FEFU Endowment Foundation grant number
   D-349-17. And the APC was funded by grant D-349-17.
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NR 42
TC 9
Z9 9
U1 2
U2 9
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 1660-3397
J9 MAR DRUGS
JI Mar. Drugs
PD SEP
PY 2019
VL 17
IS 9
AR 496
DI 10.3390/md17090496
PG 12
WC Chemistry, Medicinal; Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA JA6NS
UT WOS:000487959700026
PM 31450717
OA Green Published, gold
DA 2022-04-25
ER

PT J
AU Martinez-Delgado, G
   Felix, R
AF Martinez-Delgado, Gustavo
   Felix, Ricardo
TI Emerging Role of Ca(V)1.2 Channels in Proliferation and Migration in
   Distinct Cancer Cell Lines
SO ONCOLOGY
LA English
DT Review
DE Ca2+ channels; Ca(V)1.2 channels; Cancer; Cell proliferation; Autophagy
ID CALCIUM-CHANNEL; ION CHANNELS; FIBROBLAST CELL; COLON-CANCER; CA2+;
   GROWTH; PROGRESSION; ANTAGONISTS; EXPRESSION; PROTEIN
AB Extensive research is currently underway, seeking better diagnostic methods and treatments and a better understanding of the molecular mechanisms involved in cancer, from the role of specific genetic mutations to the intricate biochemical and molecular pathways involved. Because of their role in regulating relevant physiological events such as cell proliferation, migration, and invasion, ion channels have recently been recognized as important elements in cancer initiation and progression. Moreover, it has been reported that pharmacological intervention in ion channel activity might provide protection against diverse types of cancer, and that ion channels could be used as targets to counteract tumor growth, prevent metastasis, and overcome the therapy resistance of tumor cells. In this context, Ca2+ channels have been found to play a role in tumorigenesis and tumor progression. Specifically, L-type Ca2+ channel inhibition may affect cell proliferation, differentiation, and apoptosis. This review aims to provide insights into the potential role of these channels in cancer cell lines, emphasizing their participation in cell proliferation, migration, and autophagy induction, as well as their potential as rational targets for new cancer therapeutics. (C) 2017 S. Karger AG, Basel
C1 [Martinez-Delgado, Gustavo] Inst Nacl Med Genom, Consejo Nacl Ciencia & Tecnol CONACYT, Lab Genom Enfermedades Cardiovasc, Mexico City, DF, Mexico.
   [Felix, Ricardo] IPN, Ctr Res & Adv Studies, Dept Cell Biol, Natl Polytech Inst Cinvestav, Mexico City, DF, Mexico.
RP Martinez-Delgado, G (corresponding author), INMEGEN, Lab Genom Enfermedades Cardiovasc, Perifer Sur 4809, Mexico City 14610, DF, Mexico.; Felix, R (corresponding author), IPN, CINVESTAV, Dept Cell Biol, Ave IPN 2508, Mexico City 07360, DF, Mexico.
EM gmartinezd@inmegen.gob.mx; rfelix@cinvestav.mx
RI Felix, Ricardo/A-6989-2008; Martinez-Delgado, Gustavo/X-7033-2019
OI Felix, Ricardo/0000-0002-5383-7176; Martinez-Delgado,
   Gustavo/0000-0003-4655-3770
FU Conacyt-MexicoConsejo Nacional de Ciencia y Tecnologia (CONACyT)
   [221660]
FX The authors appreciate the critical review of Dr. Maria T. Villarreal.
   Work in the Genomics of Cardiovascular Diseases Laboratory is founded by
   the National Institute of Genomic Medicine (INMEGEN) and the National
   Council for Science and Technology (Conacyt-Mexico). Work in the Felix
   laboratory is partially founded by Conacyt-Mexico (grant 221660).
   Finally, we also thank the 3 anonymous reviewers commissioned by
   Oncology for their insightful comments and criticisms.
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NR 70
TC 4
Z9 4
U1 0
U2 4
PU KARGER
PI BASEL
PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND
SN 0030-2414
EI 1423-0232
J9 ONCOLOGY-BASEL
JI Oncology
PY 2017
VL 93
IS 1
BP 1
EP 10
DI 10.1159/000464293
PG 10
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA FA0FM
UT WOS:000405106700001
PM 28355609
DA 2022-04-25
ER

PT J
AU Zhou, L
   Li, S
   Sun, J
AF Zhou, L.
   Li, S.
   Sun, J.
TI Ginkgolic acid induces apoptosis and autophagy of endometrial carcinoma
   cells via inhibiting PI3K/Akt/mTOR pathway in vivo and in vitro
SO HUMAN & EXPERIMENTAL TOXICOLOGY
LA English
DT Article
DE Ginkgolic acid; PI3K; Akt; MTOR; endometrial cancer; apoptosis;
   autophagy
ID BREAST-CANCER; COLON-CANCER; PHOSPHATIDYLINOSITOL; EXPRESSION; GROWTH
AB Endometrial cancer (EC) is the fourth most common malignancy in women in developed countries. The prognosis of EC is extremely poor, and it is an important factor that contributes to the death of patients. Therefore, studying EC pathogenesis and therapeutic targets, and exploring effective drugs are the primary tasks to improve the prognosis of EC. In the present study, we aimed to explore the function of ginkgolic acid (GA) in EC cell apoptosis and autophagy through PI3K/Akt/mTOR signal pathway in vitro and in vivo. Firstly, MTT assay and clone formation assay were employed to analyze the Ishikawa and HEC-1-B cell viabilities and proliferation after treatment with GA. The results showed that GA inhibited endometrial cancer cell survival. Flow cytometry assay and western blot assay were applied to examine the apoptosis and apoptosis related protein Bcl-2, Bax, Cleaved caspase-3 expression levels of Ishikawa and HEC-1-B cells after treatment with GA. Next, we applied western blot assay to analyze the autophagy associated proteins LC3I, LC3II, p62 and Beclin-1 in GA treated Ishikawa and HEC-1-B cells. We found that GA promoted apoptosis and induced autophagy of endometrial cancer cells. Meanwhile, western blot assay was also used to determine the expression levels of the PI3K/Akt/mTOR signal pathway related protein and the results revealed that GA inhibited the activity of PI3K/Akt/mTOR pathway. Finally, we found that GA inhibited tumor growth in vivo through immunohistochemistry assay. In conclusion, GA induces apoptosis and autophagy of EC cells via inhibiting PI3K/Akt/mTOR pathway in vivo and vitro.
C1 [Zhou, L.; Li, S.] Henan Univ Chinese Med, Dept Obstet & Gynaecol, Affiliated Hosp 1, 19 Renmin Rd, Zhengzhou 450000, Henan, Peoples R China.
   [Sun, J.] Henan Univ Chinese Med, Dept Obstet & Gynaecol, Zhengzhou, Henan, Peoples R China.
RP Li, S (corresponding author), Henan Univ Chinese Med, Dept Obstet & Gynaecol, Affiliated Hosp 1, 19 Renmin Rd, Zhengzhou 450000, Henan, Peoples R China.
EM lishurong54321@163.com
FU Youth fund of National Natural Science Foundation of ChinaNational
   Natural Science Foundation of China (NSFC) [82004412]
FX The author(s) disclosed receipt of the following financial support for
   the research, authorship, and/or publication of this article: This work
   was supported by the Youth fund of National Natural Science Foundation
   of China (Grant No. 82004412).
CR Aghajanian C, 2018, GYNECOL ONCOL, V150, P274, DOI 10.1016/j.ygyno.2018.05.018
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NR 36
TC 0
Z9 0
U1 4
U2 6
PU SAGE PUBLICATIONS LTD
PI LONDON
PA 1 OLIVERS YARD, 55 CITY ROAD, LONDON EC1Y 1SP, ENGLAND
SN 0960-3271
EI 1477-0903
J9 HUM EXP TOXICOL
JI Hum. Exp. Toxicol.
PD DEC
PY 2021
VL 40
IS 12
BP 2156
EP 2164
AR 09603271211023789
DI 10.1177/09603271211023789
EA JUN 2021
PG 9
WC Toxicology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Toxicology
GA XG8WY
UT WOS:000669076300001
PM 34132136
DA 2022-04-25
ER

PT J
AU Zhang, N
   Peng, F
   Wang, YJ
   Yang, L
   Wu, FB
   Wang, XY
   Ye, C
   Han, B
   He, G
AF Zhang, Nan
   Peng, Fu
   Wang, Yujia
   Yang, Li
   Wu, Fengbo
   Wang, Xiaoyun
   Ye, Cui
   Han, Bo
   He, Gu
TI Shikonin induces colorectal carcinoma cells apoptosis and autophagy by
   targeting galectin-1/JNK signaling axis
SO INTERNATIONAL JOURNAL OF BIOLOGICAL SCIENCES
LA English
DT Article
DE Shikonin; Colorectal carcinoma; Galectin-1; apoptosis; autophagy
ID CANCER-CELLS; ACTIVATION; JNK; DERIVATIVES; INHIBITOR; DEATH;
   IDENTIFICATION; GLYCOSYLATION; INFLAMMATION; MODULATION
AB Colorectal carcinoma (CRC) is the third most common malignant tumor pathology worldwide. Despite progress in surgical procedures and therapy options, CRC is still a considerable cause of cancer-related mortality. In this study, we tested the antitumor effects of shikonin in CRC and tried to identify its potential mechanism. The potential target, molecular mechanism as well as in vitro and in vivo antitumor effects of shikonin in CRC cells were determined by an integrative protocol including quantitative proteomics, RT-PCR, western blotting, RNA interference and overexpression, apoptosis and autophagy assays, etc. Galectin-1 was a potential target of shikonin from the iTRAQ-based proteomic analysis in shikonin-treated SW620 cell. The overexpression and RNA silencing of galectin-1 in two CRC cells suggested that the shikonin sensitivity was correlation to galectin-1 levels. The ROS accumulation induced by shikonin was important to the formation of galectin-1 dimers. Dimer galectin-1 was found to be associated with the activation of JNK and downstream apoptosis or autophagy. Moreover, through functional in vitro studies, we showed that differences in galectin-1 level affected tumor cell proliferation, migration, and invasion. In summary, shikonin induced CRC cells apoptosis and autophagy by targeting galectin-1 and JNK signaling pathway both in vitro and in vivo, which suggested a potential novel therapy target for CRC.
C1 [Zhang, Nan; Ye, Cui; Han, Bo] Chengdu Univ Tradit Chinese Med, Sch Pharm, State Key Lab Southwestern Chinese Med Resources, Chengdu 611137, Sichuan, Peoples R China.
   [Peng, Fu; Wang, Yujia; Yang, Li; Wu, Fengbo; Wang, Xiaoyun; He, Gu] Sichuan Univ, State Key Lab Biotherapy, West China Hosp, Chengdu 610041, Sichuan, Peoples R China.
   [Peng, Fu; Wang, Yujia; Yang, Li; Wu, Fengbo; Wang, Xiaoyun; He, Gu] Sichuan Univ, Ctr Canc, West China Hosp, Chengdu 610041, Sichuan, Peoples R China.
   [Peng, Fu; Wang, Yujia; Yang, Li; Wu, Fengbo; Wang, Xiaoyun; He, Gu] Sichuan Univ, West China Sch Pharm, Chengdu 610041, Sichuan, Peoples R China.
RP Han, B (corresponding author), Chengdu Univ Tradit Chinese Med, Sch Pharm, State Key Lab Southwestern Chinese Med Resources, Chengdu 611137, Sichuan, Peoples R China.; He, G (corresponding author), Sichuan Univ, State Key Lab Biotherapy, West China Hosp, Chengdu 610041, Sichuan, Peoples R China.; He, G (corresponding author), Sichuan Univ, Ctr Canc, West China Hosp, Chengdu 610041, Sichuan, Peoples R China.; He, G (corresponding author), Sichuan Univ, West China Sch Pharm, Chengdu 610041, Sichuan, Peoples R China.
EM hanbo@cdutcm.edu.cn; hegu@scu.edu.cn
RI He, Gu/G-5446-2015
OI He, Gu/0000-0002-1536-8882
FU National Natural Science Foundation of ChinaNational Natural Science
   Foundation of China (NSFC) [21772131, 81630101, 81891012, 81573588,
   81773889]; Science & Technology Department of Sichuan Province
   [2017JZYD0001, 2017JY0323, 2019YFSY0004]
FX We are grateful for financial support from the National Natural Science
   Foundation of China (21772131, 81630101, 81891012, 81573588 and
   81773889), the Science & Technology Department of Sichuan Province
   (2017JZYD0001, 2017JY0323 and 2019YFSY0004).
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NR 73
TC 20
Z9 23
U1 4
U2 27
PU IVYSPRING INT PUBL
PI LAKE HAVEN
PA PO BOX 4546, LAKE HAVEN, NSW 2263, AUSTRALIA
SN 1449-2288
J9 INT J BIOL SCI
JI Int. J. Biol. Sci.
PY 2020
VL 16
IS 1
BP 147
EP 161
DI 10.7150/ijbs.36955
PG 15
WC Biochemistry & Molecular Biology; Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
   Topics
GA JR4VF
UT WOS:000499624000012
PM 31892852
OA Green Published, gold
DA 2022-04-25
ER

PT J
AU Xing, Y
   Wang, ZH
   Ma, DH
   Han, Y
AF Xing, Ying
   Wang, Zhi Hong
   Ma, Dong Hong
   Han, Ying
TI FTY720 enhances chemosensitivity of colon cancer cells to doxorubicin
   and etoposide via the modulation of P-glycoprotein and multidrug
   resistance protein 1
SO JOURNAL OF DIGESTIVE DISEASES
LA English
DT Article
DE apoptosis; multidrug resistance protein 1; P-glycoprotein; chemotherapy;
   multidrug resistance; FTY720
ID HEPATOCELLULAR-CARCINOMA CELLS; GASTRIC-CANCER; TUMOR-GROWTH; IN-VITRO;
   FINGOLIMOD FTY720; ABC TRANSPORTERS; DRUG-RESISTANCE; APOPTOSIS;
   EXPRESSION; AUTOPHAGY
AB Objective
   This study aimed to investigate the effects of FTY720 on inducing cell growth inhibition and enhancing the cytotoxicity of anti-cancer drugs in the human colon cancer cell line HCT-8 and its multidrug-resistant cell line HCT-8/5-fluorouracil (HCT-8/5-Fu).
   Methods
   Cell viability and apoptosis after being treated with FTY720 alone or in combination with doxorubicin (DOX) and etoposide (VP16) were tested in HCT-8 and HCT-8/5-Fu cells. The changes in P-glycoprotein (P-gp) and multidrug resistance protein 1 (MRP1) were determined at the mRNA and functional levels.
   Results
   FTY720 showed anti-proliferative activity against cancer cells in a dose-dependent and time-dependent manner and could enhance the cytotoxicity of DOX and VP16 in both HCT-8 and HCT-8/5-Fu cell lines. In addition, treatment with FTY720 resulted in the promotion of VP16-induced cell apoptosis and an increased accumulation of intracellular DOX and two specific fluorescent substrates of P-gp and MRP1 through the inhibition of efflux and the suppression of gene expression.
   Conclusion
   FTY720 exerts its chemosensitization effect in HCT-8 and HCT-8/5-Fu cell lines by promoting cell apoptosis and inhibiting P-gp and MRP1, which could be applied as a potential co-adjuvant therapeutic modality.
C1 [Xing, Ying] Gen Hosp Beijing Mil Command, Med Sch Chinese PLA, Beijing 100700, Peoples R China.
   [Wang, Zhi Hong; Ma, Dong Hong; Han, Ying] Gen Hosp Beijing Mil Command, Dept Gastroenterol, Beijing 100700, Peoples R China.
RP Han, Y (corresponding author), Gen Hosp Beijing Mil Command, Dept Gastroenterol, 5 Nanmencang, Beijing 100700, Peoples R China.
EM yh721303@sina.com
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NR 49
TC 20
Z9 22
U1 0
U2 12
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1751-2972
EI 1751-2980
J9 J DIGEST DIS
JI J. Dig. Dis.
PD MAY
PY 2014
VL 15
IS 5
BP 246
EP 259
DI 10.1111/1751-2980.12131
PG 14
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA AF4LT
UT WOS:000334684800005
PM 24868599
DA 2022-04-25
ER

PT J
AU Gao, L
   Sun, X
   Zhang, Q
   Chen, XC
   Zhao, TW
   Lu, LQ
   Zhang, JB
   Hong, YP
AF Gao, Liang
   Sun, Xin
   Zhang, Qi
   Chen, Xiaochen
   Zhao, Tongwei
   Lu, Liqing
   Zhang, Jianbin
   Hong, Yupeng
TI Histone deacetylase inhibitor trichostatin A and autophagy inhibitor
   chloroquine synergistically exert anti-tumor activity in H-ras
   transformed breast epithelial cells
SO MOLECULAR MEDICINE REPORTS
LA English
DT Article
DE trichostatin A; histone deacetylase inhibitor; apoptosis; autophagy;
   MCF10A-ras cells; chloroquine
ID APOPTOSIS; CANCER; DEATH; MECHANISMS; EXPRESSION; CARCINOMA; SURVIVAL;
   THERAPY
AB Histone deacetylase inhibitors (HDACIs) cause oncogene-transformed mammalian cell death. Our previous study indicated that HDACIs activate forkhead box O1 (FOXO1) and induce autophagy in liver and colon cancer cells. However, whether FOXO1 is involved in HDACI-mediated oncogene-transformed mammalian cell death remains unclear. In the present study, H-ras transformed MCF10A cells were used to investigate the role of FOXO1 in this pathway. Results showed that trichostatin A (TSA), a HDACI, activated apoptosis in MCF10A-ras cells, but not in MCF10A cells. Furthermore, TSA activated FOXO1 via P21 upregulation, whereas the knockdown of FOXO1 reduced TSA-induced cell death. In addition, TSA induced autophagy in MCF10A and MCF10A-ras cells by blocking the mammailian target of rapamycin signaling pathway. Furthermore, autophagy inhibition lead to higher MCF10A-ras cell death by TSA, thus indicating that autophagy is essential in cell survival. Taken together, the present study demonstrated that TSA causes oncogene-transformed cell apoptosis via activation of FOXO1 and HDACI-mediated autophagy induction, which served as important cell survival mechanisms. Notably, the present findings imply that a combination of HDACIs and autophagy inhibitors produce a synergistic anticancer effect.
C1 [Gao, Liang; Sun, Xin; Chen, Xiaochen; Zhao, Tongwei; Lu, Liqing; Zhang, Jianbin; Hong, Yupeng] Hangzhou Med Coll, Peoples Hosp, Zhejiang Prov Peoples Hosp, Dept Oncol, 158 Shangtang Rd, Hangzhou 310014, Zhejiang, Peoples R China.
   [Zhang, Qi] Zhejiang Univ, Sch Med, Affiliated Hosp 2, Dept Hepatobiliary & Pancreat Surg, Hangzhou 310002, Zhejiang, Peoples R China.
RP Zhang, JB; Hong, YP (corresponding author), Hangzhou Med Coll, Peoples Hosp, Zhejiang Prov Peoples Hosp, Dept Oncol, 158 Shangtang Rd, Hangzhou 310014, Zhejiang, Peoples R China.
EM zhangjianbin@hmc.edu.cn; hypbdn@zju.edu.cn
FU Science Technology Department of Zhejiang Province, China [2015C33173];
   Traditional Chinese Medicine Fund of Zhejiang Province, China
   [2011ZA010]; Zhejiang Provincial Natural Science Foundation of
   ChinaNatural Science Foundation of Zhejiang Province [LQ18H280006]
FX This study was financially supported by the Science Technology
   Department of Zhejiang Province, China (grant no. 2015C33173), the
   Traditional Chinese Medicine Fund of Zhejiang Province, China (grant no.
   2011ZA010) and the Zhejiang Provincial Natural Science Foundation of
   China (grant no. LQ18H280006).
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NR 27
TC 6
Z9 6
U1 0
U2 2
PU SPANDIDOS PUBL LTD
PI ATHENS
PA POB 18179, ATHENS, 116 10, GREECE
SN 1791-2997
EI 1791-3004
J9 MOL MED REP
JI Mol. Med. Rep.
PD MAR
PY 2018
VL 17
IS 3
BP 4345
EP 4350
DI 10.3892/mmr.2018.8446
PG 6
WC Oncology; Medicine, Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Research & Experimental Medicine
GA FV2MB
UT WOS:000424400000116
PM 29344672
OA hybrid, Green Submitted, Green Published
DA 2022-04-25
ER

PT J
AU Zhuang, PW
   Zhang, JB
   Wang, Y
   Zhang, MX
   Song, LL
   Lu, ZQ
   Zhang, L
   Zhang, FQ
   Wang, J
   Zhang, YJ
   Wei, HJ
   Li, HY
AF Zhuang, Pengwei
   Zhang, Jinbao
   Wang, Yan
   Zhang, Mixia
   Song, Lili
   Lu, Zhiqiang
   Zhang, Lu
   Zhang, Fengqi
   Wang, Jing
   Zhang, Yanjun
   Wei, Hongjun
   Li, Hongyan
TI Reversal of muscle atrophy by Zhimu and Huangbai herb pair via
   activation of IGF-1/Akt and autophagy signal in cancer cachexia
SO SUPPORTIVE CARE IN CANCER
LA English
DT Article
DE Cancer cachexia; Skeletal muscle atrophy; Zhimu and Huangbai herb pair;
   Autophagy; IGF-1/Akt
ID GROWTH-FACTOR-I; SKELETAL-MUSCLE; MICE; MASS; ADENOCARCINOMA;
   IDENTIFICATION; INTERLEUKIN-6; DOWNSTREAM; EXPRESSION; BERBERINE
AB Muscle atrophy is the prominent clinical feature of cancer-induced cachexia. Zhimu and Huangbai herb pair (ZBHP) has been used since ancient China times and have been phytochemically investigated for constituents that might cause anti-cancer, diabetes, and their complication. In this study, the effects and mechanisms of ZBHP on reversal of muscle atrophy were explored.
   C57BL/6 mice implanted with colon-26 adenocarcinoma were chosen to develop cancer cachexia for evaluating the effects of ZBHP on reversal of muscle atrophy. The body weight, survival time, inflammatory cytokines, and pathological changes of muscle were monitored. In addition, IGF-1/Akt and autophagy pathway members were analyzed to interpret the mechanism of drug response.
   The function and morphology of skeletal muscle in cachexia model were significantly disturbed, and the survival time was shortened. Consistently, inflammatory cytokines and muscle atrophy-related atrogin-1, MuRF1, and FOXO3 were significantly increased, and IGF-1/Akt and autophagy signal pathways were depressed. Treatment with ZBHP significantly alleviated tumor-free body weight reduction and cachexia-induced changes in cytokines and prolonged survival. ZBHP treatment not only inhibited the muscle atrophy-related genes but also activated the IGF-1/Akt and autophagy signal pathways to facilitate the protein synthesis.
   The results revealed that ZBHP treatment could inhibit the muscle atrophy induced by cancer cachexia and prolong the survival time, and ZBHP may be of value as a pharmacological alternative in treatment of cancer cachexia.
C1 [Zhuang, Pengwei; Zhang, Jinbao; Wang, Yan; Zhang, Mixia; Song, Lili; Lu, Zhiqiang; Zhang, Lu; Zhang, Fengqi; Wang, Jing; Zhang, Yanjun] Tianjin Univ Tradit Chinese Med, Chinese Mat Med Coll, 312 Anshanxi Rd, Tianjin 300193, Peoples R China.
   [Zhuang, Pengwei; Wang, Yan; Zhang, Mixia; Song, Lili; Zhang, Yanjun] Tianjin Univ Tradit Chinese Med, Tianjin State Key Lab Modern Chinese Med, 312 Anshanxi Rd, Tianjin 300193, Peoples R China.
   [Zhuang, Pengwei; Wei, Hongjun; Li, Hongyan] Tianjin JF Pharmaland Technol Dev Co Ltd, Tianjin, Peoples R China.
   [Zhang, Jinbao] Gansu Univ Chinese Med, Lanzhou, Gansu, Peoples R China.
RP Zhang, YJ (corresponding author), Tianjin Univ Tradit Chinese Med, Chinese Mat Med Coll, 312 Anshanxi Rd, Tianjin 300193, Peoples R China.; Zhang, YJ (corresponding author), Tianjin Univ Tradit Chinese Med, Tianjin State Key Lab Modern Chinese Med, 312 Anshanxi Rd, Tianjin 300193, Peoples R China.
EM zyjsunye@163.com
FU National Natural Science Foundation of ChinaNational Natural Science
   Foundation of China (NSFC) [81403213]; Program for Changjiang Scholars
   and Innovative Research Team in University ("PCSIRT")Program for
   Changjiang Scholars & Innovative Research Team in University (PCSIRT)
   [IRT 14R41]
FX This work was supported by the National Natural Science Foundation of
   China (no. 81403213) and Program for Changjiang Scholars and Innovative
   Research Team in University ("PCSIRT", IRT 14R41).
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NR 37
TC 17
Z9 20
U1 4
U2 26
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0941-4355
EI 1433-7339
J9 SUPPORT CARE CANCER
JI Support. Care Cancer
PD MAR
PY 2016
VL 24
IS 3
BP 1189
EP 1198
DI 10.1007/s00520-015-2892-5
PG 10
WC Oncology; Health Care Sciences & Services; Rehabilitation
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Health Care Sciences & Services; Rehabilitation
GA DC1WY
UT WOS:000369010000021
PM 26280404
DA 2022-04-25
ER

PT J
AU Yang, L
   Cai, YS
   Xu, K
   Zhu, JL
   Li, YB
   Wu, XQ
   Sun, J
   Lu, SM
   Xu, P
AF Yang, Le
   Cai, Yong-Song
   Xu, Ke
   Zhu, Jia-Lin
   Li, Yuan-Bo
   Wu, Xiao-Qing
   Sun, Jian
   Lu, She-Min
   Xu, Peng
TI Sodium selenite induces apoptosis and inhibits autophagy in human
   synovial sarcoma cell line SW982 in vitro
SO MOLECULAR MEDICINE REPORTS
LA English
DT Article
DE synovial sarcoma; SW982 cell line; sodium selenite; apoptosis; autophagy
ID COLON-CANCER CELLS; MITOCHONDRIAL PATHWAY; CARCINOMA-CELLS;
   DOWN-REGULATION; NB4 CELLS; CHEMOTHERAPY; SUPPRESSION; ACTIVATION;
   RAPAMYCIN; TOXICITY
AB The present study aimed to examine the effects of sodium selenite on the SW982 human synovial sarcoma cell line in relation to cell viability, apoptosis and autophagy. The results indicated that sodium selenite reduced cell viability and induced apoptosis by activating caspase-3 and members of the poly (ADP-ribose) polymerase and Bcl-2 protein families in SW982 cells. Furthermore, autophagy was also suppressed by sodium selenite treatment in SW982 cells, and apoptosis was upregulated in cells co-treated with sodium selenite and the autophagy inhibitor 3-methyladenine. By contrast, apoptosis was downregulated when sodium selenite was combined with rapamycin, an inducer of autophagy. The results indicated that autophagy may protect cells from the cytotoxicity of sodium selenite. The present study results demonstrated that sodium selenite induced apoptosis and inhibited autophagy and autophagy-protected cells from death by antagonizing sodium selenite-induced apoptosis in SW982 cells in vitro.
C1 [Yang, Le; Cai, Yong-Song; Xu, Ke; Zhu, Jia-Lin; Li, Yuan-Bo; Wu, Xiao-Qing; Xu, Peng] Xi An Jiao Tong Univ, Hlth Sci Ctr, Xian Hong Hui Hosp, Dept Joint Surg, 76 Nanguo Rd, Xian 710054, Shaanxi, Peoples R China.
   [Sun, Jian; Lu, She-Min] Xi An Jiao Tong Univ, Hlth Sci Ctr, Dept Genet & Mol Biol, Xian 710061, Shaanxi, Peoples R China.
RP Xu, P (corresponding author), Xi An Jiao Tong Univ, Hlth Sci Ctr, Xian Hong Hui Hosp, Dept Joint Surg, 76 Nanguo Rd, Xian 710054, Shaanxi, Peoples R China.
EM sousou369@163.com
RI Lu, Shemin/M-3350-2018; Lu, Shemin/AAI-6479-2021
OI Lu, Shemin/0000-0001-8250-850X; Lu, Shemin/0000-0002-5535-8320
FU National Natural Science Foundations of ChinaNational Natural Science
   Foundation of China (NSFC) [81271948, 81601877]
FX This study was supported by The National Natural Science Foundations of
   China (grant nos. 81271948 and 81601877).
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NR 34
TC 5
Z9 6
U1 6
U2 11
PU SPANDIDOS PUBL LTD
PI ATHENS
PA POB 18179, ATHENS, 116 10, GREECE
SN 1791-2997
EI 1791-3004
J9 MOL MED REP
JI Mol. Med. Rep.
PD MAY
PY 2018
VL 17
IS 5
BP 6560
EP 6568
DI 10.3892/mmr.2018.8679
PG 9
WC Oncology; Medicine, Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Research & Experimental Medicine
GA GD5OR
UT WOS:000430556800041
PM 29512717
OA hybrid, Green Published, Green Submitted
DA 2022-04-25
ER

PT J
AU Ballaro, R
   Penna, F
   Pin, F
   Gomez-Cabrera, MC
   Vina, J
   Costelli, P
AF Ballaro, Riccardo
   Penna, Fabio
   Pin, Fabrizio
   Carmen Gomez-Cabrera, Mari
   Vina, Jose
   Costelli, Paola
TI Moderate Exercise Improves Experimental Cancer Cachexia by Modulating
   the Redox Homeostasis
SO CANCERS
LA English
DT Article
DE muscle wasting; oxidative stress; autophagy; chemotherapy; mitochondria
ID SKELETAL-MUSCLE; OXIDATIVE STRESS; ANIMAL-MODEL; CHEMOTHERAPY;
   ANTIOXIDANT; AUTOPHAGY; EXPRESSION; PREVENTION; PLASTICITY; INDUCTION
AB Cachexia is a debilitating syndrome that complicates the management of cancer patients. Muscle wasting, one of the main features of cachexia, is associated with hyper-activation of protein degradative pathways and altered mitochondrial function that could both result from impaired redox homeostasis. This study aimed to investigate the contribution of oxidative stress to cancer-induced cachexia in the presence or in the absence of moderate exercise training. Mice bearing the colon C26 carcinoma, either sedentary or exercised, were used. The former showed muscle wasting and redox imbalance, with the activation of an antioxidant response and with upregulation of markers of proteasome-dependent protein degradation and autophagy. Moderate exercise was able to relieve muscle wasting and prevented the loss of muscle strength; such a pattern was associated with reduced levels of Reactive Oxygen Species (ROS), carbonylated proteins and markers of autophagy and with improved antioxidant capacity. The muscle of sedentary tumor hosts also showed increased levels of molecular markers of mitophagy and reduced mitochondrial mass. Conversely, exercise in the C26 hosts led to increased mitochondrial mass. In conclusion, moderate exercise could be an effective non-pharmacological approach to prevent muscle wasting in cancer patients, decreasing muscle protein catabolism and oxidative stress and preserving mitochondria.
C1 [Ballaro, Riccardo; Penna, Fabio; Pin, Fabrizio; Costelli, Paola] Univ Torino, Expt Med & Clin Pathol Unit, Dept Clin & Biol Sci, I-10125 Turin, Italy.
   [Ballaro, Riccardo; Penna, Fabio; Pin, Fabrizio; Costelli, Paola] Interuniv Inst Myol, I-61029 Urbino, Italy.
   [Pin, Fabrizio] Indiana Univ Sch Med, Dept Anat & Cell Biol, Indianapolis, IN 46202 USA.
   [Carmen Gomez-Cabrera, Mari; Vina, Jose] Univ Valencia, Dept Physiol, Freshage Res Grp, CIBERFES,INCLIVA, Valencia, Spain.
RP Costelli, P (corresponding author), Univ Torino, Expt Med & Clin Pathol Unit, Dept Clin & Biol Sci, I-10125 Turin, Italy.; Costelli, P (corresponding author), Interuniv Inst Myol, I-61029 Urbino, Italy.
EM riccardo.ballaro@unito.it; fabio.penna@unito.it; fpin@iu.edu;
   gomez@uv.es; jose.vina@uv.es; Carmen.Gomez@uv.es
RI Vina, Jose/AAB-3069-2021; Gomez-Cabrera, Maria Carmen/H-6911-2018;
   Ballarò, Riccardo/ABC-1988-2020; Penna, Fabio/K-5090-2016
OI Vina, Jose/0000-0001-9709-0089; Gomez-Cabrera, Maria
   Carmen/0000-0003-4000-1684; Ballarò, Riccardo/0000-0001-5505-9024;
   Penna, Fabio/0000-0002-2774-6027
FU Associazione Italiana per la Ricerca sul Cancro [AIRC]Fondazione AIRC
   per la ricerca sul cancro [IG9153]; University of Torino
FX Work supported by Associazione Italiana per la Ricerca sul Cancro [AIRC;
   grant IG9153 (PC)] Milano and University of Torino (ex-60% funds),
   Italy.
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NR 58
TC 29
Z9 29
U1 5
U2 11
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
SN 2072-6694
J9 CANCERS
JI Cancers
PD MAR
PY 2019
VL 11
IS 3
AR 285
DI 10.3390/cancers11030285
PG 20
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA HZ0RT
UT WOS:000468550200015
PM 30823492
OA Green Published, Green Submitted, gold
DA 2022-04-25
ER

PT J
AU Fu, C
   Yu, ZJ
   He, Y
   Ding, J
   Wei, MJ
AF Fu, Chen
   Yu, Zhaojin
   He, Ying
   Ding, Jian
   Wei, Minjie
TI Down-Regulation of an Autophagy-Related Gene SERPINA1 as a Superior
   Prognosis Biomarker Associates with Relapse and Distant Metastasis in
   Colon Adenocarcinoma
SO ONCOTARGETS AND THERAPY
LA English
DT Article
DE SERPINA1; autophagy; COAD; prognostic; relapse; distant metastasis
ID CANCER STATISTICS; R PACKAGE; CELLS; EXPRESSION; APOPTOSIS; PROTEINS
AB Background: The relapse and distant metastasis in colon adenocarcinoma (COAD) patients with a poor prognosis. Autophagy has gained increasing attention recently.
   Methods: This study utilized univariate Cox analysis from the TCGA database to obtain 10 prognostic autophagy-related genes (ARGs). GO and KEGG functional annotation analysis suggested that the ARGs were significantly enriched in tumor metabolic processes. We verified the autophagy-related genes screened by TCGA clinical data. Then, we compared the expression of SERPINA1 in primary and metastatic tumor cells in the GEO database, and finally verified the relationship between SERPINA1 protein expression and prognosis with the CPTAC database.
   Results: The ROC curves showed SERPINA1 had robust prediction capability in judging the prognosis and disease process compared with the other 4 ARGs and risk score in COAD. Clinical relationship analysis further indicated SERPINA1 was related to TMN stage, clinical-stage, OS, RFS, and DMFS in COAD. Besides, survival analysis presented that higher expression of SERPINA1 was significantly associated with the longer OS, RFS, or DMFS. Moreover, SERPINA1 protein was validated to be associated with OS, RFS, and DMFS through our own IHC and CPTAC database. Finally, we exploratoryly combined the SERPINA1 mRNA and SERPINA1 protein as a new index for prognostics.
   Conclusion: This new combined index showed the highest prognostic value for OS, RFS, and DMFS, and had the potential to become a practical biomarker for prognosis.
C1 [Fu, Chen; Yu, Zhaojin; He, Ying; Ding, Jian; Wei, Minjie] China Med Univ, Sch Pharm, Dept Pharmacol, Shenyang 110122, Peoples R China.
   [Fu, Chen; Yu, Zhaojin; Wei, Minjie] China Med Univ, Dept Pharmacol, Liaoning Key Lab Mol Targeted Antitumor Drug Dev, Shenyang 110122, Peoples R China.
   [He, Ying] China Med Univ, Affiliated Hosp 4, Dept Oncol, Shenyang 110000, Peoples R China.
   [Ding, Jian] Chinese Acad Sci, Shanghai Inst Mat Med, Div Antitumor Pharmacol, State Key Lab Drug Res, Shanghai 201203, Peoples R China.
   [Wei, Minjie] Liaoning Med Diag & Treatment Ctr, Shenyang 110000, Peoples R China.
RP Wei, MJ (corresponding author), China Med Univ, Sch Pharm, Dept Pharmacol, Shenyang 110122, Peoples R China.; Ding, J (corresponding author), Chinese Acad Sci, Shanghai Inst Mat Med, Div Antitumor Pharmacol, State Key Lab Drug Res, Shanghai 201203, Peoples R China.
EM carl.2000@163.com; weiminjiecmu@163.com
FU National Natural Science Foundation of China (NSFC)National Natural
   Science Foundation of China (NSFC) [82073884]; NSFC-Liaoning joint fund
   key program [U20A20413]; Major Special S&T Projects in Liaoning Province
   [2019JH1/10300005]
FX National Natural Science Foundation of China (NSFC, No. 82073884),
   NSFC-Liaoning joint fund key program (No. U20A20413), Major Special S&T
   Projects in Liaoning Province (2019JH1/10300005).
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NR 34
TC 3
Z9 3
U1 3
U2 6
PU DOVE MEDICAL PRESS LTD
PI ALBANY
PA PO BOX 300-008, ALBANY, AUCKLAND 0752, NEW ZEALAND
SN 1178-6930
J9 ONCOTARGETS THER
JI OncoTargets Ther.
PY 2021
VL 14
BP 3861
EP 3872
DI 10.2147/OTT.S306405
PG 12
WC Biotechnology & Applied Microbiology; Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biotechnology & Applied Microbiology; Oncology
GA SW6WR
UT WOS:000664655100001
PM 34188492
OA gold, Green Published
DA 2022-04-25
ER

PT J
AU Zhang, ZW
   Liu, Z
   Chen, J
   Yi, J
   Cheng, J
   Dun, WQ
   Wei, HL
AF Zhang, Zhewen
   Liu, Zhuan
   Chen, Jing
   Yi, Juan
   Cheng, Juan
   Dun, Wangqing
   Wei, Hulai
TI Resveratrol induces autophagic apoptosis via the lysosomal cathepsin D
   pathway in human drug-resistant K562/ADM leukemia cells
SO EXPERIMENTAL AND THERAPEUTIC MEDICINE
LA English
DT Article
DE resveratrol; apoptosis; autophagy; drug resistance; cathepsin D;
   K562/ADM cells
ID MULTIDRUG-RESISTANCE; COLORECTAL-CANCER; ARSENIC TRIOXIDE;
   DOWN-REGULATION; IN-VITRO; DEATH; PROLIFERATION; VIVO
AB The aim of the present study was to investigate the crosstalk between resveratrol (Res)-induced autophagy and apoptosis, and the molecular pathway by which autophagy leads to apoptotic death in drug-resistant K562/ADM leukemia cells. The viability of K562/ADM cells was determined using the MTT assay. The formation of autophagic vacuoles was detected using transmission electron microscopy and monodansylcadaverine (MDC) staining. Cell apoptosis was evaluated using flow cytometry. The expression of apoptosis-or autophagy-associated proteins was measured using western blotting. The results indicated that treatment with Res inhibited cell viability in a concentration-dependent manner. Furthermore, the numbers of MDC-positive fluorescent points, autophagic vacuoles and autolysosome-engulfed cytoplasmic materials were markedly increased in Res-treated K562/ADM cells compared with untreated cells, as determined using fluorescence microscopy and transmission electron microscopy. Res-induced apoptosis was associated with increased cleaved caspase-3 and B-cell lymphoma 2 associated X protein, and decreased B-cell lymphoma 2 (Bcl-2) protein expression levels when compared with the control (P<0.05). However, the proportion of apoptotic cells decreased from 69.6 to 41.0% (40 mu mol/l Res) and from 77.3 to 58.8% (80 mu mol/l Res) following pre-treatment with the autophagy inhibitor 3-methyladenine (P<0.01). The protein expression levels of microtubule-associated protein 1A/1B-light chain 3 and beclin 1, two markers of autophagy, were upregulated in Res-treated cells compared with the control (P<0.05). In addition, lysosomal cathepsin D (Cath D) release increased during Res-induced autophagy and apoptosis (P<0.05). The present results demonstrated that Res-induced apoptosis of K562/ADM cells was autophagy-dependent and the released Cath D may trigger caspase-dependent cell death through the Bcl-2 family of proteins. Furthermore, the present data indicate that to enhancement of the autophagy-cathepsin-apoptosis pathway may be an effective approach for overcoming anticancer drug resistance.
C1 [Zhang, Zhewen; Liu, Zhuan; Chen, Jing; Yi, Juan; Dun, Wangqing; Wei, Hulai] Lanzhou Univ, Sch Basic Med Sci, Inst Biochem & Mol Biol, Lanzhou 730000, Gansu, Peoples R China.
   [Cheng, Juan] Lanzhou Univ, Affiliated Hosp 1, Dept Hematol, Lanzhou 730000, Gansu, Peoples R China.
   [Wei, Hulai] Lanzhou Univ, Sch Basic Med Sci, Key Lab Preclin Study New Drugs Gansu Prov, 199 Donggang West Rd, Lanzhou 730000, Gansu, Peoples R China.
RP Wei, HL (corresponding author), Lanzhou Univ, Sch Basic Med Sci, Key Lab Preclin Study New Drugs Gansu Prov, 199 Donggang West Rd, Lanzhou 730000, Gansu, Peoples R China.
EM weihulai@lzu.edu.cn
FU Fundamental Research Funds for the Central UniversitiesFundamental
   Research Funds for the Central Universities [lzujbky-2014-143]; National
   Natural Science Foundation of ChinaNational Natural Science Foundation
   of China (NSFC) [81541025]
FX The present study was supported by the Fundamental Research Funds for
   the Central Universities (grant no. lzujbky-2014-143) and National
   Natural Science Foundation of China (grant no. 81541025).
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NR 30
TC 17
Z9 18
U1 0
U2 5
PU SPANDIDOS PUBL LTD
PI ATHENS
PA POB 18179, ATHENS, 116 10, GREECE
SN 1792-0981
EI 1792-1015
J9 EXP THER MED
JI Exp. Ther. Med.
PD MAR
PY 2018
VL 15
IS 3
BP 3012
EP 3019
DI 10.3892/etm.2018.5742
PG 8
WC Medicine, Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Research & Experimental Medicine
GA FZ6XI
UT WOS:000427743500119
PM 29456707
OA gold, Green Published
DA 2022-04-25
ER

PT J
AU Chen, ZH
   Li, YC
   Zhang, C
   Yi, HM
   Wu, C
   Wang, JP
   Liu, YW
   Tan, JQ
   Wen, JF
AF Chen, Zhihong
   Li, Yanchun
   Zhang, Chi
   Yi, Hongmei
   Wu, Chang
   Wang, Junpu
   Liu, Yuwu
   Tan, Jieqiong
   Wen, Jifang
TI Downregulation of Beclin1 and Impairment of Autophagy in a Small
   Population of Colorectal Cancer
SO DIGESTIVE DISEASES AND SCIENCES
LA English
DT Article
DE Colorectal cancer; Beclin 1; Autophagy; Rapamycin
ID TUMOR-SUPPRESSOR; P53 MUTATIONS; CELL-LINES; EXPRESSION; GENE;
   TUMORIGENESIS; INHIBITION; APOPTOSIS; PROTEIN; PROGNOSIS
AB Background Autophagy is a highly conserved mechanism for degradation and recycling of long-lived proteins and damaged organelle to maintain cell homeostasis. Deregulation of autophagy has been associated with tumorigenesis. Beclin 1 is an essential autophagy protein and its upregulation has been observed in most colorectal cancer tissues. However, there is a small population of colorectal cancers with downregulation of Beclin 1.
   Aim The purpose of this study was to investigate the role autophagy plays in colorectal cancers with downregulaion of Beclin 1.
   Methods LC3 protein, an autophagosome marker, was assessed by ICH and WB in colorectal cancers tissues. An anti-tumor effect of Beclin 1 was examined by introducing exogenous Beclin 1 in vitro. Colony formation assay, growth curves and mouse xenograft were analysed.
   Results Our results showed that LC3 was suppressed in the colorectal cancers (9.86 %) with downregulation of Beclin 1. Moreover, overexpression of Beclin 1 inhibited colorectal cancer cell growth and enhanced the rapamycin-induced antitumor effect in vitro.
   Conclusion Downregulation of Beclin 1 and autophagy inhibition play an important role in a part of colorectal cancers. Activating autophagy or overexperssion of Beclin 1 may be an effective treatment for some colorectal cancers. Detection of expression profile of Beclin 1 in colorectal cancers could be a strategy for new diagnostic and therapeutic methods.
C1 [Chen, Zhihong; Wu, Chang; Wang, Junpu; Liu, Yuwu; Wen, Jifang] Cent S Univ, Sch Basic Med, Dept Pathol, Changsha 410013, Hunan, Peoples R China.
   [Chen, Zhihong; Li, Yanchun; Yi, Hongmei] Hunan Prov Peoples Hosp, Dept Pathol, Changsha 410005, Hunan, Peoples R China.
   [Zhang, Chi] Univ South China, Funct Lab Ctr, Hengyang 421001, Peoples R China.
   [Tan, Jieqiong] Cent S Univ, State Key Lab Med Genet, Changsha 410078, Hunan, Peoples R China.
RP Wen, JF (corresponding author), Cent S Univ, Sch Basic Med, Dept Pathol, 172 Tong Zi Po Rd, Changsha 410013, Hunan, Peoples R China.
EM zhihong6662002@yahoo.com.cn; liyanchun99@yahoo.cn; zhangchi9966@163.com;
   yihongmei2012@yahoo.cn; wuchang_scs@163.com; junpuwang1212@yahoo.cn;
   liuyuwu_8923@yahoo.cn; tanjieqiong@sklmg.edu.cn; jifang.wen@yahoo.com.cn
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NR 37
TC 26
Z9 30
U1 0
U2 9
PU SPRINGER
PI DORDRECHT
PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS
SN 0163-2116
EI 1573-2568
J9 DIGEST DIS SCI
JI Dig. Dis. Sci.
PD OCT
PY 2013
VL 58
IS 10
BP 2887
EP 2894
DI 10.1007/s10620-013-2732-8
PG 8
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA 223BO
UT WOS:000324778900017
PM 23812859
OA hybrid, Green Published
DA 2022-04-25
ER

PT J
AU Xavier, CPR
   Lima, CF
   Pedro, DFN
   Wilson, JM
   Kristiansen, K
   Pereira-Wilson, C
AF Xavier, Cristina P. R.
   Lima, Cristovao F.
   Pedro, Dalila F. N.
   Wilson, Jonathan M.
   Kristiansen, Karsten
   Pereira-Wilson, Cristina
TI Ursolic acid induces cell death and modulates autophagy through JNK
   pathway in apoptosis-resistant colorectal cancer cells
SO JOURNAL OF NUTRITIONAL BIOCHEMISTRY
LA English
DT Article
DE Ursolic acid; Colorectal carcinoma; Cell death; Autophagy; JNK;
   5-fluorouracil
ID N-TERMINAL KINASE; SIGNALING PATHWAYS; P53; ACTIVATION; BCL-2;
   PHOSPHORYLATION; INDUCTION; CHEMOTHERAPY; EXPRESSION; QUERCETIN
AB Colorectal carcinomas (CRCs) with P53 mutations have been shown to be resistant to chemotherapy with 5-fluorouracil (5-FU), the most widely used chemotherapeutic drug for CRC treatment. Autophagy is emerging as a promising therapeutic target for drug-resistant tumors. In the present study, we tested the effects of ursolic acid (UA), a natural triterpenoid, on cell death mechanisms and its effects in combination with 5-FU in the HCf 15 p53 mutant apoptosisresistant CRC cell line. The involvement of UA in autophagy and its in vivo efficacy were evaluated. Our data show that UA induces apoptosis independent of caspases in HCT15 cells and enhances 5-FU effects associated with an activation of c-jun N-terminal kinase (INK). In this cell line, where this compound has a more pronounced effect on the induction of cell death compared to 5-FU, apoptosis corresponds only to a small percentage of the total cell death induced by UA. UA also modulated autophagy by inducing the accumulation of LC3 and p62 levels with involvement of JNK pathway, which indicates a contribution of autophagy on JNK-dependent induction of cell death by UA. By using nude mice xenografted with HCT15 cells, we verified that UA was also active in vivo decreasing tumor growth rate. In conclusion, this study shows UA's anticancer potential both in vitro and in vivo. Induction of cell death and modulation of autophagy in CRC-resistant cells were shown to involve JNK signaling. (C) 2013 Elsevier Inc. All rights reserved.
C1 [Xavier, Cristina P. R.; Pedro, Dalila F. N.; Pereira-Wilson, Cristina] Univ Minho, Dept Biol, CBMA Ctr Mol & Environm Biol, P-4710057 Braga, Portugal.
   [Lima, Cristovao F.] Univ Minho, Dept Biol, CITAB Ctr Res & Technol Agroenvironm & Biol Sci, P-4710057 Braga, Portugal.
   [Wilson, Jonathan M.] Univ Porto, CIMAR Associate Lab, Interdisciplinary Ctr Marine & Environm Res CIIMA, P-4050123 Oporto, Portugal.
   [Kristiansen, Karsten; Pereira-Wilson, Cristina] Univ Copenhagen, Dept Biol, DK-2200 Copenhagen, Denmark.
RP Pereira-Wilson, C (corresponding author), Univ Minho, Dept Biol, CBMA Ctr Mol & Environm Biol, P-4710057 Braga, Portugal.
EM cpereira@bio.uminho.pt
RI Wilson, Jonathan/I-6071-2012; Wilson, Jonathan Mark/AAG-6481-2019;
   Pereira Wilson, Cristina/F-1967-2013; Xavier, Cristina Pinto
   Ribeiro/C-7442-2015; Kristiansen, Karsten/J-5148-2014; Lima,
   Cristovao/B-6123-2009
OI Wilson, Jonathan/0000-0003-3681-1166; Wilson, Jonathan
   Mark/0000-0003-3681-1166; Xavier, Cristina Pinto
   Ribeiro/0000-0002-4613-1917; Kristiansen, Karsten/0000-0002-6024-0917;
   Lima, Cristovao/0000-0003-3557-3549; Pedro, Dalila/0000-0003-1724-7504;
   Pereira-Wilson, Cristina/0000-0002-3714-8258
FU Foundation for Science and Technology (FCT), PortugalPortuguese
   Foundation for Science and Technology [SFRH/BD/27524/2006,
   SFRH/BD/64817/2009]; University of Copenhagen [SFRH/BSAB/918/2009]; FCT
   research grants [PTDC/QUI-BI0J101392/2008, PEst-C/BIA/U14050/2011];
   QREN; European Community fund FEDEREuropean Commission
FX C.P.R.X. and D.F.N.P. were supported by the Foundation for Science and
   Technology (FCT), Portugal, through grants SFRH/BD/27524/2006 and
   SFRH/BD/64817/2009, respectively. C.P.W. was guest professor at
   University of Copenhagen through the grant SFRH/BSAB/918/2009. The work
   was supported by FCT research grants PTDC/QUI-BI0J101392/2008 (NaturAge)
   and PEst-C/BIA/U14050/2011. All projects are co-funded by the program
   COMPETE from QREN with co-participation from the European Community fund
   FEDER. We would like to thank Dr. Morten Johnsen from the Department of
   Biology, University of Copenhagen, for the technical assistance in the
   in vivo experiment.
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NR 44
TC 73
Z9 77
U1 0
U2 44
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA STE 800, 230 PARK AVE, NEW YORK, NY 10169 USA
SN 0955-2863
EI 1873-4847
J9 J NUTR BIOCHEM
JI J. Nutr. Biochem.
PD APR
PY 2013
VL 24
IS 4
BP 706
EP 712
DI 10.1016/j.jnutbio.2012.04.004
PG 7
WC Biochemistry & Molecular Biology; Nutrition & Dietetics
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Nutrition & Dietetics
GA 120IQ
UT WOS:000317164400013
PM 22841540
OA Green Submitted
DA 2022-04-25
ER

PT J
AU Yu, MS
   Henning, R
   Walker, A
   Kim, G
   Perroy, A
   Alessandro, R
   Virador, V
   Kohn, EC
AF Yu, Minshu
   Henning, Ryan
   Walker, Amanda
   Kim, Geoffrey
   Perroy, Alyssa
   Alessandro, Riccardo
   Virador, Victoria
   Kohn, Elise C.
TI L-asparaginase inhibits invasive and angiogenic activity and induces
   autophagy in ovarian cancer
SO JOURNAL OF CELLULAR AND MOLECULAR MEDICINE
LA English
DT Article
DE asparaginase; ovarian cancer; sialyl Lewis X; angiogenesis; autophagy
ID FOCAL ADHESION KINASE; COLON-CARCINOMA CELLS; INTEGRIN GLYCOSYLATION;
   GLYCOPROTEIN SYNTHESIS; PREDICTIVE BIOMARKER; EXTRACELLULAR-MATRIX;
   SIGNAL-TRANSDUCTION; LEUKEMIA CELLS; PHASE-II; EXPRESSION
AB Recent work identified L-asparaginase (L-ASP) as a putative therapeutic target for ovarian cancer. We suggest that L-ASP, a dysregulator of glycosylation, would interrupt the local microenvironment, affecting the ovarian cancer cellendothelial cell interaction and thus angiogenesis without cytotoxic effects. Ovarian cancer cell lines and human microvascular endothelial cells (HMVEC) were exposed to L-ASP at physiologically attainable concentrations and subjected to analyses of endothelial tube formation, invasion, adhesion and the assessment of sialylated proteins involved in matrix-associated and heterotypic cell adhesion. Marked reduction in HMVEC tube formation in vitro, HMVEC and ovarian cancer cell invasion, and heterotypic cell-cell and cell-matrix adhesion was observed (P < 0.05-0.0001). These effects were associated with reduced binding to beta 1integrin, activation of FAK, and cell surface sialyl LewisX (sLex) expression. No reduction in HMVEC E-selectin expression was seen consistent with the unidirectional inhibitory actions observed. L-ASP concentrations were non-toxic to either ovarian cancer or HMVEC lines in the time frame of the assays. However, early changes of autophagy were observed in both cell types with induction of ATG12, beclin-1, and cleavage of LC-3, indicating cell injury did occur. These data and the known mechanism of action of L-ASP on glycosylation of nascent proteins suggest that L-ASP reduces of ovarian cancer dissemination and progression through modification of its microenvironment. The reduction of ovarian cancer cell surface sLex inhibits interaction with HMVEC and thus HMVEC differentiation into tubes, inhibits interaction with the local matrix reducing invasive behaviour, and causes cell injury initiating autophagy in tumour and vascular cells.
C1 [Yu, Minshu; Henning, Ryan; Walker, Amanda; Kim, Geoffrey; Perroy, Alyssa; Virador, Victoria; Kohn, Elise C.] NCI, Mol Signaling Sect, Med Oncol Branch, Ctr Canc Res, Bethesda, MD 20892 USA.
   [Alessandro, Riccardo] Univ Palermo, Sez Biol & Genet, Dipartimento Biopatol & Biotecnol Med & Forensi, Palermo, Italy.
RP Kohn, EC (corresponding author), 10 Ctr Dr,MSC 1906, Bethesda, MD 20892 USA.
EM ek1b@nih.gov
RI Virador, Victoria M./A-8173-2009
FU NIH, National Cancer Institute, Center for Cancer ResearchUnited States
   Department of Health & Human ServicesNational Institutes of Health (NIH)
   - USANIH National Cancer Institute (NCI); NATIONAL CANCER
   INSTITUTEUnited States Department of Health & Human ServicesNational
   Institutes of Health (NIH) - USANIH National Cancer Institute (NCI)
   [ZIASC009375, ZIASC009163, ZIASC009374] Funding Source: NIH RePORTER
FX This research was supported by the Intramural Research Program of the
   NIH, National Cancer Institute, Center for Cancer Research.
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NR 54
TC 35
Z9 37
U1 0
U2 5
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
EI 1582-4934
J9 J CELL MOL MED
JI J. Cell. Mol. Med.
PD OCT
PY 2012
VL 16
IS 10
BP 2369
EP 2378
DI 10.1111/j.1582-4934.2012.01547.x
PG 10
WC Cell Biology; Medicine, Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Cell Biology; Research & Experimental Medicine
GA 012LK
UT WOS:000309237500013
PM 22333033
OA Green Submitted, Green Accepted, gold, Green Published
DA 2022-04-25
ER

PT J
AU Wang, WL
   Zhu, DR
   Chen, C
   Zhu, TY
   Han, C
   Liu, FY
   Li, LN
   Luo, JG
   Kong, LY
AF Wang, Wen-Li
   Zhu, Dong-Rong
   Chen, Chen
   Zhu, Tian-Yu
   Han, Chao
   Liu, Fei-Yan
   Li, Ling-Nan
   Luo, Jian-Guang
   Kong, Ling-Yi
TI Taicrypnacids A and B, a Pair of C-37 Heterodimeric Diterpenoid
   Stereoisomers fronn Taiwania cryptomerioides
SO JOURNAL OF NATURAL PRODUCTS
LA English
DT Article
ID DEHYDROABIETANE DERIVATIVES; OXIDATIVE STRESS; ER STRESS; APOPTOSIS;
   CELLS; AUTOPHAGY; MEROTERPENOIDS; CYCLOADDUCTS; ACTIVATION; PROTEASOME
AB Two uncommon C-37 heterodimeric diterpenoids, taicrypnacids A (1) and B (2), and a known labdane-type diterpenoid (3) were isolated from the leaves of Taiwania cryptomerioides. Several techniques, such as comprehensive spectroscopic analysis, chemical conversion, X-ray crystallography, and ECD data, were employed to define the structures. The two new compounds displayed cytotoxicity against human breast cancer (MCF-7), osteosarcoma (U-2 OS), and human colon carcinoma (HCT-116) cell lines, while the methyl ester la showed no activity. Compound 1 induced Ca2+-ROS pathway-mediated endoplasmic reticulum stress, and excessive stress led to cell death by activating apoptosis and autophagy.
C1 [Wang, Wen-Li; Zhu, Dong-Rong; Chen, Chen; Zhu, Tian-Yu; Han, Chao; Liu, Fei-Yan; Li, Ling-Nan; Luo, Jian-Guang; Kong, Ling-Yi] China Pharmaceut Univ, Sch Tradit Chinese Pharm, Jiangsu Key Lab Bioact Nat Prod Res, 24 Tong Jia Xiang, Nanjing 210009, Jiangsu, Peoples R China.
   [Wang, Wen-Li; Zhu, Dong-Rong; Chen, Chen; Zhu, Tian-Yu; Han, Chao; Liu, Fei-Yan; Li, Ling-Nan; Luo, Jian-Guang; Kong, Ling-Yi] China Pharmaceut Univ, Sch Tradit Chinese Pharm, State Key Lab Nat Med, 24 Tong Jia Xiang, Nanjing 210009, Jiangsu, Peoples R China.
RP Luo, JG; Kong, LY (corresponding author), China Pharmaceut Univ, Sch Tradit Chinese Pharm, Jiangsu Key Lab Bioact Nat Prod Res, 24 Tong Jia Xiang, Nanjing 210009, Jiangsu, Peoples R China.
EM luojg@cpu.edu.cn; cpu_lykong@126.com
FU Drug Innovation Major Project [2018ZX09735002-003]; Program for
   Changjiang Scholars and Innovative Research Team in UniversityProgram
   for Changjiang Scholars & Innovative Research Team in University
   (PCSIRT) [IRT_15R63]
FX This research was supported by the Drug Innovation Major Project
   (2018ZX09735002-003) and the Program for Changjiang Scholars and
   Innovative Research Team in University (IRT_15R63).
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NR 41
TC 1
Z9 1
U1 4
U2 24
PU AMER CHEMICAL SOC
PI WASHINGTON
PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA
SN 0163-3864
EI 1520-6025
J9 J NAT PROD
JI J. Nat. Prod.
PD AUG
PY 2019
VL 82
IS 8
BP 2087
EP 2093
DI 10.1021/acs.jnatprod.8b00815
PG 7
WC Plant Sciences; Chemistry, Medicinal; Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED); Index Chemicus (IC)
SC Plant Sciences; Pharmacology & Pharmacy
GA IU2UJ
UT WOS:000483435000003
PM 31347365
DA 2022-04-25
ER

PT J
AU Chen, YJ
   Hao, Q
   Wang, SS
   Cao, MM
   Huang, YD
   Weng, XL
   Wang, JQ
   Zhang, Z
   He, XH
   Lu, H
   Zhou, X
AF Chen, Yajie
   Hao, Qian
   Wang, Shanshan
   Cao, Mingming
   Huang, Yingdan
   Weng, Xiaoling
   Wang, Jieqiong
   Zhang, Zhen
   He, Xianghuo
   Lu, Hua
   Zhou, Xiang
TI Inactivation of the tumor suppressor p53 by long noncoding RNA RMRP
SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF
   AMERICA
LA English
DT Article
DE p53; long noncoding RNA; RMRP; SNRPA1; PARP inhibition
ID PROCESSING ENDORIBONUCLEASE; EMBRYONIC LETHALITY; MDM2-DEFICIENT MICE;
   PARP INHIBITORS; MUTATIONS; PROTEIN; TRANSLATION; COMPONENT; RESCUE;
   DOMAIN
AB p53 inactivation is highly associated with tumorigenesis and drug resistance. Here, we identify a long noncoding RNA, the RNA component of mitochondrial RNA-processing endoribonuclease (RMRP), as an inhibitor of p53. RMRP is overexpressed and associated with an unfavorable prognosis in colorectal cancer. Ectopic RMRP suppresses p53 activity by promoting MDM2-induced p53 ubiquitination and degradation, while depletion of RMRP activates the p53 pathway. RMRP also promotes colorectal cancer growth and proliferation in a p53-dependent fashion in vitro and in vivo. This anti-p53 action of RMRP is executed through an identified partner protein, SNRPA1. RMRP can interact with SNRPA1 and sequester it in the nucleus, consequently blocking its lysosomal proteolysis via chaperone-mediated autophagy. The nuclear SNRPA1 then interacts with p53 and enhances MDM2-induced proteasomal degradation of p53. Remarkably, ablation of SNRPA1 completely abrogates RMRP regulation of p53 and tumor cell growth, indicating that SNRPA1 is indispensable for the anti-p53 function of RMRP. Interestingly and significantly, poly (ADP-ribose) polymerase (PARP) inhibitors induce RMRP expression through the transcription factor C/EBPI3, and RMRP confers tumor resistance to PARP inhibition by preventing p53 activation. Altogether, our study demonstrates that RMRP plays an oncogenic role by inactivating p53 via SNRPA1 in colorectal cancer.
C1 [Chen, Yajie; Hao, Qian; Wang, Shanshan; Cao, Mingming; Huang, Yingdan; Weng, Xiaoling; He, Xianghuo; Zhou, Xiang] Fudan Univ, Shanghai Canc Ctr, Shanghai 200032, Peoples R China.
   [Chen, Yajie; Hao, Qian; Wang, Shanshan; Cao, Mingming; Huang, Yingdan; Weng, Xiaoling; He, Xianghuo; Zhou, Xiang] Fudan Univ, Inst Biomed Sci, Shanghai 200032, Peoples R China.
   [Chen, Yajie; Hao, Qian; Wang, Shanshan; Cao, Mingming; Huang, Yingdan; Weng, Xiaoling; He, Xianghuo; Zhou, Xiang] Fudan Univ, Shanghai Med Coll, Dept Oncol, Shanghai 200032, Peoples R China.
   [Chen, Yajie; Zhang, Zhen] Fudan Univ, Shanghai Canc Ctr, Dept Radiat Oncol, Shanghai 200032, Peoples R China.
   [Wang, Jieqiong; Lu, Hua] Tulane Univ, Dept Biochem & Mol Biol, Sch Med, New Orleans, LA 70112 USA.
   [Wang, Jieqiong; Lu, Hua] Tulane Univ, Tulane Canc Ctr, Sch Med, New Orleans, LA 70112 USA.
   [He, Xianghuo; Zhou, Xiang] Fudan Univ, Shanghai Canc Ctr, Key Lab Breast Canc Shanghai, Shanghai 200032, Peoples R China.
   [Zhou, Xiang] Fudan Univ, Minist Sci & Technol Inst Biomed Sci, Shanghai Key Lab Med Epigenet, Int Colab Med Epigenet & Metab, Shanghai 200032, Peoples R China.
RP Hao, Q; Zhou, X (corresponding author), Fudan Univ, Shanghai Canc Ctr, Shanghai 200032, Peoples R China.; Hao, Q; Zhou, X (corresponding author), Fudan Univ, Inst Biomed Sci, Shanghai 200032, Peoples R China.; Hao, Q; Zhou, X (corresponding author), Fudan Univ, Shanghai Med Coll, Dept Oncol, Shanghai 200032, Peoples R China.; Zhou, X (corresponding author), Fudan Univ, Shanghai Canc Ctr, Key Lab Breast Canc Shanghai, Shanghai 200032, Peoples R China.; Zhou, X (corresponding author), Fudan Univ, Minist Sci & Technol Inst Biomed Sci, Shanghai Key Lab Med Epigenet, Int Colab Med Epigenet & Metab, Shanghai 200032, Peoples R China.
EM qhao15@hotmail.com; xiangzhou@fudan.edu.cn
RI He, Xianghuo/I-1497-2014; Zhou, Xiang/J-5046-2017
OI He, Xianghuo/0000-0001-8872-668X; Zhou, Xiang/0000-0002-1172-7948; Wang,
   Shanshan/0000-0002-6651-2821
FU National Natural Science Foundation of ChinaNational Natural Science
   Foundation of China (NSFC) [81702352]; Reynolds and Ryan Families Chair
   Fund of Translational Cancer
FX We thank the laboratory members for active and helpful discussion,
   Yazhen Gui for laboratory assistance, Ping Zhang for flow cytometry, and
   the innovative research team of the high-level local univer-sity in
   Shanghai. X.Z. was supported by the National Natural Science Foundation
   of China (Grants 81874053 and 82072879) , Q.H. was supported by the
   National Natural Science Foundation of China (Grant 81702352) , and H.L.
   was supported by the Reynolds and Ryan Families Chair Fund of
   Translational Cancer.
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NR 47
TC 7
Z9 7
U1 9
U2 10
PU NATL ACAD SCIENCES
PI WASHINGTON
PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 USA
SN 0027-8424
EI 1091-6490
J9 P NATL ACAD SCI USA
JI Proc. Natl. Acad. Sci. U. S. A.
PD JUL 20
PY 2021
VL 118
IS 29
AR e2026813118
DI 10.1073/pnas.2026813118
PG 12
WC Multidisciplinary Sciences
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Science & Technology - Other Topics
GA UA3BQ
UT WOS:000685037700013
PM 34266953
OA hybrid, Green Published
DA 2022-04-25
ER

PT J
AU Yang, XD
   Xu, XH
   Zhu, JJ
   Zhang, SY
   Wu, Y
   Wu, YY
   Zhao, K
   Xing, CG
   Cao, JP
   Zhu, H
   Li, M
   Ye, ZY
   Peng, W
AF Yang, Xiaodong
   Xu, Xiaohui
   Zhu, Junjia
   Zhang, Shuyu
   Wu, Yong
   Wu, Yongyou
   Zhao, Kui
   Xing, Chungen
   Cao, Jianping
   Zhu, Hong
   Li, Ming
   Ye, Zhenyu
   Peng, Wei
TI miR-31 affects colorectal cancer cells by inhibiting autophagy in
   cancer-associated fibroblasts
SO ONCOTARGET
LA English
DT Article
DE miR-31; colorectal cancer; CAFs; autophagy; biological behaviors
ID EXPRESSION PROFILES; TUMOR-GROWTH; MICRORNA-31; GLYCOLYSIS; METASTASIS;
   SENESCENCE; SURVIVAL; STAGE
AB Autophagy is a double-edged sword in tumor development. Recent studies have found that miRNAs have an inhibitory effect on the regulation of autophagy. It has been reported that miR-31 plays an important role in the development of colorectal cancer. However, what role miR-31 plays in colorectal cancer-associated fibroblasts (CAFs) has not been determined. In this study, we confirmed that the expression of miR-31 in CAFs was higher than in normal colorectal fibroblasts (NFs). We also found that treatment of CAFs with miR-31 mimic inhibited the expression of the autophagy-related genes Beclin-1, ATG, DRAM and LC3. In addition, we found up-regulation of miR-31 significantly affected colorectal cancer cell behaviors, including proliferation, invasion and apoptosis. Also, up-regulation of miR-31 in CAF could increase the radiosensitivity of colorectal cancer cells co-cultured with CAF. In summary, miR-31 can inhibit autophagy in colorectal CAFs, affect colorectal cancer development, and increase the radiosensitivity of colorectal cancer cells co-cultured with CAF. We hypothesize that miR-31 may become a new target of treatments for colorectal cancer.
C1 [Yang, Xiaodong; Xu, Xiaohui; Zhu, Junjia; Wu, Yong; Wu, Yongyou; Zhao, Kui; Xing, Chungen; Ye, Zhenyu; Peng, Wei] Soochow Univ, Affiliated Hosp 2, Dept Gen Surg, Suzhou 215004, Peoples R China.
   [Xu, Xiaohui] Soochow Univ, Peoples Hosp Taicang City 1, Dept Gen Surg, Taicang Affiliated Hosp, Suzhou 215400, Peoples R China.
   [Zhang, Shuyu; Cao, Jianping; Li, Ming] Soochow Univ, Coll Med, Sch Radiat Med & Protect, Suzhou 215123, Peoples R China.
   [Zhu, Hong] Soochow Univ, Affiliated Hosp 1, Oncol Dept, Suzhou 215006, Peoples R China.
RP Xing, CG (corresponding author), Soochow Univ, Affiliated Hosp 2, Dept Gen Surg, Suzhou 215004, Peoples R China.; Cao, JP (corresponding author), Soochow Univ, Coll Med, Sch Radiat Med & Protect, Suzhou 215123, Peoples R China.
EM xingcg@126.com; jpcao@suda.edu.cn
FU National Natural Science Foundation of ChinaNational Natural Science
   Foundation of China (NSFC) [81672970, 81301933, 81472917, 81572345];
   Health Research Projects in Jiangsu Province [H201313]; Suzhou
   Technology Bureau [SYSD2013090, SYS201552, SYSD2015034]; Priority
   Academic Program Development of Jiangsu Higher Education Institutions
   (PAPD); Suzhou Science and Education health youth projects
   [kjxw2015050]; Taicang Municipal Science and Technology Bureau of Basic
   Research Program [TC2015YYYL01]; focus of clinical disease treatment
   technology special funds of Suzhou city [LCZX201505]; Soochow university
FX This work was partially supported by the National Natural Science
   Foundation of China (Grant No: 81672970, 81301933, 81472917 and
   81572345), Health Research Projects in Jiangsu Province (H201313), the
   projects of Suzhou Technology Bureau (SYSD2013090, SYS201552,
   SYSD2015034) and the Priority Academic Program Development of Jiangsu
   Higher Education Institutions (PAPD), Suzhou Science and Education
   health youth projects (kjxw2015050), Taicang Municipal Science and
   Technology Bureau of Basic Research Program (TC2015YYYL01), the focus of
   clinical disease treatment technology special funds of Suzhou city
   (LCZX201505), and the second affiliated hospital of Soochow university
   preponderant clinic discipline group project funding.
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NR 27
TC 44
Z9 48
U1 0
U2 6
PU IMPACT JOURNALS LLC
PI ORCHARD PARK
PA 6666 E QUAKER ST, STE 1, ORCHARD PARK, NY 14127 USA
EI 1949-2553
J9 ONCOTARGET
JI Oncotarget
PD NOV 29
PY 2016
VL 7
IS 48
BP 79603
EP 79614
DI 10.18632/oncotarget.12873
PG 12
WC Oncology; Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Cell Biology
GA EE5HH
UT WOS:000389636000113
PM 27793031
OA Green Published, Green Submitted, gold
DA 2022-04-25
ER

PT J
AU Wei, FJ
   Wang, YM
   Luo, ZW
   Li, Y
   Duan, YX
AF Wei, Fujing
   Wang, Yimin
   Luo, Zewei
   Li, Yu
   Duan, Yixiang
TI New findings of silica nanoparticles induced ER autophagy in human colon
   cancer cell
SO SCIENTIFIC REPORTS
LA English
DT Article
ID SIZE-DEPENDENT CYTOTOXICITY; SELECTIVE AUTOPHAGY; ENDOPLASMIC-RETICULUM;
   IN-VITRO; PROTEIN; COMPARTMENTS; MATURATION; INDUCTION; PATHWAY; LC3
AB Nanoparticle-induced autophagy has been extensively studied, however, real time information about the endoplasmic reticulum involved autophagic process (ER autophagy) induced by nanomaterials remains unknown. In this work, silica nanoparticles (SNPs) were synthesized with characteristics of low toxicity, good biocompatibility and excellent water dispersibility to treat cells. Results show that either low concentration (10 mu g/mL) or high concentration (200 mu g/mL) of SNPs could increase the quantity of processing from microtubule-associated protein 1-light chain 3-I (LC3-I) to the other variant of LC3 (LC3-II). Interestingly, the level of autophagy induced by the SNPs is associated with the treated time but not the concentrations of SNPs. Importantly, for the first time, SNP accumulation in ER was discovered through co-localization analysis, which incurs ER autophagy. These new findings about SNPs-induced ER autophagy could open an effective way for securely designing silica-based nanoparticles and enable us to know more about ER autophagy.
C1 [Wei, Fujing; Wang, Yimin; Luo, Zewei; Li, Yu; Duan, Yixiang] Sichuan Univ, Coll Life Sci, Res Ctr Analyt Instrumentat, Key Lab Bioresource & Ecoenvironm,Minist Educ, Chengdu 610065, Peoples R China.
RP Duan, YX (corresponding author), Sichuan Univ, Coll Life Sci, Res Ctr Analyt Instrumentat, Key Lab Bioresource & Ecoenvironm,Minist Educ, Chengdu 610065, Peoples R China.
EM yduan@scu.edu.cn
OI Luo, Zewei/0000-0001-9178-9868
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NR 50
TC 26
Z9 26
U1 4
U2 52
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 2045-2322
J9 SCI REP-UK
JI Sci Rep
PD FEB 14
PY 2017
VL 7
AR 42591
DI 10.1038/srep42591
PG 11
WC Multidisciplinary Sciences
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Science & Technology - Other Topics
GA EK3ZR
UT WOS:000393867400001
PM 28195184
OA Green Published, gold
DA 2022-04-25
ER

PT J
AU Suhaimi, SA
   Hong, SL
   Malek, SNA
AF Suhaimi, Shafinah Ahmad
   Hong, Sok Lai
   Malek, Sri Nurestri Abdul
TI Rutamarin, an Active Constituent from Ruta angustifolia Pers., Induced
   Apoptotic Cell Death in the HT29 Colon Adenocarcinoma Cell Line
SO PHARMACOGNOSY MAGAZINE
LA English
DT Article
DE Apoptosis; cancer; cytotoxicity; in vitro; Ruta angustifolia; rutamarin
ID GROWTH-INHIBITION; CYCLE ARREST; CANCER; GRAVEOLENS; COUMARINS;
   AUTOPHAGY; PATHWAYS
AB Background: Ruta angustifolia Pers. is a perennial herb that is cultivated worldwide, including Southeast Asia, for the treatment of various diseases as traditional medicine. Objective: The purpose of the study was to identify an active principle of R. angustifolia and to investigate its effect on the HT29 cell death. Materials and Methods: The methanol and fractionated extracts (hexane, chloroform, ethyl acetate, and water) of R. angustifolia Pers. were initially investigated for their cytotoxic activity against two human carcinoma cell lines (MCF7 and HT29) and a normal human colon fibroblast cell line (CCD-18Co) using sulforhodamine B cytotoxicity assay. Eight compounds including rutamarin were isolated from the active chloroform extract and evaluated for their cytotoxic activity against HT29 human colon carcinoma cell line and CCD-18Co noncancer cells. Further studies on the induction of apoptosis such as morphological examinations, biochemical analyses, cell cycle analysis, and caspase activation assay were conducted in rutamarin-treated HT29 cells. Results: Rutamarin exhibited remarkable cytotoxic activity against HT29 cells (IC., value of 5.6 mu M) but was not toxic to CCD-18Co cells. The morphological and biochemical hallmarks of apoptosis including activation of caspases 3, 8, and 9 were observed in rutamarin-treated HT29 cells. These may be associated with cell cycle arrest at the GO/GI and G2/M checkpoints, which was also observed in HT29 cells. Conclusions: The present study describes rutamarin-induced apoptosis in the HT29 cell line for the first time and suggests that rutamarin has the potential to be developed as an anticancer agent.
C1 [Suhaimi, Shafinah Ahmad; Malek, Sri Nurestri Abdul] Univ Malaya, Fac Sci, Inst Biol Sci, Kuala Lumpur 50603, Malaysia.
   [Hong, Sok Lai] Univ Malaya, Inst Res Management & Monitoring, Ctr Res Serv, Res Management & Innovat Complex, Kuala Lumpur 50603, Malaysia.
RP Malek, SNA (corresponding author), Univ Malaya, Fac Sci, Inst Biol Sci, Kuala Lumpur 50603, Malaysia.
EM srimalek@yahoo.com
RI Malek, Sri Nurestri Abd/B-9834-2010; Malek, Sri Nurestri/W-8556-2019;
   Hong, Sok Lai/H-9892-2013
OI Malek, Sri Nurestri Abd/0000-0001-6278-8559; Malek, Sri
   Nurestri/0000-0001-6278-8559; Hong, Sok Lai/0000-0003-0721-4012; Ahmad
   Suhaimi, Shafinah/0000-0002-2727-3231
FU High Impact Research MoE from Ministry of Education Malaysia
   [UM.C/625/1/HIR/MoE/SC/02]; Ministry of Education Malaysia; Universiti
   Sains Malaysia (USM)Universiti Sains Malaysia
FX The research is supported by the High Impact Research MoE Grant
   UM.C/625/1/HIR/MoE/SC/02 from the Ministry of Education Malaysia. The
   scholarship to Shafinah Ahmad Suhaimi for financial assistance is
   provided by the Ministry of Education Malaysia as well as Universiti
   Sains Malaysia (USM).
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NR 34
TC 9
Z9 9
U1 1
U2 12
PU MEDKNOW PUBLICATIONS & MEDIA PVT LTD
PI MUMBAI
PA B-9, KANARA BUSINESS CENTRE, OFF LINK RD, GHAKTOPAR-E, MUMBAI, 400075,
   INDIA
SN 0973-1296
EI 0976-4062
J9 PHARMACOGN MAG
JI Pharmacogn. Mag.
PD APR-JUN
PY 2017
VL 13
IS 50
SU 2
BP S179
EP S188
AR PMID 28808378
DI 10.4103/pm.pm_432_16
PG 10
WC Chemistry, Medicinal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA FK7RG
UT WOS:000413704300004
PM 28808378
OA Green Published
DA 2022-04-25
ER

PT J
AU Kim, SH
   Kim, H
AF Kim, Suhn Hyung
   Kim, Hyeyoung
TI Astaxanthin Modulation of Signaling Pathways That Regulate Autophagy
SO MARINE DRUGS
LA English
DT Review
DE AMP activated protein kinase (AMPK); autophagy; astaxanthin; cellular
   homolog of murine thymoma virus akt8 oncogene (Akt); mitogen-activated
   protein kinases (MAPK); c-Jun N-terminal kinase (JNK); p38
ID ACTIVATED PROTEIN-KINASE; ENDOPLASMIC-RETICULUM STRESS; N-TERMINAL
   KINASE; OXIDATIVE STRESS; CELL-DEATH; UP-REGULATION; INDUCED
   CYTOTOXICITY; INDUCED APOPTOSIS; TUMOR-SUPPRESSOR; COLON-CANCER
AB Autophagy is a lysosomal pathway that degrades and recycles unused or dysfunctional cell components as well as toxic cytosolic materials. Basal autophagy favors cell survival. However, the aberrant regulation of autophagy can promote pathological conditions. The autophagy pathway is regulated by several cell-stress and cell-survival signaling pathways that can be targeted for the purpose of disease control. In experimental models of disease, the carotenoid astaxanthin has been shown to modulate autophagy by regulating signaling pathways, including the AMP-activated protein kinase (AMPK), cellular homolog of murine thymoma virus akt8 oncogene (Akt), and mitogen-activated protein kinase (MAPK), such as c-Jun N-terminal kinase (JNK) and p38. Astaxanthin is a promising therapeutic agent for the treatment of a wide variety of diseases by regulating autophagy.
C1 [Kim, Suhn Hyung; Kim, Hyeyoung] Yonsei Univ, Coll Human Ecol, Brain Korea 21 PLUS Project, Dept Food & Nutr, Seoul 03722, South Korea.
RP Kim, H (corresponding author), Yonsei Univ, Coll Human Ecol, Brain Korea 21 PLUS Project, Dept Food & Nutr, Seoul 03722, South Korea.
EM cigdoli2@naver.com; kim626@yonsei.ac.kr
OI Kim, Hyeyoung/0000-0002-7019-917X
FU National Research Foundation (NRF) of Korea - Korean Government
   [NRF-2018 R1A2A2A01004855]
FX This study was supported financially by a grant from the National
   Research Foundation (NRF) of Korea, which is funded by the Korean
   Government (NRF-2018 R1A2A2A01004855).
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NR 135
TC 16
Z9 18
U1 5
U2 13
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 1660-3397
J9 MAR DRUGS
JI Mar. Drugs
PD OCT
PY 2019
VL 17
IS 10
AR 546
DI 10.3390/md17100546
PG 22
WC Chemistry, Medicinal; Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA JP1XI
UT WOS:000498064500006
PM 31547619
OA Green Published, gold
DA 2022-04-25
ER

PT J
AU Xu, W
   Yu, MH
   Qin, J
   Luo, Y
   Zhong, M
AF Xu, Wei
   Yu, Minhao
   Qin, Jun
   Luo, Yang
   Zhong, Ming
TI LACTB Regulates PIK3R3 to Promote Autophagy and Inhibit EMT and
   Proliferation Through the PI3K/AKT/mTOR Signaling Pathway in Colorectal
   Cancer
SO CANCER MANAGEMENT AND RESEARCH
LA English
DT Article
DE colorectal cancer; LACTB; PIK3R3; EMT; proliferation; autophagy
ID RETINAL-PIGMENT EPITHELIUM; CELL-CYCLE ARREST; MESENCHYMAL TRANSITION;
   THERAPEUTIC TARGET; ACTIVATION; CARCINOMA; APOPTOSIS; EXPRESSION;
   MIGRATION; PROTEIN
AB Background: Colorectal cancer (CRC) is one of the most common aggressive malignancies. LACTB functions as a tumor suppressor, and previous findings have demonstrated that LACTB can inhibit epithelial-to-mesenchymal transition (EMT) and proliferation of breast cancer and CRC cells. However, few studies have investigated the roles of LACTB in autophagy and proliferation in CRC. The current study aimed to identify the roles of LACTB in EMT and proliferation associated with autophagy in CRC and to elucidate the probable molecular mechanisms through which LACTB are involved in these processes.
   Materials and Methods: Transwell invasion, MTT, transmission electron microscopy, RNA-seq, immunoprecipitation, immunohistochemistry and Western blotting assays were performed to evaluate the migratory, invasive, proliferative and autophagic abilities of CRC cells, and the levels of active molecules involved in PI3K/AKT signaling were examined through Western blotting analysis. In addition, the in vivo function of LACTB was assessed using a tumor xenograft model.
   Results: Weaker LACTB expression was found in CRC tissue samples than in nonmalignant tissue samples, and LACTB inhibited cell invasion, migration, and proliferation by promoting autophagy in vitro. Furthermore, the regulatory effects of LACTB on autophagy and EMT were partially attributed to the PI3K/AKT signaling pathway. The in vivo results also showed that LACTB modulated CRC tumorigenesis.
   Conclusion: LACTB can regulate the activity of PIK3R3 to influence the level of PI3K, and it also promotes autophagy and inhibits EMT and proliferation in part through the PI3K/AKT/mTOR signaling pathway.
C1 [Xu, Wei; Yu, Minhao; Qin, Jun; Luo, Yang; Zhong, Ming] Shanghai Jiao Tong Univ, Renji Hosp, Sch Med, Dept Gastrointestinal Surg, Shanghai 200127, Peoples R China.
RP Zhong, M (corresponding author), Shanghai Jiao Tong Univ, Renji Hosp, Sch Med, Dept Gastrointestinal Surg, Shanghai 200127, Peoples R China.
EM drzhongming1966@163.com
FU National Natural Science Foundation of ChinaNational Natural Science
   Foundation of China (NSFC) [81860435, 81873555, 81672347]
FX This work was supported by grants from the National Natural Science
   Foundation of China (grant numbers 81860435, 81873555, and 81672347).
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NR 63
TC 15
Z9 15
U1 1
U2 4
PU DOVE MEDICAL PRESS LTD
PI ALBANY
PA PO BOX 300-008, ALBANY, AUCKLAND 0752, NEW ZEALAND
SN 1179-1322
J9 CANCER MANAG RES
JI Cancer Manag. Res.
PY 2020
VL 12
BP 5181
EP 5200
DI 10.2147/CMAR.S250661
PG 20
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA MJ7NK
UT WOS:000548274500003
PM 32636680
OA gold, Green Published
DA 2022-04-25
ER

PT J
AU Zhang, HG
   Wang, FJ
   Wang, Y
   Zhao, ZX
   Qiao, PF
AF Zhang, Hao-Gang
   Wang, Fu-Jing
   Wang, Yao
   Zhao, Zi-Xing
   Qiao, Peng-Fei
TI lncRNA GAS5 inhibits malignant progression by regulating macroautophagy
   and forms a negative feedback regulatory loop with the
   miR-34a/mTOR/SIRT1 pathway in colorectal cancer
SO ONCOLOGY REPORTS
LA English
DT Article
DE colorectal cancer; lncRNA GAS5; macroautophagy; miR-34a; negative
   feedback regulatory loop
ID NONCODING RNA GAS5; TUMOR-SUPPRESSOR; AUTOPHAGY; METASTASIS; EXPRESSION;
   RESISTANCE; ACTIVATION; APOPTOSIS; PROMOTES; CELLS
AB Long non-coding RNA growth arrest specific 5 (GAS5) exerts inhibitory effects through the modulation of several target microRNAs (miRs) in cancer. However, its potential roles and underlying relationship during colorectal cancer (CRC) progression are unclear. Therefore, we explored the role of the negative feedback loop formed by the GAS5/miR-34a axis and mammalian target of rapamycin/sirtuin 1 (mTOR/SIRT1) pathway on macroautophagy and apoptosis in CRC. Expression of GAS5, miR-34a, SIRT1 and mTOR in CRC patients and cell lines was detected by quantitative reverse transcription polymerase chain reaction. Online bioinformatic analysis was used to predict the downstream miRs of GAS5. Luciferase assay and western blotting were performed to demonstrate miR-34a as a downstream target gene of GAS5 in CRC cells. The effects of the GAS5/miR-34a axis on apoptosis, macroautophagy, and the mTOR/SIRT1 pathway were assessed by flow cytometry, transmission electron microscopy and western blotting, respectively. Our results suggested that GAS5 was downregulated and acted as a molecular sponge of miR-34a during CRC progression. miR-34a participated in regulating GAS5-suppressed CRC cell macroautophagy and induced apoptosis through the mTOR/SIRT1 pathway. GAS5-mediated macroautophagy was maintained in an equilibrium state that might have a protective effect on CRC cell apoptosis. The mTOR signaling pathway suppressed GAS5 expression and formed a negative regulation feedback loop with miR-34a in CRC cells. Our results suggested that the GAS5/miR-34a/SIRT1/mTOR negative regulatory feedback loop mediated CRC cell macroautophagy, and maintained the cells in an autonomous equilibrium state, but not excessive activation state, which functions as a strong antiapoptotic phenotype during human CRC progression.
C1 [Zhang, Hao-Gang; Wang, Fu-Jing; Wang, Yao; Zhao, Zi-Xing; Qiao, Peng-Fei] Harbin Med Univ, Affiliated Hosp 2, Dept Gen Surg, 246 Xuefu Rd, Harbin 150001, Heilongjiang, Peoples R China.
RP Qiao, PF (corresponding author), Harbin Med Univ, Affiliated Hosp 2, Dept Gen Surg, 246 Xuefu Rd, Harbin 150001, Heilongjiang, Peoples R China.
EM lunwenqpf@126.com
FU Science Foundation of the Health Commission of Heilongjiang Province
   [2018346]
FX The present study was supported by The Science Foundation of the Health
   Commission of Heilongjiang Province (2018346).
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NR 43
TC 3
Z9 3
U1 0
U2 1
PU SPANDIDOS PUBL LTD
PI ATHENS
PA POB 18179, ATHENS, 116 10, GREECE
SN 1021-335X
EI 1791-2431
J9 ONCOL REP
JI Oncol. Rep.
PD JAN
PY 2021
VL 45
IS 1
BP 202
EP 216
DI 10.3892/or.2020.7825
PG 15
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA PF0LU
UT WOS:000598757000019
PM 33416133
OA hybrid, Green Published
DA 2022-04-25
ER

PT J
AU Zhu, CL
   Liu, F
   Qian, WB
   Zhang, TY
   Li, F
AF Zhu, Changlai
   Liu, Fang
   Qian, Wenbo
   Zhang, Tianyi
   Li, Feng
TI Combined Effect of Sodium Selenite and Ginsenoside Rh2 on HCT116 Human
   Colorectal Carcinoma Cells
SO ARCHIVES OF IRANIAN MEDICINE
LA English
DT Article
DE Colorectal carcinoma; ginsenoside-Rh2; sodiumselenite; synergistic
   effect
ID CANCER PREVENTION; APOPTOSIS; AUTOPHAGY; BAX; ACTIVATION; BCL-2;
   MECHANISMS; INDUCTION; DISEASE; CYCLE
AB Background: Sodium selenite and ginsenoside Rh2 (G-Rh2) are well known for their anticancer properties and have been exploited as a new therapeutic approach. In this study, we are interested to evaluate if sodium selenite and G-Rh2 combination results in a synergistic anticancer effect that could contribute to lower systemic toxicity.
   Methods: We observed the synergistic antitumor effect by combination of sodium selenite and G-Rh2 on HCT-116 human colorectal carcinoma cells in vitro. Cell growth, viability, cell cycle progression and cell apoptosis, Bax/Bc12 ratio, caspase-3 expression, reactive oxygen species (ROS) production and autophagy were evaluated.
   Results: The results showed that sodium selenite and G-Rh2 combination have a synergistic effect on cell growth inhibition (57%) compared with sodium selenite (25%) and G-Rh2 alone (28%) after 24 hours of treatment. This combination also induced G1 and S phase arrest simultaneously and increased apoptosis rate. The results also indicated that Bax/Bc12 ratio and caspase-3 expression, known as proapoptotic factors, were increased in the presence of sodium selenite and G-Rh2 alone. However, combined drug treatment results in a more significant increase in Bax/Bc12 ratio and caspase-3 expression (P < 0.05). In addition, this combination significantly induces a depletion of ROS production and autophagy, compared to control, sodium selenite and G-Rh2 alone (P < 0.05).
   Conclusion: Sodium selenite and ginsenoside Rh2 combination may be a more effective treatment for human colorectal carcinoma and is a promising chemotherapeutic approach for malignant tumors.
C1 [Zhu, Changlai; Liu, Fang] Nantong Univ, Coinnovat Ctr Neuroregenerat, Jiangsu Key Lab Neuroregenerat, Nantong, Jiangsu, Peoples R China.
   [Qian, Wenbo; Zhang, Tianyi] Nantong Univ, Coll Med, Nantong, Jiangsu, Peoples R China.
   [Li, Feng] Nantong Univ, Affiliated Hosp, Dept Gastroenterol, 20 Xisi Rd, Nantong 226001, Jiangsu, Peoples R China.
RP Li, F (corresponding author), Nantong Univ, Affiliated Hosp, Dept Gastroenterol, 20 Xisi Rd, Nantong 226001, Jiangsu, Peoples R China.
EM willim118@hotmail.com
FU Scientific and Technical Development Program of Nanton [K2010018]
FX This study was supported by Scientific and Technical Development Program
   of Nanton (Grant No. K2010018).
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NR 35
TC 14
Z9 17
U1 1
U2 6
PU ACAD MEDICAL SCIENCES I R IRAN
PI TEHRAN
PA PO BOX 19395-5655, TEHRAN, 00000, IRAN
SN 1029-2977
EI 1735-3947
J9 ARCH IRAN MED
JI Arch. Iran. Med.
PD JAN
PY 2016
VL 19
IS 1
BP 23
EP 29
PG 7
WC Medicine, General & Internal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC General & Internal Medicine
GA DC9LK
UT WOS:000369542900003
PM 26702744
DA 2022-04-25
ER

PT J
AU Tyciakova, S
   Valova, V
   Svitkova, B
   Matuskova, M
AF Tyciakova, Silvia
   Valova, Valeria
   Svitkova, Barbora
   Matuskova, Miroslava
TI Overexpression of TNF alpha induces senescence, autophagy and
   mitochondrial dysfunctions in melanoma cells
SO BMC CANCER
LA English
DT Article
DE TNF alpha; Melanoma; Senescence; Autophagy; Aldehyde dehydrogenase
   activity; Mitochondrial status; Cancer stem cell-related markers
ID TUMOR-NECROSIS-FACTOR; CANCER STEM-CELLS
AB BackgroundTumor necrosis factor alpha (TNF alpha) is a pleiotropic cytokine with both anti-tumorigenic and pro-tumorigenic activity, affecting tumor cell biology, the balance between cell survival and death. The final effect of TNF alpha is dependent on the type of malignant cells, with the potential to arrest cancer progression.MethodsIn order to explain the diverse cellular response to TNF alpha, we engineered melanoma and colorectal carcinoma cell lines stably overexpressing this cytokine.ResultsUnder the TNF alpha overexpression, significant upregulation of two genes was observed: proinflammatory cytokine IL6 gene in melanoma cells A375 and gene for pro-apoptotic ligand TRAIL in colorectal carcinoma cells HT29, both mediated by TNF alpha /TNFR1 signaling. Malignant melanoma line A375 displayed also increased autophagy on day 3, followed by premature senescence on day 6. Both processes seem to be interconnected, following earlier apoptosis induction and deregulation of mitochondrial functions. We documented altered mitochondrial status, lowered ATP production, lowered mitochondrial mass, and changes in mitochondrial morphology (shortened and condensed mitochondria) both in melanoma and colorectal carcinoma cells. Overexpression of TNF alpha was not linked with significant affection of the subpopulation of cancer stem-like cells in vitro. However, we could demonstrate a decrease in aldehyde dehydrogenase (ALDH) activity up to 50%, which is associated with to the stemness phenotype.ConclusionsOur in vitro study of direct TNF alpha influence demonstrates two distinct outcomes in tumor cells of different origin, in non-epithelial malignant melanoma cells of neural crest origin, and in colorectal carcinoma cells derived from the epithelium.
C1 [Tyciakova, Silvia; Valova, Valeria; Svitkova, Barbora; Matuskova, Miroslava] Slovak Acad Sci, Biomed Res Ctr, Canc Res Inst, Dubravska Cesta 9, Bratislava 84505, Slovakia.
   [Valova, Valeria] Comenius Univ, Dept Genet, Fac Nat Sci, Ilkovicova 6, Bratislava 84215, Slovakia.
RP Tyciakova, S (corresponding author), Slovak Acad Sci, Biomed Res Ctr, Canc Res Inst, Dubravska Cesta 9, Bratislava 84505, Slovakia.
EM silvia.tyciakova@savba.sk
RI Svitkova, Barbora/AAV-9228-2020; Tyciakova, Silvia/F-7089-2018
OI Tyciakova, Silvia/0000-0003-2919-0410; Svitkova (Buliakova),
   Barbora/0000-0001-8927-3934
FU VEGAVedecka grantova agentura MSVVaS SR a SAV (VEGA)European Commission
   [02/178/17, 02/0050/19]; Ministry of Health of the Slovak Republic
   [2019/60-BMCSAV-4]; EU Horizon 2020 Research and Innovation programme
   [857381]; UVP BIOMED [ITMS 26240220087]; Slovak Cancer Research
   Foundation [RFL2009, RFL2012]
FX This work was supported by VEGA grants no. 02/178/17, 02/0050/19; by
   Ministry of Health of the Slovak Republic under the project registration
   number 2019/60-BMCSAV-4, EU Horizon 2020 Research and Innovation
   programme under grant agreement No 857381 (VISION), by UVP BIOMED -
   project ITMS 26240220087 and by Slovak Cancer Research Foundation
   RFL2009 and RFL2012 programs. The funding did not affect the design of
   the study, collection, analysis or interpretation of data or preparation
   of the manuscript.
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NR 43
TC 0
Z9 0
U1 1
U2 4
PU BMC
PI LONDON
PA CAMPUS, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
EI 1471-2407
J9 BMC CANCER
JI BMC Cancer
PD MAY 6
PY 2021
VL 21
IS 1
AR 507
DI 10.1186/s12885-021-08237-1
PG 13
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA SI5TC
UT WOS:000654886600005
PM 33957885
OA Green Published, gold
DA 2022-04-25
ER

PT J
AU Yang, Z
   Liang, SQ
   Saliakoura, M
   Yang, HT
   Vassella, E
   Konstantinidou, G
   Tschan, M
   Hegedus, B
   Zhao, L
   Gao, YY
   Xu, D
   Deng, HB
   Marti, TM
   Kocher, GJ
   Wang, WX
   Schmid, RA
   Peng, RW
AF Yang, Zhang
   Liang, Shun-Qing
   Saliakoura, Maria
   Yang, Haitang
   Vassella, Eric
   Konstantinidou, Georgia
   Tschan, Mario
   Hegedus, Balazs
   Zhao, Liang
   Gao, Yanyun
   Xu, Duo
   Deng, Haibin
   Marti, Thomas M.
   Kocher, Gregor J.
   Wang, Wenxiang
   Schmid, Ralph A.
   Peng, Ren-Wang
TI Synergistic effects of FGFR1 and PLK1 inhibitors target a metabolic
   liability in KRAS-mutant cancer
SO EMBO MOLECULAR MEDICINE
LA English
DT Article
DE autophagy; fibroblast growth factor receptor 1; KRAS-mutant cancer;
   polo-like kinase 1; synthetic lethal vulnerability
ID NON-ONCOGENE ADDICTION; CELL LUNG-CANCER; KINASE INHIBITOR; AUTOPHAGY;
   THERAPY; GROWTH; PHOSPHORYLATION; VULNERABILITIES; PROGRESSION;
   MUTATIONS
AB KRAS oncoprotein is commonly mutated in human cancer, but effective therapies specifically targeting KRAS-driven tumors remain elusive. Here, we show that combined treatment with fibroblast growth factor receptor 1 (FGFR1) and polo-like kinase 1 (PLK1) inhibitors evoke synergistic cytotoxicity in KRAS-mutant tumor models in vitro and in vivo. Pharmacological and genetic suppression of FGFR1 and PLK1 synergizes to enhance anti-proliferative effects and cell death in KRAS-mutant lung and pancreatic but not colon nor KRAS wild-type cancer cells. Mechanistically, co-targeting FGFR1 and PLK1 upregulates reactive oxygen species (ROS), leading to oxidative stress-activated c-Jun N-terminal kinase (JNK)/p38 pathway and E2F1-induced apoptosis. We further delineate that autophagy protects from PLK1/FGFR1 inhibitor cytotoxicity and that antagonizing the compensation mechanism by clinically approved chloroquine fully realizes the therapeutic potential of PLK1 and FGFR1 targeting therapy, producing potent and durable responses in KRAS-mutant patient-derived xenografts and a genetically engineered mouse model of Kras-induced lung adenocarcinoma. These results suggest a previously unappreciated role for FGFR1 and PLK1 in the surveillance of metabolic stress and demonstrate a synergistic drug combination for treating KRAS-mutant cancer.
C1 [Yang, Zhang; Liang, Shun-Qing; Yang, Haitang; Zhao, Liang; Gao, Yanyun; Xu, Duo; Deng, Haibin; Marti, Thomas M.; Kocher, Gregor J.; Schmid, Ralph A.; Peng, Ren-Wang] Univ Bern, Bern Univ Hosp, Inselspital, Div Gen Thorac Surg,Dept BioMed Res DBMR, Bern, Switzerland.
   [Yang, Zhang] Fujian Med Univ, Union Hosp, Dept Thorac Surg, Fuzhou, Peoples R China.
   [Saliakoura, Maria; Konstantinidou, Georgia] Univ Bern, Inst Pharmacol, Bern, Switzerland.
   [Vassella, Eric; Tschan, Mario] Univ Bern, Inst Pathol, Bern, Switzerland.
   [Hegedus, Balazs] Univ Duisburg Essen, Univ Med Essen, Ruhrlandklin, Dept Thorac Surg, Essen, Germany.
   [Wang, Wenxiang] Cent South Univ, Hunan Canc Hosp, Thorac Surg Dept 2, Changsha, Peoples R China.
   [Wang, Wenxiang] Cent South Univ, Affiliated Canc Hosp, Xiangya Sch Med, Changsha, Peoples R China.
RP Schmid, RA; Peng, RW (corresponding author), Univ Bern, Bern Univ Hosp, Inselspital, Div Gen Thorac Surg,Dept BioMed Res DBMR, Bern, Switzerland.
EM ralph.schmid@insel.ch; renwang.peng@insel.ch
RI Hegedus, Balazs/B-6076-2008; Konstantinidou, Georgia/O-9192-2016; Yang,
   Haitang/M-9742-2017
OI Hegedus, Balazs/0000-0002-4341-4153; Konstantinidou,
   Georgia/0000-0001-9513-0286; Tschan, Mario P./0000-0001-5897-3647; Peng,
   Ren-Wang/0000-0003-1199-6520; Yang, Haitang/0000-0002-8732-5910; Yang,
   Zhang/0000-0001-8592-5800; Gao, Yanyun/0000-0002-1226-3073
FU Swiss National Science Foundation (SNSF)Swiss National Science
   Foundation (SNSF) [310030_192648]; Swiss Cancer League/Swiss Cancer
   Research Foundation [KFS-4851-08-2019]; Cancer League of the Canton of
   Bern; China Scholarship CouncilChina Scholarship Council
FX We acknowledge Matteo Rossi Sebastiano (Institute of Pharmacology,
   University of Bern) for animal studies and in vitro experiments. The
   PF139 and PF563 cell lines were established in collaboration with the
   West-German Biobank Essen (WBE). This work was supported by grants from
   Swiss National Science Foundation (SNSF; #310030_192648; to R-W. Peng),
   Swiss Cancer League/Swiss Cancer Research Foundation (#KFS-4851-08-2019;
   to R-W. Peng), Cancer League of the Canton of Bern (to R-W. Peng; G. J.
   Kocher.), and PhD fellowships from China Scholarship Council (to Z.Y.,
   H.Y., Y. G., H.D.).
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NR 67
TC 2
Z9 2
U1 6
U2 8
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1757-4676
EI 1757-4684
J9 EMBO MOL MED
JI EMBO Mol. Med.
PD SEP 7
PY 2021
VL 13
IS 9
AR e13193
DI 10.15252/emmm.202013193
EA AUG 2021
PG 19
WC Medicine, Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Research & Experimental Medicine
GA UM2IP
UT WOS:000682868100001
PM 34369083
OA Green Published, gold
DA 2022-04-25
ER

PT J
AU Roy, K
   Kanwar, RK
   Krishnakumar, S
   Cheung, CHA
   Kanwar, JR
AF Roy, Kislay
   Kanwar, Rupinder K.
   Krishnakumar, Subramanian
   Cheung, Chun Hei Antonio
   Kanwar, Jagat R.
TI Competitive inhibition of survivin using a cell-permeable recombinant
   protein induces cancer-specific apoptosis in colon cancer model
SO INTERNATIONAL JOURNAL OF NANOMEDICINE
LA English
DT Article
DE nanoparticle; chitosan; mucoadhesive; cytotoxicity; xenograft
ID CHITOSAN NANOPARTICLES; TARGETING SURVIVIN; EXPRESSION; DELIVERY; DEATH;
   DRUG; PROLIFERATION; DEGRADATION; ENHANCERS; RELEASE
AB Endogenous survivin expression has been related with cancer survival, drug resistance, and metastasis. Therapies targeting survivin have been shown to significantly inhibit tumor growth and recurrence. We found out that a cell-permeable dominant negative survivin (SurR9-C84A, referred to as SR9) competitively inhibited endogenous survivin and blocked the cell cycle at the G(1)/S phase. Nanoencapsulation in mucoadhesive chitosan nanoparticles (CHNP) substantially increased the bioavailability and serum stability of SR9. The mechanism of nanoparticle uptake was studied extensively in vitro and in ex vivo models. Our results confirmed that CHNP-SR9 protected primary cells from autophagy and successfully induced tumor-specific apoptosis via both extrinsic and intrinsic apoptotic pathways. CHNP-SR9 significantly reduced the tumor spheroid size (three-dimensional model) by nearly 7-fold. Effects of SR9 and CHNP-SR9 were studied on 35 key molecules involved in the apoptotic pathway. Highly significant (4.26-fold, P <= 0.005) reduction in tumor volume was observed using an in vivo mouse xenograft colon cancer model. It was also observed that net apoptotic (6.25-fold, P <= 0.005) and necrotic indexes (3.5-fold, P <= 0.05) were comparatively higher in CHNP-SR9 when compared to void CHNP and CHNP-SR9 internalized more in cancer stem cells (4.5-fold, P <= 0.005). We concluded that nanoformulation of SR9 did not reduce its therapeutic potential; however, nanoformulation provided SR9 with enhanced stability and better bioavailability. Our study presents a highly tumor-specific protein-based cancer therapy that has several advantages over the normally used chemotherapeutics.
C1 [Roy, Kislay; Kanwar, Rupinder K.; Kanwar, Jagat R.] Deakin Univ, Fac Hlth, MMR Strateg Res Ctr, Sch Med,NLIMBR, Waurn Ponds, Vic 3217, Australia.
   [Krishnakumar, Subramanian] Vis Res Fdn, Kamalnayan Bajaj Inst Res Vis & Ophthalmol, Dept Nanobiotechnol, Madras, Tamil Nadu, India.
   [Krishnakumar, Subramanian] Vis Res Fdn, Kamalnayan Bajaj Inst Res Vis & Ophthalmol, L&T Ocular Pathol Dept, Madras, Tamil Nadu, India.
   [Cheung, Chun Hei Antonio] Natl Cheng Kung Univ, Coll Med, Dept Pharmacol, Tainan 70101, Taiwan.
RP Kanwar, JR (corresponding author), Deakin Univ, Fac Hlth, MMR Strateg Res Ctr, Sch Med,NLIMBR, Waurn Ponds, Vic 3217, Australia.
EM jagat.kanwar@deakin.edu.au
OI Cheung, Chun Hei Antonio/0000-0003-4181-1435
FU Australia-India Strategic Research Fund (AISRF)Australian
   GovernmentDepartment of Industry, Innovation and Science; National
   Health and Medical Research Council (NHMRC)National Health and Medical
   Research Council (NHMRC) of Australia
FX The authors would like to thank the Australia-India Strategic Research
   Fund (AISRF) and the National Health and Medical Research Council
   (NHMRC) for financial support.
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NR 44
TC 19
Z9 21
U1 1
U2 14
PU DOVE MEDICAL PRESS LTD
PI ALBANY
PA PO BOX 300-008, ALBANY, AUCKLAND 0752, NEW ZEALAND
SN 1178-2013
J9 INT J NANOMED
JI Int. J. Nanomed.
PY 2015
VL 10
BP 1019
EP 1043
DI 10.2147/IJN.S73916
PG 25
WC Nanoscience & Nanotechnology; Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Science & Technology - Other Topics; Pharmacology & Pharmacy
GA CA2HT
UT WOS:000348730300002
PM 25678789
OA Green Published, gold, Green Submitted
DA 2022-04-25
ER

PT J
AU Cho, DH
   Jo, YK
   Kim, SC
   Park, IJ
   Kim, JC
AF Cho, Dong-Hyung
   Jo, Yoon Kyung
   Kim, Seung Cheol
   Park, In Ja
   Kim, Jin Cheon
TI Down-regulated Expression of ATG5 in Colorectal Cancer
SO ANTICANCER RESEARCH
LA English
DT Article
DE ATG5; autophagy; colorectal cancer; tumor suppressor; LVI
ID AUTOPHAGY; GENE; TUMORIGENESIS; DEFICIENT; ROLES
AB The role of autophagy in tumor development is paradoxical. Although some genetic evidence has indicated that autophagy has as a tumor suppressor function, it also provides some advantages to tumors under metabolic stress conditions. Autophagy is regulated by several autophagy-related gene (ATG) proteins. In mammals, 16 different ATG genes have been identified. To investigate the clinicopathological role of ATG5 in colorectal cancer, we firstly investigated its expression in patients with sporadic colorectal cancer. Expression analysis revealed ATG5 to be strongly down-regulated in colorectal cancer (38140 patients). Interestingly, immunohistochemical analysis of colorectal cancer tissues indicated that increased ATG5 expression is associated with lymphovascular invasion (p=0.035). The findings in our limited clinical cohort indicate that ATG5 could be a potential prognostic or diagnostic biomarker.
C1 [Cho, Dong-Hyung; Jo, Yoon Kyung] Kyung Hee Univ, Grad Sch EW Med Sci, Yongin 446701, Gyeonggi Do, South Korea.
   [Jo, Yoon Kyung; Kim, Seung Cheol; Kim, Jin Cheon] Asan Med Ctr, Inst Innovat Canc Res, Seoul, South Korea.
   [Kim, Seung Cheol; Park, In Ja; Kim, Jin Cheon] Univ Ulsan, Coll Med, Dept Surg, Seoul, South Korea.
RP Cho, DH (corresponding author), Kyung Hee Univ, Grad Sch EW Med Sci, 1 Seocheon Dong, Yongin 446701, Gyeonggi Do, South Korea.
EM dhcho@khu.ac.kr; jckim@amc.seoul.kr
RI Park, In Ja/U-2371-2019
OI Park, In Ja/0000-0001-5355-3969
FU Asan Institute for Life Sciences [2011-069]; Center for Development and
   Commercialization of Anti-Cancer Therapeutics; Korean Health 21 RD
   Project [A062254, A102059]; Ministry of Health, Welfare and Family
   Affairs, Korea), and the Basic Science Research Program [2010-0009164];
   National Research Foundation, KoreaNational Research Foundation of Korea
FX This work was supported by the Asan Institute for Life Sciences
   (2011-069, Asan Foundation, Seoul, Korea), the Center for Development
   and Commercialization of Anti-Cancer Therapeutics and the Korean Health
   21 R&D Project (A062254 and A102059, Ministry of Health, Welfare and
   Family Affairs, Korea), and the Basic Science Research Program
   (2010-0009164, the National Research Foundation, Korea).
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NR 29
TC 45
Z9 50
U1 0
U2 5
PU INT INST ANTICANCER RESEARCH
PI ATHENS
PA EDITORIAL OFFICE 1ST KM KAPANDRITIOU-KALAMOU RD KAPANDRITI, PO BOX 22,
   ATHENS 19014, GREECE
SN 0250-7005
EI 1791-7530
J9 ANTICANCER RES
JI Anticancer Res.
PD SEP
PY 2012
VL 32
IS 9
BP 4091
EP 4096
PG 6
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA 012NN
UT WOS:000309243200070
PM 22993366
DA 2022-04-25
ER

PT J
AU Rosati, A
   Basile, A
   Falco, A
   d'Avenia, M
   Festa, M
   Graziano, V
   De Laurenzi, V
   Arra, C
   Pascale, M
   Turco, MC
AF Rosati, Alessandra
   Basile, Anna
   Falco, Antonia
   d'Avenia, Morena
   Festa, Michelina
   Graziano, Vincenzo
   De Laurenzi, Vincenzo
   Arra, Claudio
   Pascale, Maria
   Turco, Maria Caterina
TI Role of BAG3 protein in leukemia cell survival and response to therapy
SO BIOCHIMICA ET BIOPHYSICA ACTA-REVIEWS ON CANCER
LA English
DT Review
DE BAG3; Cancer; Apoptosis; Leukemia; Autophagy
ID ACUTE LYMPHOBLASTIC-LEUKEMIA; COLON-CANCER CELLS; INDUCED APOPTOSIS;
   TUMOR-SUPPRESSOR; GENE-EXPRESSION; DILATED CARDIOMYOPATHY; BCL-2-BINDING
   PROTEIN; SELECTIVE AUTOPHAGY; REACTIVE ASTROCYTES; CHAPERONE ACTIVITY
AB The ability of BAG3, a member of the BAG family of heat shock protein (Hsp) 70 - cochaperones, to sustain the survival of human primary B-CLL and ALL cells was recognized about nine years ago. Since then, the anti-apoptotic activity of BAG3 has been confirmed in other tumor types, where it has been shown to regulate the intracellular concentration and localization of apoptosis-regulating factors, including NF-kappa B-activating (IKK gamma) and Bcl2-family (Bax) proteins. Furthermore, growing evidences support its role in lymphoid and myeloid leukemia response to therapy. Moreover in the last years, the contribution of BAG3 to autophagy, a process known to be involved in the pathogenesis and response to therapy of leukemia cells, has been disclosed, opening a new avenue for the interpretation of the role of this protein in leukemias' biology. (C) 2012 Elsevier B.V. All rights reserved.
C1 [Pascale, Maria] Univ Salerno, Div Biomed Arturo Leone, FAMABIOMED, BIOUNIVERSA Srl, I-84084 Fisciano, SA, Italy.
   [Rosati, Alessandra; Basile, Anna; Falco, Antonia; d'Avenia, Morena; Festa, Michelina; Pascale, Maria; Turco, Maria Caterina] Univ Salerno, FARMABIOMED, I-84084 Fisciano, SA, Italy.
   [Graziano, Vincenzo; De Laurenzi, Vincenzo] Univ G dAnnunzio, Fdn G DAnnunzio, Ce SI, Dept Biomed Sci, Chieti, Italy.
   [Arra, Claudio] Pascale Tumor Inst, Anim Facil, Naples, Italy.
RP Pascale, M (corresponding author), Univ Salerno, Div Biomed Arturo Leone, FAMABIOMED, BIOUNIVERSA Srl, Via Ponte Don Melillo 11-C, I-84084 Fisciano, SA, Italy.
EM pascale@unisa.it
RI TURCO, Maria Caterina/AAC-5282-2022; De Laurenzi, Vincenzo/K-7471-2016
OI TURCO, Maria Caterina/0000-0002-7835-359X; Rosati,
   Alessandra/0000-0001-6675-0857; Arra, Claudio/0000-0003-3162-2091; De
   Laurenzi, Vincenzo/0000-0002-7506-1743; Graziano,
   Vincenzo/0000-0001-7656-824X
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NR 89
TC 21
Z9 21
U1 0
U2 15
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0304-419X
EI 0006-3002
J9 BBA-REV CANCER
JI Biochim. Biophys. Acta-Rev. Cancer
PD DEC
PY 2012
VL 1826
IS 2
BP 365
EP 369
DI 10.1016/j.bbcan.2012.06.001
PG 5
WC Biochemistry & Molecular Biology; Biophysics; Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Biophysics; Oncology
GA 024JG
UT WOS:000310104900009
PM 22710027
DA 2022-04-25
ER

PT J
AU Choi, PR
   Kang, YJ
   Sung, B
   Kim, JH
   Moon, HR
   Chung, HY
   Kim, SE
   Park, MI
   Park, SJ
   Kim, ND
AF Choi, Pyoung Rak
   Kang, Yong Jung
   Sung, Bokyung
   Kim, Jae Hyun
   Moon, Hyung Ryong
   Chung, Hae Young
   Kim, Sung Eun
   Park, Moo In
   Park, Seun Ja
   Kim, Nam Deuk
TI MHY218-induced apoptotic cell death is enhanced by the inhibition of
   autophagy in AGS human gastric cancer cells
SO INTERNATIONAL JOURNAL OF ONCOLOGY
LA English
DT Article
DE MHY218; gastric cancer cells; apoptosis; autophagy
ID HISTONE DEACETYLASE INHIBITOR; HYDROXAMIC ACID; CLASS-I; EXPRESSION
   PROFILE; GROWTH; COMBINATION; MODULATION; INDUCTION; PATTERNS; SURVIVAL
AB We previously reported the anticancer effects of MHY218, which is a hydroxamic acid derivative, in HCT116 human colon cancer cells. In the present study, the involvement of autophagy in the MHY218-induced apoptotic cell death of AGS human gastric cancer cells was investigated. MHY218 treatment induced growth inhibition and apoptotic cell death in a concentration- and time-dependent manner. The induction of apoptosis was confirmed by observations of decreased viability, DNA fragmentation, and an increase in late apoptosis and sub-G1 DNA, which were detected with a flow cytometric analysis. Western blot analyses showed that MHY218 treatment resulted in decreased protein levels of procaspase-8, -9, and -3; cleavage of poly(ADP-ribose) polymerase (PARP); and alterations in the ratio of Bax/Bcl-2 protein expression. Apoptosis induced by MHY218 was involved in the activation of caspase-8, -9, and -3, and it was blocked by the addition of Z-VAD-FMK, a pan-caspase inhibitor. In addition, autophagy-inducing effects of MHY218 were indicated by cytoplasmic vacuolation, the accumulation of acidic vesicular organelles, the appearance of green fluorescent protein-light-chain 3 (LC3) punctate dots, and increased levels of Beclin-1 and LC3-II protein expression. Pretreatment with the autophagy inhibitors LY294002, 3-methyladenine, chloroquine, and bafilomycin Al enhanced the induction of apoptosis by MHY218, and this was accompanied by an increase in PARP cleavage. Taken together, these results provide new insights into the role of MHY218 as a potential antitumor agent. The combination of MHY218 with an autophagy inhibitor might be a useful candidate for the chemoprevention and/or treatment of gastric cancer.
C1 [Kang, Yong Jung; Sung, Bokyung; Moon, Hyung Ryong; Chung, Hae Young; Kim, Nam Deuk] Pusan Natl Univ, Coll Pharm, Mol Inflammat Res Ctr Aging Intervent MRCA, Busan 609735, South Korea.
   [Choi, Pyoung Rak; Kim, Jae Hyun; Kim, Sung Eun; Park, Moo In; Park, Seun Ja] Kosin Univ, Gospel Hosp, Dept Gastroenterol, Busan 602702, South Korea.
RP Kim, ND (corresponding author), Pusan Natl Univ, Coll Pharm, Dept Pharm, Busan 609735, South Korea.
EM nadkim@pusan.ac.kr
RI Sung, Bokyung/AAX-5697-2021; Kim, Jae Hyun/AAI-9800-2020
OI Kim, Jae Hyun/0000-0002-4272-8003
FU National Research Foundation of Korea (NRF) - Korea government (MSIP)
   [2009-0083538]
FX This study was supported by the National Research Foundation of Korea
   (NRF) grant funded by the Korea government (MSIP) (no. 2009-0083538). We
   thank the Aging Tissue Bank for providing research information.
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NR 47
TC 14
Z9 14
U1 0
U2 12
PU SPANDIDOS PUBL LTD
PI ATHENS
PA POB 18179, ATHENS, 116 10, GREECE
SN 1019-6439
EI 1791-2423
J9 INT J ONCOL
JI Int. J. Oncol.
PD AUG
PY 2015
VL 47
IS 2
BP 563
EP 572
DI 10.3892/ijo.2015.3031
PG 10
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA CM8QC
UT WOS:000357965700018
PM 26043797
OA Bronze
DA 2022-04-25
ER

PT J
AU Zeng, XH
   Kinsella, TJ
AF Zeng, Xuehuo
   Kinsella, Timothy J.
TI Mammalian target of rapamycin and S6 kinase 1 positively regulate
   6-thioguanine-induced autophagy
SO CANCER RESEARCH
LA English
DT Article
ID DNA MISMATCH REPAIR; DROSOPHILA FAT-BODY; HUMAN TUMOR-CELLS; MONITORING
   AUTOPHAGY; CANCER-CELLS; MTOR; TUMORIGENESIS; SUPPRESSOR; GROWTH; GENE
AB DNA mismatch repair (MMR) ensures the fidelity of DNA replication and is required for activation of cell cycle arrest and apoptosis in response to certain classes of DNA damage. We recently reported that MMR is also implicated in initiation of an autophagic response after MMR processing of 6-thioguanine (6-TG). It is now generally believed that autophagy is negatively controlled by mammalian target of rapamycin (mTOR) activity. To determine whether mTOR is involved in 6-TG-induced autophagy, we used rapamycin, a potential anticancer agent, to inhibit mTOR activity. Surprisingly, we find that rapamycin cotreatment inhibits 6-TG-induced autophagy in MMR-proficient human colorectal cancer HCT116 (MLH1(+)) and HT29 cells as measured by LC3 immunoblotting, GFP-LC3 relocalization, and acridine orange staining. Consistently, short interfering RNA silencing of the 70-kDa ribosomal S6 kinase 1 (S6K1), the downstream effector of mTOR, markedly reduces 6-TG-induced autophagy. Furthermore, we show that inhibition of mTOR by rapamycin induces the activation of Akt as shown by increased Akt phosphorylation at Ser(473) and the inhibition of 6-TG-induced apoptosis and cell death. Activated Akt is a well-known inhibitor of autophagy. In conclusion, our data indicate that mTOR-S6K1 positively regulates autophagy after MMR processing of 6-TG probably through its negative feedback inhibition of Akt.
C1 Case Western Reserve Univ, Univ Hosp Case Med Ctr, Dept Radiat Oncol, Cleveland, OH 44106 USA.
   Univ Hosp Case Med Ctr, Case Comprehens Canc Ctr, Case Integrat Canc Biol Program, Cleveland, OH 44106 USA.
RP Kinsella, TJ (corresponding author), Case Western Reserve Univ, Univ Hosp Case Med Ctr, Dept Radiat Oncol, LTR6068,11100 Euclid Ave, Cleveland, OH 44106 USA.
EM timothy.kinsella@uhhospitals.org
FU NCI NIH HHSUnited States Department of Health & Human ServicesNational
   Institutes of Health (NIH) - USANIH National Cancer Institute (NCI)
   [CA50595, R01 CA050595, CA112963, U56 CA112963] Funding Source: Medline;
   NATIONAL CANCER INSTITUTEUnited States Department of Health & Human
   ServicesNational Institutes of Health (NIH) - USANIH National Cancer
   Institute (NCI) [R01CA050595] Funding Source: NIH RePORTER
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NR 46
TC 90
Z9 93
U1 0
U2 7
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
J9 CANCER RES
JI Cancer Res.
PD APR 1
PY 2008
VL 68
IS 7
BP 2384
EP 2390
DI 10.1158/0008-5472.CAN-07-6163
PG 7
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA 284WU
UT WOS:000254738500041
PM 18381446
DA 2022-04-25
ER

PT J
AU Cheng, X
   Feng, HR
   Wu, HX
   Jin, ZJ
   Shen, XN
   Kuang, J
   Huo, Z
   Chen, XZ
   Gao, HJ
   Ye, F
   Ji, XP
   Jing, XQ
   Zhang, YQ
   Zhang, T
   Qiu, WH
   Zhao, R
AF Cheng, Xi
   Feng, Haoran
   Wu, Haoxuan
   Jin, Zhijian
   Shen, Xiaonan
   Kuang, Jie
   Huo, Zhen
   Chen, Xianze
   Gao, Haoji
   Ye, Feng
   Ji, Xiaopin
   Jing, Xiaoqian
   Zhang, Yaqi
   Zhang, Tao
   Qiu, Weihua
   Zhao, Ren
TI Targeting autophagy enhances apatinib-induced apoptosis via endoplasmic
   reticulum stress for human colorectal cancer
SO CANCER LETTERS
LA English
DT Article
DE Tyrosine kinase inhibitor; Chloroquine; IRE1 alpha; Drug resistance
ID RESISTANCE; PATHWAY; ER
AB Apatinib, a novel tyrosine kinase inhibitor (TKI), has been confirmed for its efficacy and safety in the treatment of advanced gastric carcinoma and some other solid tumors. However, the direct functional mechanisms of tumor lethality mediated by apatinib have not yet been fully characterized, and the precise mechanisms of drug resistance are largely unknown. Here, in this study, we demonstrated that apatinib could induce both apoptosis and autophagy in human colorectal cancer (CRC) via a mechanism that involved endoplasmic reticulum (ER) stress. Moreover, activation of the IRE1 alpha pathway from apatinib-induced ER stress is responsible for the induction of autophagy; however, blocking autophagy could enhance the apoptosis in apatinib-treated human CRC cell lines. Furthermore, the combination of apatinib with autophagy inhibitor chloroquine (CQ) tends to have the most significant anti-tumor effect of CRC both in vitro and in vivo. Overall, our data show that because apatinib treatment could induce ER stress-related apoptosis and protective autophagy in human CRC cell lines, targeting autophagy is a promising therapeutic strategy to relieve apatinib drug resistance in CRC.
C1 [Cheng, Xi; Feng, Haoran; Wu, Haoxuan; Jin, Zhijian; Kuang, Jie; Huo, Zhen; Chen, Xianze; Gao, Haoji; Ye, Feng; Ji, Xiaopin; Jing, Xiaoqian; Zhang, Yaqi; Zhang, Tao; Qiu, Weihua; Zhao, Ren] Shanghai Jiao Tong Univ, Ruijin Hosp, Dept Gen Surg, Sch Med, Shanghai 200025, Peoples R China.
   [Cheng, Xi; Feng, Haoran; Wu, Haoxuan; Jin, Zhijian; Kuang, Jie; Huo, Zhen; Chen, Xianze; Gao, Haoji; Ye, Feng; Ji, Xiaopin; Jing, Xiaoqian; Zhang, Yaqi; Zhang, Tao; Qiu, Weihua; Zhao, Ren] Shanghai Jiao Tong Univ, Ruijin Hosp, Shanghai Inst Digest Surg, Sch Med, Shanghai 200025, Peoples R China.
   [Cheng, Xi; Zhao, Ren] Shanghai Jiao Tong Univ, Ruijin North Hosp, Dept Gen Surg, Sch Med, Shanghai 201801, Peoples R China.
   [Shen, Xiaonan] Shanghai Jiao Tong Univ, Renji Hosp, Dept Gastroenterol, Sch Med, Shanghai 200001, Peoples R China.
RP Zhang, T; Qiu, WH; Zhao, R (corresponding author), Shanghai Jiao Tong Univ, Ruijin Hosp, Dept Gen Surg, Sch Med, Shanghai 200025, Peoples R China.
EM woodyhom@yahoo.com; qwh11072@rjh.com.cn; rjzhaoren@139.com
FU Nature Science Foundation of China NSFCNational Natural Science
   Foundation of China (NSFC) [81772558]; Clinical Skill and Innovation
   3-year program of Shanghai Hospital Development Center [16CR2064B];
   Ph.D. Innovation Fund of Shanghai Jiaotong University School of Medicine
   [BXJ201709]
FX Nature Science Foundation of China NSFC (81772558), Clinical Skill and
   Innovation 3-year program of Shanghai Hospital Development Center
   (16CR2064B), Ph.D. Innovation Fund of Shanghai Jiaotong University
   School of Medicine (BXJ201709) and "Visiting Programs for Graduate
   Students of Shanghai Jiaotong University School of Medicine".
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NR 34
TC 63
Z9 67
U1 1
U2 18
PU ELSEVIER IRELAND LTD
PI CLARE
PA ELSEVIER HOUSE, BROOKVALE PLAZA, EAST PARK SHANNON, CO, CLARE, 00000,
   IRELAND
SN 0304-3835
EI 1872-7980
J9 CANCER LETT
JI Cancer Lett.
PY 2018
VL 431
BP 105
EP 114
DI 10.1016/j.canlet.2018.05.046
PG 10
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA GM8KM
UT WOS:000438477500011
PM 29859300
OA hybrid
DA 2022-04-25
ER

PT J
AU Aredia, F
   Czaplinski, S
   Fulda, S
   Scovassi, AI
AF Aredia, Francesca
   Czaplinski, Sebastian
   Fulda, Simone
   Scovassi, A. Ivana
TI Molecular features of the cytotoxicity of an NHE inhibitor: Evidence of
   mitochondrial alterations, ROS overproduction and DNA damage
SO BMC CANCER
LA English
DT Article
DE Apoptosis; Autophagy; HMA; Mitochondria; NHE; PAR; RIPK3; ROS
ID CELL-DEATH; CANCER; NECROPTOSIS; APOPTOSIS; STRESS; POLY(ADP-RIBOSE);
   MECHANISMS; AMILORIDE; WARBURG; PATHWAY
AB Background: NH exchangers (NHEs) play a crucial role in regulating intra/extracellular pH, which is altered in cancer cells, and are therefore suitable targets to alter cancer cell metabolism in order to inhibit cell survival and proliferation. Among NHE inhibitors, amiloride family members are commonly used in clinical practice as diuretics; we focused on the amiloride HMA, reporting a net cytotoxic effect on a panel of human cancer cell lines; now we aim to provide new insights into the molecular events leading to cell death by HMA.
   Methods: Colon cancer cell lines were treated with HMA and analysed with: morphological and cellular assays for cell viability and death, and autophagy; biochemical approaches to evaluate mitochondrial function and ROS production; in situ detection of DNA damage; molecular tools to silence crucial autophagy/necroptosis factors.
   Results: HMA affects cellular morphology, alters mitochondrial structure and function, causes an increase in ROS, which is detrimental to DNA integrity, stimulates poly(ADP-ribose) synthesis, activates RIPK3-dependent death and triggers autophagy, which is unable to rescue cell survival. These features are hot points of an intricate network of processes, including necroptosis and autophagy, regulating the homeostasis between survival and death.
   Conclusion: Our results allow the identification of multiple events leading to cell death in cancer cells treated with HMA. The here-defined intricate network activated by HMA could be instrumental to selectively target the key players of each pathway in the attempt to improve the global response to HMA. Our data could be the starting point for developing a newly designed targeted therapy.
C1 [Aredia, Francesca; Scovassi, A. Ivana] CNR, Ist Genet Mol, Via Abbiategrasso 207, I-27100 Pavia, Italy.
   [Aredia, Francesca] Univ Pavia, Dipartimento Biol & Biotecnol L Spallanzani, Via Ferrata 9, I-27100 Pavia, Italy.
   [Czaplinski, Sebastian; Fulda, Simone] Goethe Univ, Inst Expt Canc Res Pediat, Komturstr 3A, D-60528 Frankfurt, Germany.
RP Scovassi, AI (corresponding author), CNR, Ist Genet Mol, Via Abbiategrasso 207, I-27100 Pavia, Italy.
EM scovassi@igm.cnr.it
OI Fulda, Simone/0000-0002-0459-6417
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NR 49
TC 9
Z9 10
U1 0
U2 4
PU BMC
PI LONDON
PA CAMPUS, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 1471-2407
J9 BMC CANCER
JI BMC Cancer
PD NOV 5
PY 2016
VL 16
AR 851
DI 10.1186/s12885-016-2878-9
PG 14
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA EB8KL
UT WOS:000387639800001
PM 27816051
OA Green Published, gold
DA 2022-04-25
ER

PT J
AU Gong, K
   Chen, C
   Zhan, Y
   Chen, Y
   Huang, ZB
   Li, WH
AF Gong, Ke
   Chen, Chao
   Zhan, Yao
   Chen, Yan
   Huang, Zebo
   Li, Wenhua
TI Autophagy-related Gene 7 (ATG7) and Reactive Oxygen
   Species/Extracellular Signal-regulated Kinase Regulate
   Tetrandrine-induced Autophagy in Human Hepatocellular Carcinoma
SO JOURNAL OF BIOLOGICAL CHEMISTRY
LA English
DT Article
ID COLON-CANCER CELLS; CYTOCHROME-C; APOPTOSIS; DEATH; ACTIVATION; PATHWAY;
   MITOCHONDRIA; THERAPY; GROWTH; PERMEABILIZATION
AB Tetrandrine, a bisbenzylisoquinoline alkaloid isolated from the broadly used Chinese medicinal herb Stephaniae tetrandrae, exhibits potent antitumor effects and has the potential to be used as a cancer chemotherapeutic agent. We previously reported that high concentrations of tetrandrine induce apoptosis in liver cancer cells. Here, we found that in human hepatocellular carcinoma (HCC) cells, a low dose of tetrandrine (5 mu M) induced the expression of LC3-II, resulted in the formation of acidic autophagolysosome vacuoles (AVOs), and caused a punctate fluorescence pattern with the GFP-LC3 protein, which all are markers for cellular autophagy. Tetrandrine induced the production of intracellular reactive oxygen species (ROS), and treatment with ROS scavengers significantly abrogated the tetrandrine-induced autophagy. These results suggest that the generation of ROS plays an important role in promoting tetrandrine-induced autophagy. Tetrandrine-induced mitochondrial dysfunction resulted in ROS accumulation and autophagy. ROS generation activated the ERK MAP kinase, and the ERK signaling pathway at least partially contributed to tetrandrine-induced autophagy in HCC cells. Moreover, we found that tetrandrine transcriptionally regulated the expression of autophagy related gene 7 (ATG7), which promoted tetrandrine-induced autophagy. In addition to in vitro studies, similar results were also observed in vivo, where tetrandrine caused the accumulation of ROS and induced cell autophagy in a tumor xenograft model. Interestingly, tetrandrine treatment also induced autophagy in a ROS-dependent manner in C. elegans muscle cells. Therefore, these findings suggest that tetrandrine is a potent autophagy agonist and may be a promising clinical chemotherapeutic agent.
C1 [Gong, Ke; Chen, Chao; Zhan, Yao; Li, Wenhua] Wuhan Univ, Coll Life Sci, Wuhan 430072, Peoples R China.
   [Chen, Yan; Huang, Zebo] Wuhan Univ, Coll Pharm, Wuhan 430071, Peoples R China.
RP Li, WH (corresponding author), Wuhan Univ, Coll Life Sci, Wuhan 430072, Peoples R China.
EM whli@whu.edu.cn
RI Huang, Zebo/AAF-2382-2019
OI Huang, Zebo/0000-0003-2431-3741
FU National Basic Research Program of ChinaNational Basic Research Program
   of China [2010CB529800]; National Nature Science Foundation of
   ChinaNational Natural Science Foundation of China (NSFC) [81273540];
   Chinese 111 projectMinistry of Education, China - 111 Project [B06018];
   major scientific and technological special project for "Significant
   Creation of New Drugs" [2011ZX09102-001-32, 2011ZX09401-302-4]
FX This work was supported by National Basic Research Program of China
   Grant 2010CB529800, National Nature Science Foundation of China Grant
   81273540, The Chinese 111 project (B06018), and the major scientific and
   technological special project for "Significant Creation of New Drugs"
   Grants 2011ZX09102-001-32 and 2011ZX09401-302-4.
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   Shao YF, 2004, P NATL ACAD SCI USA, V101, P18030, DOI 10.1073/pnas.0408345102
   Shen YC, 2001, MOL PHARMACOL, V60, P1083, DOI 10.1124/mol.60.5.1083
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   Sung BK, 2010, J BIOL CHEM, V285, P35418, DOI 10.1074/jbc.M110.172767
   Tracy K, 2007, MOL CELL BIOL, V27, P6229, DOI 10.1128/MCB.02246-06
   Wu JM, 2010, CANCER LETT, V287, P187, DOI 10.1016/j.canlet.2009.06.009
   Xie CM, 2011, FREE RADICAL BIO MED, V51, P1365, DOI 10.1016/j.freeradbiomed.2011.06.016
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   Zhang M, 2011, FREE RADICAL BIO MED, V50, P1252, DOI 10.1016/j.freeradbiomed.2011.02.031
NR 57
TC 95
Z9 105
U1 1
U2 35
PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3996 USA
EI 1083-351X
J9 J BIOL CHEM
JI J. Biol. Chem.
PD OCT 12
PY 2012
VL 287
IS 42
BP 35576
EP 35588
DI 10.1074/jbc.M112.370585
PG 13
WC Biochemistry & Molecular Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology
GA 022OF
UT WOS:000309968000070
PM 22927446
OA Green Published, hybrid
DA 2022-04-25
ER

PT J
AU Yuan, DP
   Zhu, YN
AF Yuan, Danping
   Zhu, Yanan
TI Knockdown of LINC01224 Suppresses Colon Cancer Progression by Sponging
   miR-485-5p to Downregulate MCL1
SO CANCER MANAGEMENT AND RESEARCH
LA English
DT Article
DE colon cancer; LINC01224; miR-485-5p; MCL1
ID LONG NONCODING RNAS; CLASSIFICATION; AUTOPHAGY; BCL2
AB Background: Colon cancer (CC) is the most commonly occurring malignant tumor in the world. The current cancer treatment options have been less effective especially in the advanced stages of CC and patients have poor overall survival. Hence, there is an urgent need to explore novel molecular therapeutic targets for CC treatment. Methods: qRT-PCR was performed to detect the levels of lncRNA LINC01224 (LINC01224), microRNA-485-5p (miR-485-5p), MCL1 in CC tumor tissues or cell lines. Two si-RNAs against LINC01224 were used to silence the level of LINC01224, and CCK-8 assay, colony formation assay, and transwell assay were performed to explore the role of LINC01224 on the proliferation, migration, and invasion of CC cell lines. Kaplan-Meier method was applied for evaluating the association between LINC01224 level and the overall survival of CC patients. Through bioinformatics analysis, we found that LINC01224 sponged miR-485-5p and consequently targeted MCL1. Dual-luciferase reporter assay, RNA pull down assay, qRT-PCR, and Western blot assay were conducted for verification of the interactions among LINC01224, miR-485-5p, and MCL1. Furthermore, the role of LINC01224/miR-485-5p/MCL1 axis in CC progression was investigated by CCK-8 assay, colony formation assay, and transwell assay. Results: LINC01224 was highly expressed in CC tumor tissues and CC cell lines, and its expression was associated with the overall survival of CC patients. The LINC01224-siRNAs (si-LINC01224) markedly suppressed the level of LINC01224 in CC cell lines (HT29 and SW480 cells) and consequently significantly suppressed the proliferation, migration, and invasion of the HT29 and SW480 cells. LINC01224 was verified to sponge miR-485-5p and consequently targeted MCL1. MiR-485-5p inhibitor or MCL1 overexpression (MCL1 OE) markedly restored the repressive effect of the si-LINC01224 pool on MCL1 expression level, as well as proliferation, migration, and invasion of HT29 and SW480 cells. Conclusion: This study identified LINC01224/miR-485-5p/MCL1 axis as a novel molecular therapeutic target involved in CC progression.
C1 [Yuan, Danping] Ningbo First Hosp, Dept Colorectal Surg, Ningbo 315010, Zhejiang, Peoples R China.
   [Zhu, Yanan] Taizhou Hosp Zhejiang Prov, Dept Emergency, 150 Ximen St, Linhai 317000, Zhejiang, Peoples R China.
RP Zhu, YN (corresponding author), Taizhou Hosp Zhejiang Prov, Dept Emergency, 150 Ximen St, Linhai 317000, Zhejiang, Peoples R China.
EM zya_cs@163.com
CR Burki TK, 2017, LANCET ONCOL, V18, pE437, DOI 10.1016/S1470-2045(17)30502-8
   Campbell KJ, 2018, OPEN BIOL, V8, DOI 10.1098/rsob.180002
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NR 27
TC 0
Z9 0
U1 0
U2 0
PU DOVE MEDICAL PRESS LTD
PI ALBANY
PA PO BOX 300-008, ALBANY, AUCKLAND 0752, NEW ZEALAND
SN 1179-1322
J9 CANCER MANAG RES
JI Cancer Manag. Res.
PY 2021
VL 13
BP 7803
EP 7812
DI 10.2147/CMAR.S289024
PG 10
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA WH1VT
UT WOS:000707475300002
PM 34675675
OA Green Published, gold
DA 2022-04-25
ER

PT J
AU Raposo, LR
   Silva, A
   Silva, D
   Roma-Rodrigues, C
   Espadinha, M
   Baptista, PV
   Santos, MMM
   Fernandes, AR
AF Raposo, Luis R.
   Silva, Ana
   Silva, Dario
   Roma-Rodrigues, Catarina
   Espadinha, Margarida
   Baptista, Pedro, V
   Santos, Maria M. M.
   Fernandes, Alexandra R.
TI Exploiting the antiproliferative potential of spiropyrazoline oxindoles
   in a human ovarian cancer cell line
SO BIOORGANIC & MEDICINAL CHEMISTRY
LA English
DT Article
DE Chemotherapy; Compound-DNA interaction; Cytotoxicity; Ovarian cancer;
   Spiropyrazoline oxindoles
ID SPIROOXINDOLE; DNA; MITOCHONDRIA
AB Cancer is still one of the deadliest diseases worldwide despite the efforts in its early detection and treatment strategies. However, most chemotherapeutic agents still present side effects in normal tissues and acquired resistance that limit their efficacy. Spiropyrazoline oxindoles might be good alternatives as they have shown antiproliferative activity in human breast and colon cancer cell lines, without eliciting cytotoxicity in healthy cells. However, their potential for ovarian cancer was never tested. In this work, the antiproliferative activity of five spiropyrazoline oxindoles was assessed in ovarian cancer cells A2780 and the biological targets and mechanism of action of the most promising compound evaluated. Compound la showed the highest antiproliferative effect, as well as the highest selectivity for A2780 cells compared to healthy fibroblasts. This antiproliferative effect results from the induction of cell death by mitochondria-mediated apoptosis and autophagy. In vitro DNA interaction studies demonstrated that la interacts with DNA by groove-binding, without triggering genotoxicity. In addition, la showed a strong affinity to bovine serum albumin that might be important for further inclusion in drug delivery platforms. Proteomic studies reinforced la role in promoting A2780 endoplasmatic reticulum (ER) stress by destabilizing the correct protein folding which triggers cell death via apoptosis and autophagy.
C1 [Raposo, Luis R.; Silva, Ana; Roma-Rodrigues, Catarina; Baptista, Pedro, V; Fernandes, Alexandra R.] Univ Nova Lisboa, Dept Ciencias Vida, UCIBIO, Fac Ciencias & Tecnol, Campus Caparica, P-2829516 Caparica, Portugal.
   [Silva, Dario; Espadinha, Margarida; Santos, Maria M. M.] Univ Lisbon, Fac Pharm, Res Inst Med iMedULisboa, Ave Prof Gama Pinto, P-1649003 Lisbon, Portugal.
RP Fernandes, AR (corresponding author), Univ Nova Lisboa, Dept Ciencias Vida, UCIBIO, Fac Ciencias & Tecnol, Campus Caparica, P-2829516 Caparica, Portugal.; Santos, MMM (corresponding author), Univ Lisbon, Fac Pharm, Res Inst Med iMedULisboa, Ave Prof Gama Pinto, P-1649003 Lisbon, Portugal.
EM mariasantos@ff.ulisboa.pt; ma.fernandes@fct.unl.pt
RI Raposo, Luís R/T-3754-2017; Espadinha, Margarida/AAW-9881-2021;
   Roma-Rodrigues, Catarina/AAT-5658-2021; Roma-Rodrigues,
   Catarina/S-6144-2016; Raposo, Luís/AAX-1610-2021; Baptista,
   Pedro/A-1237-2009; Fernandes, Alexandra/C-7465-2011; Santos,
   Maria/I-7189-2013
OI Raposo, Luís R/0000-0002-8637-346X; Roma-Rodrigues,
   Catarina/0000-0002-8676-6562; Roma-Rodrigues,
   Catarina/0000-0002-8676-6562; Raposo, Luís/0000-0002-8637-346X;
   Baptista, Pedro/0000-0001-5255-7095; Fernandes,
   Alexandra/0000-0003-2054-4438; Santos, Maria/0000-0002-2239-9353; Silva,
   Dario/0000-0002-2565-089X
FU FCTPortuguese Foundation for Science and TechnologyEuropean Commission
   [UIDB/04378/2020, UIDB/04138/2020, PTDC/QUI-QOR/29664/2017,
   CEECIND/01772/2017, SFRH/BPD/124612/2016, SFRH/BD/117931/2016,
   PTDC/NAN-MAT/31100/2017]
FX We thank A. Carvalho for preliminary data management. This work was
   financed by national funds from FCT through the Applied Molecular
   Biosciences Unit - UCIBIO (UIDB/04378/2020), iMed.ULisboa
   (UIDB/04138/2020), project PTDC/QUI-QOR/29664/2017, Principal Researcher
   grant CEECIND/01772/2017 (M. M. M. Santos), and fellowships
   SFRH/BPD/124612/2016 (C. Roma-Rodrigues), SFRH/BD/117931/2016 (M.
   Espadinha) and PTDC/NAN-MAT/31100/2017 (L.R. Raposo).
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NR 57
TC 2
Z9 2
U1 4
U2 8
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0968-0896
EI 1464-3391
J9 BIOORGAN MED CHEM
JI Bioorg. Med. Chem.
PD JAN 15
PY 2021
VL 30
AR 115880
DI 10.1016/j.bmc.2020.115880
PG 11
WC Biochemistry & Molecular Biology; Chemistry, Medicinal; Chemistry,
   Organic
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Pharmacology & Pharmacy; Chemistry
GA QE2NF
UT WOS:000616047600007
PM 33348171
DA 2022-04-25
ER

PT J
AU Ambrose, AJ
   Zerio, CJ
   Sivinski, J
   Schmidlin, CJ
   Shi, TD
   Ross, AB
   Widrick, KJ
   Johnson, SM
   Zhang, DD
   Chapman, E
AF Ambrose, Andrew J.
   Zerio, Christopher J.
   Sivinski, Jared
   Schmidlin, Cody J.
   Shi, Taoda
   Ross, Alison B.
   Widrick, Kimberly J.
   Johnson, Steven M.
   Zhang, Donna D.
   Chapman, Eli
TI A high throughput substrate binding assay reveals hexachlorophene as an
   inhibitor of the ER-resident HSP70 chaperone GRP78
SO BIOORGANIC & MEDICINAL CHEMISTRY LETTERS
LA English
DT Article
DE Chaperone; HSP70; GRP78/BiP; Cancer; ER stress; UPR; ERAD; Autophagy
ID HEAT-SHOCK-PROTEIN-70 FAMILY; PROTEINS
AB Glucose-regulated protein 78 (GRP78) is the ER resident 70 kDa heat shock protein 70 (HSP70) and has been hypothesized to be a therapeutic target for various forms of cancer due to its role in mitigating proteotoxic stress in the ER, its elevated expression in some cancers, and the correlation between high levels for GRP78 and a poor prognosis. Herein we report the development and use of a high throughput fluorescence polarization-based peptide binding assay as an initial step toward the discovery and development of GRP78 inhibitors. This assay was used in a pilot screen to discover the anti-infective agent, hexachlorophene, as an inhibitor of GRP78. Through biochemical characterization we show that hexachlorophene is a competitive inhibitor of the GRP78-peptide interaction. Biological investigations showed that this molecule induces the unfolded protein response, induces autophagy, and leads to apoptosis in a colon carcinoma cell model, which is known to be sensitive to GRP78 inhibition.
C1 [Ambrose, Andrew J.; Zerio, Christopher J.; Sivinski, Jared; Schmidlin, Cody J.; Shi, Taoda; Ross, Alison B.; Widrick, Kimberly J.; Zhang, Donna D.; Chapman, Eli] Univ Arizona, Coll Pharm, Dept Pharmacol & Toxicol, 1703 East Mabel St,POB 210207, Tucson, AZ 85721 USA.
   [Johnson, Steven M.] Indiana Univ, Sch Med, Dept Biochem & Mol Biol, 635 Barnhill Dr, Indianapolis, IN 46202 USA.
RP Chapman, E (corresponding author), Univ Arizona, Coll Pharm, Dept Pharmacol & Toxicol, 1703 East Mabel St,POB 210207, Tucson, AZ 85721 USA.
EM chapman@pharmacy.arizona.edu
RI Ambrose, Andrew/AAP-3641-2021
OI Ambrose, Andrew/0000-0002-2932-4514; Ross, Alison/0000-0003-1047-3031;
   Sivinski, Jared/0000-0003-2696-6279; Chapman, Eli/0000-0002-6310-1664;
   Zerio, Christopher/0000-0003-4053-4835
FU National Institutes of Health T32 Training GrantUnited States Department
   of Health & Human ServicesNational Institutes of Health (NIH) - USA
   [GM008804]; National Institute of General Medical Sciences (NIGMS) of
   the National Institutes of Health (NIH)United States Department of
   Health & Human ServicesNational Institutes of Health (NIH) - USANIH
   National Institute of General Medical Sciences (NIGMS) [R01GM120350];
   NATIONAL INSTITUTE OF ENVIRONMENTAL HEALTH SCIENCESUnited States
   Department of Health & Human ServicesNational Institutes of Health (NIH)
   - USANIH National Institute of Environmental Health Sciences (NIEHS)
   [P30ES006694] Funding Source: NIH RePORTER; NATIONAL INSTITUTE OF
   GENERAL MEDICAL SCIENCESUnited States Department of Health & Human
   ServicesNational Institutes of Health (NIH) - USANIH National Institute
   of General Medical Sciences (NIGMS) [R01GM120350, T32GM008804] Funding
   Source: NIH RePORTER
FX This work was supported by funding from the National Institutes of
   Health T32 Training Grant GM008804 and National Institute of General
   Medical Sciences (NIGMS) of the National Institutes of Health (NIH)
   under Award Number R01GM120350.
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NR 17
TC 3
Z9 4
U1 0
U2 18
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0960-894X
EI 1464-3405
J9 BIOORG MED CHEM LETT
JI Bioorg. Med. Chem. Lett.
PD JUL 15
PY 2019
VL 29
IS 14
BP 1689
EP 1693
DI 10.1016/j.bmcl.2019.05.041
PG 5
WC Chemistry, Medicinal; Chemistry, Organic
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy; Chemistry
GA IA8CP
UT WOS:000469785600001
PM 31129054
OA Green Accepted, Bronze, Green Submitted
DA 2022-04-25
ER

PT J
AU Chaurasia, M
   Bhatt, AN
   Das, A
   Dwarakanath, BS
   Sharma, K
AF Chaurasia, Madhuri
   Bhatt, Anant Narayan
   Das, Asmita
   Dwarakanath, Bilikere S.
   Sharma, Kulbhushan
TI Radiation-induced autophagy: mechanisms and consequences
SO FREE RADICAL RESEARCH
LA English
DT Review
DE Calcium; DNA damage response; ER stress; mitophagy; oxidative stress
ID ENDOPLASMIC-RETICULUM STRESS; UNFOLDED PROTEIN RESPONSE;
   PHOSPHATIDYLINOSITOL 3-KINASE COMPLEXES; COLON-CANCER CELLS; DNA-DAMAGE;
   ER STRESS; IONIZING-RADIATION; INDUCED APOPTOSIS; REACTIVE OXYGEN;
   OXIDATIVE STRESS
AB Autophagy is an evolutionary conserved, indispensable, lysosome-mediated degradation process, which helps in maintaining homeostasis during various cellular traumas. During stress, a context-dependent role of autophagy has been observed which drives the cell towards survival or death depending upon the type, time, and extent of the damage. The process of autophagy is stimulated during various cellular insults, e.g. oxidative stress, endoplasmic reticulum stress, imbalances in calcium homeostasis, and altered mitochondrial potential. Ionizing radiation causes ROS-dependent as well as ROS-independent damage in cells that involve macromolecular (mainly DNA) damage, as well as ER stress induction, both capable of inducing autophagy. This review summarizes the current understanding on the roles of oxidative stress, ER stress, DNA damage, altered mitochondrial potential, and calcium imbalance in radiation-induced autophagy as well as the merits and limitations of targeting autophagy as an approach for radioprotection and radiosensitization.
C1 [Chaurasia, Madhuri; Bhatt, Anant Narayan; Dwarakanath, Bilikere S.; Sharma, Kulbhushan] Inst Nucl Med & Allied Sci, Div Metab Cell Signaling Res, Brig SK Mazumdar Marg, Delhi 110054, India.
   [Chaurasia, Madhuri; Das, Asmita] Delhi Technol Univ, Dept Biotechnol, Delhi, India.
   [Dwarakanath, Bilikere S.] Sri Ramachandra Univ, Cent Res Facil, Madras, Tamil Nadu, India.
RP Dwarakanath, BS; Sharma, K (corresponding author), Inst Nucl Med & Allied Sci, Div Metab Cell Signaling Res, Brig SK Mazumdar Marg, Delhi 110054, India.
EM dwarakanathdrbs@gmail.com; kulsinmas@gmail.com
RI SHARMA, KULBHUSHAN/AAD-7713-2019
OI SHARMA, KULBHUSHAN/0000-0001-5226-4209; Dwarakanath, Bilikere
   S./0000-0001-6988-2601; Das, Asmita/0000-0001-9846-1005
FU DRDO, Govt. of IndiaDefence Research & Development Organisation (DRDO)
   [INM-311]; ICMR, Govt. of IndiaIndian Council of Medical Research (ICMR)
FX The authors report that they have no conflicts of interest. The authors
   alone are responsible for the content and writing of the paper. Work in
   author's laboratories is supported by grants from DRDO, Govt. of India
   (INM-311). Ms Madhuri Chaurasia is a recipient of fellowship from ICMR,
   Govt. of India.
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NR 179
TC 50
Z9 52
U1 3
U2 50
PU TAYLOR & FRANCIS LTD
PI ABINGDON
PA 2-4 PARK SQUARE, MILTON PARK, ABINGDON OR14 4RN, OXON, ENGLAND
SN 1071-5762
EI 1029-2470
J9 FREE RADICAL RES
JI Free Radic. Res.
PD MAR 3
PY 2016
VL 50
IS 3
BP 273
EP 290
DI 10.3109/10715762.2015.1129534
PG 18
WC Biochemistry & Molecular Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology
GA DB6GD
UT WOS:000368611500001
PM 26764568
DA 2022-04-25
ER

PT J
AU Liu, F
   Ai, FY
   Zhang, DC
   Tian, L
   Yang, ZY
   Liu, SJ
AF Liu, Fen
   Ai, Fei-Yan
   Zhang, De-Cai
   Tian, Li
   Yang, Zhen-Yun
   Liu, Shao-Jun
TI LncRNA NEAT1 knockdown attenuates autophagy to elevate 5-FU sensitivity
   in colorectal cancer via targeting miR-34a
SO CANCER MEDICINE
LA English
DT Article
DE autophagy; colorectal carcinoma; HMGB1; LncRNA NEAT1; miR-34a
ID CELL-PROLIFERATION; PROMOTES; CHEMORESISTANCE; OSTEOSARCOMA; SURVIVAL;
   INVASION; GROWTH; HMGB1; AXIS
AB Backgrounds Colorectal carcinoma (CRC) is a common malignant tumor. Increasing evidences indicated that CRC showed a resistance to 5-fluorouracil (5-FU) and further resulted in a poor prognosis. In this study, we aim to investigate the effect of long noncoding RNA nuclear paraspeckle assembly transcript 1 (LncRNA NEAT1) on cell viability, sensitivity to 5-FU, and autophagy of CRC cell lines. Methods MTT (3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-Htetrazolium bromide) was used to detect cell viability, immunofluorescent staining was used to detect autophagy puncta, and luciferase reporter system was used to determine binding ability between miR-34a and NEAT1 or putative targets. Additionally, indicated mRNAs and protein expressions were determined by qRT-PCR or western blotting, respectively. Results We found that NEAT1 expression was increased in CRC tissues and cells, which showed a negative correlation with miR-34a expression. In addition, NEAT1 knockdown noticeably inhibited the proliferation of CRC cells and enhanced 5-FU sensitivity. It revealed that NEAT1 knockdown suppressed the LC3 puncta and the expressions of Beclin-1, ULK1, and ratio of LC3II/I. Overexpression of miR-34a showed similar trends with NEAT1 knockdown. miR-34a was validated to target the putative binding sites in 3 '-UTR of HMGB1, ATG9A, and ATG4B, which are involved in the activation of autophagy. Inhibition of miR-34a or overexpression of HMGB1 could effectively reverse elevated 5-FU sensitivity upon NEAT1 knockdown. In addition, 3-MA reversed NEAT1 overexpression-induced resistance in HT29 cells. Conclusion These findings indicate that LncRNA NEAT1 could target miR-34a and promote autophagy to facilitate 5-FU chemoresistance in CRC.
C1 [Liu, Fen; Ai, Fei-Yan; Zhang, De-Cai; Tian, Li; Yang, Zhen-Yun; Liu, Shao-Jun] Cent South Univ, Xiangya Hosp 3, Dept Gastroenterol, 138 Tongzipo Rd, Changsha 410013, Hunan, Peoples R China.
   [Liu, Fen; Ai, Fei-Yan; Zhang, De-Cai] Hunan Key Lab Nonresolving Inflammat & Canc, Changsha, Hunan, Peoples R China.
RP Liu, SJ (corresponding author), Cent South Univ, Xiangya Hosp 3, Dept Gastroenterol, 138 Tongzipo Rd, Changsha 410013, Hunan, Peoples R China.
EM cslsj169@163.com
FU Hunan Natural Science Foundation of Youth Fund Project [2018JJ3802]
FX This work was supported by Hunan Natural Science Foundation of Youth
   Fund Project (no. 2018JJ3802).
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NR 34
TC 36
Z9 37
U1 0
U2 2
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 2045-7634
J9 CANCER MED-US
JI Cancer Med.
PD FEB
PY 2020
VL 9
IS 3
BP 1079
EP 1091
DI 10.1002/cam4.2746
EA DEC 2019
PG 13
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA KH4IZ
UT WOS:000500541500001
PM 31802650
OA gold, Green Published
DA 2022-04-25
ER

PT J
AU Marion-Letellier, R
   Raman, M
   Savoye, G
   Dechelotte, P
   Ghosh, S
AF Marion-Letellier, Rachel
   Raman, Maitreyi
   Savoye, Guillaume
   Dechelotte, Pierre
   Ghosh, Subrata
TI Nutrient Modulation of Autophagy: Implications for Inflammatory Bowel
   Diseases
SO INFLAMMATORY BOWEL DISEASES
LA English
DT Article
DE autophagy; Crohn's disease; nutrients; PPAR-gamma
ID ACTIVATED-RECEPTOR-GAMMA; GENOME-WIDE ASSOCIATION; COLON-CANCER CELLS;
   CROHNS-DISEASE; FATTY-ACIDS; PPAR-GAMMA; DIFFERENTIAL MODULATION;
   SIGNALING PATHWAYS; DIETARY MODULATION; PROTEIN-SYNTHESIS
AB During nutrient deprivation, autophagy provides the constituents required to maintain the metabolism essential for survival. Recently, genome-wide association studies have identified genetic determinants for susceptibility to Crohn's disease (CD) such as ATG16L1 and IRGM that are involved in the autophagy pathway. Both disease-carrying NOD2 mutations and ATG16L1 mutations may result in impairment of autophagy. Impairment in autophagy results in impaired clearance of microbes. Ileal CD is associated with Paneth cell loss of function such as decreased production of alpha-defensins, which may arise from mutations in NOD2 or autophagy genes. Nutrients are able to modify several cellular pathways and in particular autophagy. We summarize the contribution of a variety of dietary components to activate autophagy. Understanding the crosstalk between nutrients and autophagy in the intestine may provide novel targets that have therapeutics potential in intestinal inflammation. Nutrient activation of autophagy may contribute to restoring the Paneth cell loss of function in ileal CD. (Inflamm Bowel Dis 2013;19:205-212)
C1 [Marion-Letellier, Rachel; Savoye, Guillaume; Dechelotte, Pierre] Univ Rouen, INSERM, Unit U1073, Rouen, France.
   [Marion-Letellier, Rachel; Savoye, Guillaume; Dechelotte, Pierre] Rouen Univ Hosp, Rouen, France.
   [Raman, Maitreyi; Ghosh, Subrata] Univ Calgary, Div Gastroenterol, Calgary, AB T2N 1N4, Canada.
   [Savoye, Guillaume] Rouen Univ Hosp, Dept Gastroenterol, Rouen, France.
RP Ghosh, S (corresponding author), Univ Calgary, Dept Med, Div Gastroenterol, Calgary, AB T2N 1N4, Canada.
EM subrata.ghosh@albertahealthservices.ca
RI Marion-Letellier, Rachel/ABB-8213-2021
OI Marion-Letellier, Rachel/0000-0002-3006-5943; Savoye,
   Guillaume/0000-0002-9200-2067
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NR 80
TC 73
Z9 77
U1 0
U2 18
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 1078-0998
EI 1536-4844
J9 INFLAMM BOWEL DIS
JI Inflamm. Bowel Dis.
PD JAN
PY 2013
VL 19
IS 1
BP 205
EP 212
DI 10.1002/ibd.23001
PG 8
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA 109VL
UT WOS:000316397200032
PM 23328774
DA 2022-04-25
ER

PT J
AU Kopustinskiene, DM
   Jakstas, V
   Savickas, A
   Bernatoniene, J
AF Kopustinskiene, Dalia M.
   Jakstas, Valdas
   Savickas, Arunas
   Bernatoniene, Jurga
TI Flavonoids as Anticancer Agents
SO NUTRIENTS
LA English
DT Review
DE flavonoids; cancer; ROS; antioxidants; pro-oxidants; mitochondria
ID NF-KAPPA-B; ELECTRON-TRANSPORT CHAIN; MITOCHONDRIAL
   OXIDATIVE-PHOSPHORYLATION; HESPERETIN INDUCES APOPTOSIS; OVARIAN-CANCER
   CELLS; GREEN TEA CATECHINS; TOLL-LIKE RECEPTOR; HUMAN COLON-CANCER; GUT
   MICROBIOTA; ANTIOXIDANT CAPACITY
AB Flavonoids are polyphenolic compounds subdivided into 6 groups: isoflavonoids, flavanones, flavanols, flavonols, flavones and anthocyanidins found in a variety of plants. Fruits, vegetables, plant-derived beverages such as green tea, wine and cocoa-based products are the main dietary sources of flavonoids. Flavonoids have been shown to possess a wide variety of anticancer effects: they modulate reactive oxygen species (ROS)-scavenging enzyme activities, participate in arresting the cell cycle, induce apoptosis, autophagy, and suppress cancer cell proliferation and invasiveness. Flavonoids have dual action regarding ROS homeostasis-they act as antioxidants under normal conditions and are potent pro-oxidants in cancer cells triggering the apoptotic pathways and downregulating pro-inflammatory signaling pathways. This article reviews the biochemical properties and bioavailability of flavonoids, their anticancer activity and its mechanisms of action.
C1 [Kopustinskiene, Dalia M.; Jakstas, Valdas; Bernatoniene, Jurga] Lithuanian Univ Hlth Sci, Med Acad, Inst Pharmaceut Technol, Fac Pharm, LT-50161 Kaunas, Lithuania.
   [Jakstas, Valdas] Lithuanian Univ Hlth Sci, Med Acad, Dept Pharmacognosy, LT-50161 Kaunas, Lithuania.
   [Savickas, Arunas; Bernatoniene, Jurga] Lithuanian Univ Hlth Sci, Med Acad, Dept Drug Technol & Social Pharm, Fac Pharm, Sukileliu Pr 13, LT-50161 Kaunas, Lithuania.
RP Bernatoniene, J (corresponding author), Lithuanian Univ Hlth Sci, Med Acad, Inst Pharmaceut Technol, Fac Pharm, LT-50161 Kaunas, Lithuania.; Bernatoniene, J (corresponding author), Lithuanian Univ Hlth Sci, Med Acad, Dept Drug Technol & Social Pharm, Fac Pharm, Sukileliu Pr 13, LT-50161 Kaunas, Lithuania.
EM DaliaMarija.Kopustinskiene@lsmuni.lt; Valdas.Jakstas@lsmuni.lt;
   Arunas.Savickas@lsmuni.lt; Jurga.Bernatoniene@lsmuni.lt
OI Jakstas, Valdas/0000-0001-7627-6263
FU Pharmaceutical and Health technology Open access center
FX The authors wish to thank Pharmaceutical and Health technology Open
   access center for support of this study.
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NR 225
TC 134
Z9 136
U1 100
U2 185
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 2072-6643
J9 NUTRIENTS
JI Nutrients
PD FEB
PY 2020
VL 12
IS 2
AR 457
DI 10.3390/nu12020457
PG 25
WC Nutrition & Dietetics
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Nutrition & Dietetics
GA KY3GF
UT WOS:000522458700184
PM 32059369
OA Green Published, gold
HC Y
HP Y
DA 2022-04-25
ER

PT J
AU Wang, HS
   Li, W
   Xu, J
   Zhang, T
   Zuo, DQ
   Zhou, ZF
   Lin, BH
   Wang, GY
   Wang, ZY
   Sun, W
   Sun, MX
   Chang, SM
   Cai, ZD
   Hua, YQ
AF Wang, Hongsheng
   Li, Wen
   Xu, Jing
   Zhang, Tao
   Zuo, Dongqing
   Zhou, Zifei
   Lin, Binhui
   Wang, Gangyang
   Wang, Zhuoying
   Sun, Wei
   Sun, Mengxiong
   Chang, Shimin
   Cai, Zhengdong
   Hua, Yingqi
TI NDRG1 inhibition sensitizes osteosarcoma cells to combretastatin A-4
   through targeting autophagy
SO CELL DEATH & DISEASE
LA English
DT Article
ID DOWNSTREAM-REGULATED GENE-1; COLON-CANCER CELLS; METASTASIS SUPPRESSOR;
   A4 PHOSPHATE; SIGNALING PATHWAYS; LUNG-CANCER; CHLOROQUINE; PROMOTES;
   PROTEIN; ANGIOGENESIS
AB Combretastatin A-4 (CA-4), a tubulin-depolymerizing agent, shows promising antitumor efficacy and has been under several clinical trials in solid tumors for 10 years. Autophagy has an important pro-survival role in cancer therapy, thus targeting autophagy may improve the efficacy of antitumor agents. N-myc downstream-regulated gene 1 (NDRG1) is a significant stress regulatory gene, which mediates cell survival and chemoresistance. Here we reported that CA-4 could induce cell-protective autophagy, and combination treatment of CA-4 and autophagy inhibitor chloroquine (CQ) exerted synergistic cytotoxic effect on human osteosarcoma (OS) cells. Meanwhile, CA-4 or CQ could increase the expression of NDRG1 independently. We further performed mechanistic study to explore how CA-4 and CQ regulate the expression of NDRG1. Using luciferase reporter assay, we found that CA-4 transcriptionally upregulated NDRG1 expression, whereas CQ triggered colocalization of NDRG1 and lysosome, which subsequently prevented lysosome-dependent degradation of NDRG1. Further, we showed that knockdown of NDRG1 caused the defect of lysosomal function, which accumulated LC3-positive autophagosomes by decreasing their fusion with lysosomes. Moreover, NDRG1 inhibition increased apoptosis in response to combination treatment with CA-4 and CQ. Taken together, our study revealed abrogation of NDRG1 expression sensitizes OS cells to CA-4 by suppression of autophagosome-lysosome fusion. These results provide clues for developing more effective cancer therapeutic strategies by the concomitant treatment with CA-4 and clinical available autophagy inhibitors.
C1 [Wang, Hongsheng; Chang, Shimin] Tongji Univ, Yangpu Hosp, Dept Orthopaed, Shanghai 200090, Peoples R China.
   [Wang, Hongsheng; Xu, Jing; Zhang, Tao; Zuo, Dongqing; Zhou, Zifei; Lin, Binhui; Wang, Gangyang; Wang, Zhuoying; Sun, Wei; Sun, Mengxiong; Cai, Zhengdong; Hua, Yingqi] Shanghai Jiao Tong Univ, Sch Med, Shanghai Gen Hosp, Dept Orthopaed, Shanghai, Peoples R China.
   [Li, Wen] Shanghai Univ Tradit Chinese Med, Municipal Hosp Tradit Chinese Med, Dept Oncol, Shanghai, Peoples R China.
   [Cai, Zhengdong; Hua, Yingqi] Shanghai Bone Tumor Inst, Shanghai, Peoples R China.
RP Chang, SM; Cai, ZD; Hua, YQ (corresponding author), Tongji Univ, Yangpu Hosp, Dept Orthopaed, Shanghai 200090, Peoples R China.
EM shiminchang11@aliyun.com; czd856@vip.163.com; yhua@shsmu.edu.cn
OI Chang, Shimin/0000-0003-2691-7987
FU NSFCNational Natural Science Foundation of China (NSFC) [81202115];
   Shanghai Municipal Commission of Health and Family Planning
   [XYQ2013108]; Shanghai Hospital Development Center [SHDC12013107];
   School of Mesdicine, Shanghai Jiao Tong University [81450110092];
   Shanghai Municipal Human Resources and Social Security Bureau
   [0403N14001]; Shanghai Charity cancer research center [0703N14012];
   Shanghai Science and Technology CommissionShanghai Science & Technology
   CommitteeScience & Technology Commission of Shanghai Municipality
   (STCSM) [14140904000]
FX This work was supported by NSFC (81202115); the excellent young talent
   program of Shanghai Municipal Commission of Health and Family Planning
   (XYQ2013108); Research Grant from Shanghai Hospital Development Center
   (SHDC12013107), School of Mesdicine, Shanghai Jiao Tong University
   (81450110092), Shanghai Municipal Human Resources and Social Security
   Bureau (0403N14001), Shanghai Charity cancer research center
   (0703N14012) and Shanghai Science and Technology Commission
   (14140904000).
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NR 52
TC 11
Z9 12
U1 2
U2 13
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 2041-4889
J9 CELL DEATH DIS
JI Cell Death Dis.
PD SEP
PY 2017
VL 8
AR e3048
DI 10.1038/cddis.2017.438
PG 12
WC Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Cell Biology
GA FI9KB
UT WOS:000412324800002
PM 28906492
OA Green Published, gold
DA 2022-04-25
ER

PT J
AU Zhang, YY
   Xu, ZB
   Sun, YW
   Chi, P
   Lu, XR
AF Zhang, Yiyi
   Xu, Zongbin
   Sun, Yanwu
   Chi, Pan
   Lu, Xingrong
TI Knockdown of KLK11 reverses oxaliplatin resistance by inhibiting
   proliferation and activating apoptosis via suppressing the PI3K/AKT
   signal pathway in colorectal cancer cell
SO ONCOTARGETS AND THERAPY
LA English
DT Article
DE colorectal cancer; kallikrein 11; oxaliplatin; drug resistance;
   apoptosis
ID KALLIKREIN-RELATED PEPTIDASES; HUMAN TISSUE KALLIKREINS; COLON-CANCER;
   EXPRESSION; GENE; SURVIVAL; CHEMORESISTANCE; CHEMOTHERAPY; AUTOPHAGY;
   PROSTATE
AB Introduction: Kallikrein 11 (KLK11) plays a crucial role in drug-resistance to oxaliplatin (L-OHP) in the treatment of metastatic colorectal cancer (mCRC). The study aimed to investigate the role of KLK11 in chemoresistance, and to clarify the mechanism underlying reverse of L-OHP resistance by knockdown of KLK11.
   Materials and Methods: Resistance to oxaliplatin was induced in HCT-8 (HCT-8/L-OHP) colorectal adenocarcinoma cell lines by exposing cells to increasing concentrations of L-OHP. MTT, RT-qPCR, and Western blot were used to evaluate the resistance to L-OHP. We then knocked down KLK11 in HCT-8/L-OHP cells to explore the mechanism through which KLK11 reverses L-OHP resistance. The mRNA and protein expression of KLK11 in tissues from mCRC patients were detected by RT-qPCR and immunohistochemistry.
   Results: The drug resistance index (RI) of HCT-8/L-OHP cell line to L-OHP, 5-Fluorouracil (5-FU), Irinotecan (CPT-11), Vincristine (VCR) and Cis-diamminedichloroplatinum (CDDP) were 10, 5.35, 3.23, 1.28, and 6.64, respectively. Increased expression of multi-drug resistant genes ABCC1, ABCB1, GSTP1 and ERCC1 were detected in HCT-8/L-OHP cell line. Moreover, the activated PI3K/AKT pathway was related to L-OHP-resistance. Knockdown of KLK11 in HCT-8/L-OHP cell reversed L-OHP-resistance by inhibiting cell growth and activating apoptosis via suppressing the PI3K/AKT signaling pathway. Moreover, high expression of KLK11 in chemoresistant-patients was associated with lymph node metastases and histopathology.
   Conclusion: KLK11 was highly expressed in chemoresistant-patients and L-OHP-resistant cell lines. Moreover, L-OHP resistance was associated with activated PI3K/AKT signal pathway. Knockdown of KLK11 can reverse L-OHP resistance by blocking PI3K/AKT signaling pathway.
C1 [Zhang, Yiyi; Xu, Zongbin; Sun, Yanwu; Chi, Pan; Lu, Xingrong] Fujian Med Univ, Dept Colorectal Surg, Union Hosp, 29 Xinquan Rd, Fuzhou 350001, Fujian, Peoples R China.
RP Chi, P; Lu, XR (corresponding author), Fujian Med Univ, Dept Colorectal Surg, Union Hosp, 29 Xinquan Rd, Fuzhou 350001, Fujian, Peoples R China.
EM chipan363@163.com; fjxhlxr@163.com
FU National Natural Science Foundation of ChinaNational Natural Science
   Foundation of China (NSFC) [81472777]; Training Plan of Middle-aged and
   Young Talents of Fujian Province Health and Family Planning Commission
   [2013-ZQN-ZD-11]; Science Foundation of the Fujian ProvinceNatural
   Science Foundation of Fujian Province [2017J01296]; National Clinical
   Key Specialty Construction Project (General Surgery) of China [2012-649]
FX This study was supported by the National Natural Science Foundation of
   China (No 81472777), Training Plan of Middle-aged and Young Talents of
   Fujian Province Health and Family Planning Commission (No
   2013-ZQN-ZD-11), Science Foundation of the Fujian Province, (No
   2017J01296), and National Clinical Key Specialty Construction Project
   (General Surgery) of China (No 2012-649).
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NR 43
TC 20
Z9 20
U1 0
U2 3
PU DOVE MEDICAL PRESS LTD
PI ALBANY
PA PO BOX 300-008, ALBANY, AUCKLAND 0752, NEW ZEALAND
SN 1178-6930
J9 ONCOTARGETS THER
JI OncoTargets Ther.
PY 2018
VL 11
BP 809
EP 821
DI 10.2147/OTT.S151867
PG 13
WC Biotechnology & Applied Microbiology; Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biotechnology & Applied Microbiology; Oncology
GA FW5HT
UT WOS:000425348000001
PM 29497313
OA gold, Green Submitted, Green Published
DA 2022-04-25
ER

PT J
AU Liu, LY
   Zhang, JL
   Liu, HD
   Shi, M
   Zhang, J
   Chen, L
   Huang, LQ
   Li, B
   Xu, P
AF Liu, Liyan
   Zhang, Jilin
   Liu, Hongdong
   Shi, Min
   Zhang, Jie
   Chen, Li
   Huang, Luqi
   Li, Bin
   Xu, Peng
TI Correlation of autophagy-related genes for predicting clinical prognosis
   in colorectal cancer
SO BIOMARKERS IN MEDICINE
LA English
DT Article
DE ARGs; autophagy; autophagy-related genes; clinical prognosis; colorectal
   cancer; gene ontology; KEGG; Kyoto Encyclopedia of Genes and Genomes;
   TCGA; The Cancer Genome Atlas
ID BIOLOGICAL FUNCTIONS; CELL BIOLOGY; COLON-CANCER; INVASION; BECLIN-1;
   LC3; IDENTIFICATION; PROLIFERATION; ACTIVATION; MECHANISMS
AB Aim: Autophagy plays a controversial role in cancer. The role of autophagy-related genes (ARGs) in colorectal cancer (CRC) was evaluated based on publicly available data from The Cancer Genome Atlas and the Human Autophagy Database. Materials & methods: After collecting CRC-related transcript and clinical data and a list of ARGs from public databases, the Wilcoxon test was used to identify the differentially expressed ARGs between CRC and paired normal tissues. Gene Ontology and Kyoto Encyclopedia of Genes and Genomes enrichment analyses were used to identify the major biological properties and pathways associated with these genes. Univariate Cox regression was used to identify the prognosis-associated ARGs, and a forest plot was used to visualize the results. Kaplan-Meier analysis of the 5-year survival rate was performed. Univariate and multivariate Cox analyses were used to verify the impact of the prognosis-associated ARGs. Results: A total of 36 differentially expressed genes (16 upregulated and 20 downregulated in CRC) were obtained from among 206 ARGs. There were 53 enriched pathways, including the p53 signaling pathway, platinum drug resistance, apoptosis, EGFR tyrosine kinase inhibitor resistance and ErbB signaling pathway (p- and q-values <0.05). Kaplan-Meier analysis showed that the 5-year survival rate was 46.0% (95% CI: 0.335-0.631) and 76.0% (95% CI: 0.651-0.886) in the high- and low-risk groups, respectively. The high-risk patients had worse survival probability (p = 6.256 x 10(-5)). Independent-samples t-tests revealed that MAP1LC3C expression was higher in patients aged <= 65 than >65 (p = 0.022); RAB7A expression was higher in patients aged <= 65 than >65 (p = 7.31 x 10(-4)), higher in M1 than M0 (p = 0.042), higher in N1-3 than N0 (p = 0.002) and higher in stage III and IV than I and II (p = 0.042); risk score was higher in N1-3 than N0 (p = 0.001) and in stage III and IV than I and II (p = 0.002); and WIPI2 expression was higher in M1 than M0 (p = 0.002), higher in N1-3 than N0 (p = 2.059 x 10(-7)) and higher in stage III and IV than I and II (p = 2.299 x 10(-7)). There were no differences in risk score between males and females (p = 0.593), T1-2 and T3-4 (p = 0.082) or M0 and M1 (p = 0.072). Univariate and multivariate Cox analyses showed that RAB7A was a lower-risk gene, while MAP1LC3C, WIPI2, DAPK1, ULK3 and PELP1 were high-risk genes. Conclusion: Certain ARGs are potential prognostic molecular markers of poor prognosis in CRC. Additionally, the p53 signaling pathway, platinum drug resistance, apoptosis, EGFR tyrosine kinase inhibitor resistance and ErbB signaling pathway may be critical pathways regulated by ARGs in CRC.
C1 [Liu, Liyan] Jiangxi Canc Hosp, Dept Pharm, 519 Beijing East Rd, Nanchang 330029, Jiangxi, Peoples R China.
   [Liu, Liyan] Nanchang Univ, Affiliated Canc Hosp, Dept Pharm, 519 Beijing East Rd, Nanchang 330029, Jiangxi, Peoples R China.
   [Liu, Liyan; Liu, Hongdong; Shi, Min; Zhang, Jie; Li, Bin; Xu, Peng] Jiangxi Univ Tradit Chinese Med, Coll Tradit Chinese Med, Workstat Acad, Lab Anim Sci & Technol Ctr, 1688 Meiling Rd, Nanchang 330004, Jiangxi, Peoples R China.
   [Zhang, Jilin] Jiangxi Prov Peoples Hosp, Dept Tradit Chinese Med, 92 Aiguo Rd, Nanchang 330006, Jiangxi, Peoples R China.
   [Zhang, Jie] Chengdu Univ Tradit Chinese Med, Coll Pharm, 1166 Liutai Ave, Chengdu 611137, Peoples R China.
   [Huang, Luqi] China Acad Chinese Med Sci, Natl Resource Ctr Chinese Mat Med, State Key Lab Breeding Base Daodi Herbs, 16 Nanxiao St, Beijing 100700, Peoples R China.
RP Li, B; Xu, P (corresponding author), Jiangxi Univ Tradit Chinese Med, Coll Tradit Chinese Med, Workstat Acad, Lab Anim Sci & Technol Ctr, 1688 Meiling Rd, Nanchang 330004, Jiangxi, Peoples R China.
EM lbin@crjz.com; xp0420@163.com
FU Projects of Increase and Decrease of Central Level Major [2060302];
   Workstation Project of Jiangxi University of Traditional Chinese
   Medicine [YSGZZ201801]; First-Class Subject Project of Jiangxi
   University of Traditional Chinese Medicine [JXSYLXK-ZHYAO144]; Chinese
   Medicine Science and Technology Project of the Health Commission of
   Jiangxi Province [2014A026, 2018A310]
FX This study was supported by the Projects of Increase and Decrease of
   Central Level Major (2060302), the Workstation Project of Jiangxi
   University of Traditional Chinese Medicine (YSGZZ201801), the
   First-Class Subject Project of Jiangxi University of Traditional Chinese
   Medicine (JXSYLXK-ZHYAO144) and the Chinese Medicine Science and
   Technology Project of the Health Commission of Jiangxi Province
   (2014A026, 2018A310). The authors have no other relevant affiliations or
   financial involvement with any organization or entity with a financial
   interest in or financial conflict with the subjectmatter ormaterials
   discussed in the manuscript apart from those disclosed.
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NR 51
TC 0
Z9 0
U1 3
U2 5
PU FUTURE MEDICINE LTD
PI LONDON
PA UNITEC HOUSE, 3RD FLOOR, 2 ALBERT PLACE, FINCHLEY CENTRAL, LONDON, N3
   1QB, ENGLAND
SN 1752-0363
EI 1752-0371
J9 BIOMARK MED
JI Biomark. Med.
PD JUN
PY 2021
VL 15
IS 10
BP 715
EP 729
DI 10.2217/bmm-2020-0292
EA JUN 2021
PG 15
WC Medicine, Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Research & Experimental Medicine
GA TC4IC
UT WOS:000665759300002
PM 34169735
DA 2022-04-25
ER

PT J
AU Si, YR
   Yang, ZG
   Ge, QX
   Yu, LB
   Yao, MY
   Sun, XF
   Ren, Z
   Ding, CS
AF Si, Yaoran
   Yang, Zhaoguo
   Ge, Quanxing
   Yu, Lingbing
   Yao, Meiying
   Sun, Xinfang
   Ren, Zheng
   Ding, Chunsheng
TI Long non-coding RNA Malat1 activated autophagy, hence promoting cell
   proliferation and inhibiting apoptosis by sponging miR-101 in colorectal
   cancer
SO CELLULAR & MOLECULAR BIOLOGY LETTERS
LA English
DT Article
DE Colorectal cancer; Long noncoding RNA Malat1; Autophagy; Proliferation;
   Apoptosis; miR-101
ID LNCRNA MALAT1; METASTASIS; EXPRESSION; CROSSTALK
AB BackgroundLong non-coding RNA Malat1 has been widely identified as an oncogene which shows a significant relationship with tumorigenesis in colorectal cancer (CRC). Nonetheless, whether Malat1 participates in the autophagy of colorectal cancer remains unclear.Materials and methodsFirst, the expression level of Malat1 in 96 pairs of colorectal cancer tissues and four cell lines was detected by qRT-PCR. Subsequently, the autophagy activity in colorectal cancer tissues and cell lines was detected by western blot. Furthermore, the CCK-8 assay and flow cytometry (FCM) were performed to detect the role of autophagy activated by Malat1 in colorectal cancer cell lines.ResultsIn this study, significantly increased Malat1 expression and autophagy activity were found in colorectal cancer tissues compared with the adjacent normal tissues. Also, the Malat1 level was positively correlated with the expression of LC3-II mRNA in vivo. Moreover, autophagy activation and cell proliferation were significantly facilitated by Malat1 in colorectal cancer cells, while apoptosis decreased. Above all, the inhibition of autophagy by 3-MA not only relieved the Malat1-induced cell proliferation but also promoted the Malat1-induced cell apoptosis. In addition, Malat1 was found to act as an endogenous sponge by directly binding to miR-101 to reduce miR-101. Furthermore, the suppressive effects of miR-101 on the autophagy, proliferation, and apoptosis of CRC were abolished by Malat1.ConclusionLong non-coding RNA Malat1 activated autophagy and promoted cell proliferation, yet inhibited apoptosis by sponging miR-101 in colorectal cancer cells.
C1 [Si, Yaoran; Ge, Quanxing; Yu, Lingbing; Yao, Meiying; Sun, Xinfang; Ren, Zheng; Ding, Chunsheng] Henan Univ, Huaihe Hosp, Dept Gastroenterol, Kaifeng 475000, Henan, Peoples R China.
   [Yang, Zhaoguo] Kaifeng Cent Hosp, Dept Gen Surg, Kaifeng, Henan, Peoples R China.
RP Ding, CS (corresponding author), Henan Univ, Huaihe Hosp, Dept Gastroenterol, Kaifeng 475000, Henan, Peoples R China.
EM ding_chunsheng@yeah.net
FU Henan Science and Technology Development Plan Project [182102310367]
FX Henan Science and Technology Development Plan Project: 182102310367.
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NR 28
TC 53
Z9 55
U1 1
U2 7
PU BMC
PI LONDON
PA CAMPUS, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 1425-8153
EI 1689-1392
J9 CELL MOL BIOL LETT
JI Cell. Mol. Biol. Lett.
PD JUL 27
PY 2019
VL 24
AR 50
DI 10.1186/s11658-019-0175-8
PG 12
WC Biochemistry & Molecular Biology; Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Cell Biology
GA IM0KK
UT WOS:000477676900001
PM 31372165
OA Green Published, gold
DA 2022-04-25
ER

PT J
AU Pirol, SC
   Caliskan, B
   Durmaz, I
   Atalay, R
   Banoglu, E
AF Pirol, Seyma Cankara
   Caliskan, Burcu
   Durmaz, Irem
   Atalay, Rengul
   Banoglu, Erden
TI Synthesis and preliminary mechanistic evaluation of
   5-(p-tolyl)-1-(quinolin-2-yl)pyrazole-3-carboxylic acid amides with
   potent antiproliferative activity on human cancer cell lines
SO EUROPEAN JOURNAL OF MEDICINAL CHEMISTRY
LA English
DT Article
DE Diarylpyrazole; Quinoline; Cytotoxicity; Autophagy; Apoptosis
ID BIOLOGICAL EVALUATION; PYRAZOLE DERIVATIVES; HYDRAZONE DERIVATIVES;
   DISCOVERY; APOPTOSIS; AUTOPHAGY; INHIBITORS; AGENTS; LC3
AB We synthesized a series of novel amide derivatives of 5-(p-tolyl)-1-(quinolin-2-yl)pyrazole-3-carboxylic acid and assessed their antiproliferative activities against three human cancer cell lines (Huh7, human liver; MCF7, breast and HCT116, colon carcinoma cell lines) with the sulforhodamine B assay. Compound 4j with 2-chloro-4-pyridinyl group in the amide part exhibited promising cytotoxic activity against all cell lines with IC50 values of 1.6 mu M, 3.3 mu M and 1.1 mu M for Huh7. MCF7 and HCT116 cells, respectively, and produced dramatic cell cycle arrest at SubG1/G1 phase as an indicator of apoptotic cell death induction. On the basis of their high potency in cellular environment, these straightforward pyrazole-3-carboxamide derivatives may possess potential in the design of more potent compounds for intervention with cancer cell proliferation. (C) 2014 Elsevier Masson SAS. All rights reserved.
C1 [Pirol, Seyma Cankara; Caliskan, Burcu; Banoglu, Erden] Gazi Univ, Fac Pharm, Dept Pharmaceut Chem, TR-06330 Ankara, Turkey.
   [Durmaz, Irem; Atalay, Rengul] Bilkent Univ, Dept Mol Biol & Genet, TR-06800 Ankara, Turkey.
   [Atalay, Rengul] Bilkent Univ, Genet & Biotechnol Res Ctr BilGen, TR-06800 Ankara, Turkey.
RP Banoglu, E (corresponding author), Gazi Univ, Fac Pharm, Dept Pharmaceut Chem, TR-06330 Ankara, Turkey.
EM ebanoglu@gmail.com
RI Banoglu, Erden/W-2131-2017; Caliskan, Burcu/AAD-1957-2019; Cetin-Atalay,
   Rengul/O-9826-2014; Sahin, Irem Durmaz/A-3501-2019; Çalışkan,
   Burcu/AAF-9101-2021
OI Banoglu, Erden/0000-0003-4737-1733; Caliskan, Burcu/0000-0003-2391-5644;
   Cetin-Atalay, Rengul/0000-0003-2408-6606; Sahin, Irem
   Durmaz/0000-0001-5037-7883; 
FU Gazi UniversityGazi University [BAP 02/2011-44]; Turkish Academy of
   Sciences (TUBA)Turkish Academy of Sciences
FX This work was supported by Gazi University (BAP 02/2011-44) and partly
   supported by Turkish Academy of Sciences (TUBA).
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NR 27
TC 39
Z9 39
U1 3
U2 24
PU ELSEVIER FRANCE-EDITIONS SCIENTIFIQUES MEDICALES ELSEVIER
PI ISSY-LES-MOULINEAUX
PA 65 RUE CAMILLE DESMOULINS, CS50083, 92442 ISSY-LES-MOULINEAUX, FRANCE
SN 0223-5234
EI 1768-3254
J9 EUR J MED CHEM
JI Eur. J. Med. Chem.
PD NOV 24
PY 2014
VL 87
BP 140
EP 149
DI 10.1016/j.ejmech.2014.09.056
PG 10
WC Chemistry, Medicinal
WE Science Citation Index Expanded (SCI-EXPANDED); Index Chemicus (IC)
SC Pharmacology & Pharmacy
GA CU3NE
UT WOS:000363431300013
PM 25247770
OA Green Published
DA 2022-04-25
ER

PT J
AU Zhang, XN
   Fryknas, M
   Hernlund, E
   Fayad, W
   De Milito, A
   Olofsson, MH
   Gogvadze, V
   Dang, L
   Pahlman, S
   Schughart, LAK
   Rickardson, L
   Darcy, P
   Gullbo, J
   Nygren, P
   Larsson, R
   Linder, S
AF Zhang, Xiaonan
   Fryknas, Marten
   Hernlund, Emma
   Fayad, Walid
   De Milito, Angelo
   Olofsson, Maria Hagg
   Gogvadze, Vladimir
   Dang, Long
   Pahlman, Sven
   Schughart, Leoni A. Kunz
   Rickardson, Linda
   Darcy, Padraig
   Gullbo, Joachim
   Nygren, Peter
   Larsson, Rolf
   Linder, Stig
TI Induction of mitochondrial dysfunction as a strategy for targeting
   tumour cells in metabolically compromised microenvironments
SO NATURE COMMUNICATIONS
LA English
DT Article
ID CANCER-CELLS; IN-SITU; HYPOXIA; METFORMIN; SPHEROIDS; GROWTH; AUTOPHAGY;
   THERAPY; COMPLEX; RHODAMINE-123
AB Abnormal vascularization of solid tumours results in the development of microenvironments deprived of oxygen and nutrients that harbour slowly growing and metabolically stressed cells. Such cells display enhanced resistance to standard chemotherapeutic agents and repopulate tumours after therapy. Here we identify the small molecule VLX600 as a drug that is preferentially active against quiescent cells in colon cancer 3-D microtissues. The anticancer activity is associated with reduced mitochondrial respiration, leading to bioenergetic catastrophe and tumour cell death. VLX600 shows enhanced cytotoxic activity under conditions of nutrient starvation. Importantly, VLX600 displays tumour growth inhibition in vivo. Our findings suggest that tumour cells in metabolically compromised microenvironments have a limited ability to respond to decreased mitochondrial function, and suggest a strategy for targeting the quiescent populations of tumour cells for improved cancer treatment.
C1 [Zhang, Xiaonan; Hernlund, Emma; Fayad, Walid; De Milito, Angelo; Olofsson, Maria Hagg; Darcy, Padraig; Linder, Stig] Karolinska Inst, Dept Oncol Pathol, S-17176 Stockholm, Sweden.
   [Fryknas, Marten; Rickardson, Linda; Gullbo, Joachim; Larsson, Rolf; Linder, Stig] Uppsala Univ, Div Clin Pharmacol, Dept Med Sci, S-75185 Uppsala, Sweden.
   [Gogvadze, Vladimir] Karolinska Inst, Inst Environm Med, Div Toxicol, S-17177 Stockholm, Sweden.
   [Dang, Long] Univ Florida, Shands Canc Ctr, Div Hematol Oncol, Dept Internal Med, Gainesville, FL 32601 USA.
   [Pahlman, Sven] Lund Univ, Skane Univ Hosp, Dept Lab Med, Ctr Mol Pathol,CREATE Hlth, S-20502 Malmo, Sweden.
   [Schughart, Leoni A. Kunz] Tech Univ Dresden, OncoRay Natl Ctr Radiat Res Oncol, D-01307 Dresden, Germany.
   [Gullbo, Joachim; Nygren, Peter] Uppsala Univ, Div Oncol, Dept Radiol Oncol & Radiat Sci, S-75185 Uppsala, Sweden.
RP Linder, S (corresponding author), Karolinska Inst, Dept Oncol Pathol, S-17176 Stockholm, Sweden.
EM Stig.Linder@ki.se
RI Gogvadze, Vladimir/A-4392-2014; D'Arcy, Pádraig/AAB-5045-2019; D'Arcy,
   Pádraig/F-7633-2018; Fayad, Walid M. O. H./O-7269-2018
OI D'Arcy, Pádraig/0000-0001-6671-7600; D'Arcy,
   Pádraig/0000-0001-6671-7600; Fayad, Walid M. O. H./0000-0002-7975-0343;
   De Milito, Angelo/0000-0003-2591-2914
FU Cancerfonden, Radiumhemmets Forskningsfonder, Vetenskapsradet; Alex and
   Eva Wallstrom Foundation; Lions Cancer Research Fund; Strategiska
   Forskningsstiftelsen (S.S.F.)
FX This work was supported by Cancerfonden, Radiumhemmets Forskningsfonder,
   Vetenskapsradet, the Alex and Eva Wallstrom Foundation, the Lions Cancer
   Research Fund and Strategiska Forskningsstiftelsen (S.S.F.). We are
   grateful to Hans Rosen, Vivolux AB, for continuous support and
   management of projects, Maria Rydaker, Lena Lenhammar and Christina
   Leek, Hanna Goransson Kultima and the Uppsala Array platform for
   excellent technical support and Ingrid Holmberg for artwork.
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NR 63
TC 150
Z9 154
U1 2
U2 58
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 2041-1723
J9 NAT COMMUN
JI Nat. Commun.
PD FEB
PY 2014
VL 5
AR 3295
DI 10.1038/ncomms4295
PG 14
WC Multidisciplinary Sciences
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Science & Technology - Other Topics
GA AC6WX
UT WOS:000332667600042
PM 24548894
OA hybrid, Green Published
DA 2022-04-25
ER

PT J
AU Wang, F
   Song, ZY
   Qu, XJ
   Li, F
   Zhang, L
   Li, WB
   Cui, SX
AF Wang, Feng
   Song, Zhi-Yu
   Qu, Xian-Jun
   Li, Feng
   Zhang, Liang
   Li, Wen-Bao
   Cui, Shu-Xiang
TI M10, a novel derivative of Myricetin, prevents ulcerative colitis and
   colorectal tumor through attenuating robust endoplasmic reticulum stress
SO CARCINOGENESIS
LA English
DT Article
ID UNFOLDED PROTEIN RESPONSE; INFLAMMATION; DISEASE; CELLS; ER; CANCER;
   RISK
AB Chronic gut inflammation disposes to an increased risk of colitis-associated cancer. Chemoprevention is an attractive complementary strategy. We aimed to evaluate the chemopreventive effects of M10, a novel derivative of Myricetin, in the murine azoxymethane/dextran sodium sulfate model. Oral administration of M10 at 50-100 mg/kg once a day for consecutive 12 weeks significantly prevented ulcerative colitis (UC) and colorectal tumor. Pathological analysis of intestines showed that M10 reduced the degree of chronic inflammation and prevented the progression of colorectal tumorigenesis. Flow cytometry analysis of the immunocytes isolated from intraepithelial and lamina propria showed that M10 prevented the infiltration of myeloid-derived suppressor cells and increased CD8(+)T and CD4(+)T cells in colorectal tissues. Enzyme-linked immunosorbent analysis revealed the reduction of pro-inflammatory mediators granulocyte-macrophage colony-stimulating factor/macrophage colony-stimulating factor, IL-6 and TNF-alpha in colonic mucosa. Western blot assay also showed M10 prevention of the NF-kappa B/IL-6/STAT3 pathways and the biomarkers of inflammation and colorectal tumorigenesis. Electron microscopy analysis revealed that M10 prevent robust endoplasmic reticulum (ER) stress-induced autophagy in inflamed colonic mucosal cells. In conclusion, oral administration of Myricetin derivative M10 exerts chemoprevention of UC and colorectal tumor in mice. The mechanism of chemoprevention is associated with the reduction of biomarkers of chronic inflammation and proliferation through attenuating robust ER stress in inflamed colonic mucosal cells. M10 exerts chemoprevention activity without evidence of toxicity in mice. These results justify further evaluation of M10 in clinical trials. M10 could develop a promising regimen in the chemoprevention of colitis and colorectal cancer.
C1 [Wang, Feng; Cui, Shu-Xiang] Capital Med Univ, Sch Publ Hlth, Dept Toxicol & Sanit Chem, Beijing Key Lab Environm Toxicol, Beijing, Peoples R China.
   [Song, Zhi-Yu; Qu, Xian-Jun] Capital Med Univ, Sch Basic Med Sci, Dept Pharmacol, Beijing, Peoples R China.
   [Li, Feng; Zhang, Liang; Li, Wen-Bao] Marine Biomed Res Inst Qingdao, Dept Med Chem, Qingdao, Shandong, Peoples R China.
RP Cui, SX (corresponding author), Capital Med Univ, Sch Publ Hlth, Dept Toxicol & Sanit Chem, Beijing Key Lab Environm Toxicol, Beijing, Peoples R China.; Li, WB (corresponding author), Marine Biomed Res Inst Qingdao, Dept Med Chem, Qingdao, Shandong, Peoples R China.
EM wbli92128@163.com; sxccui@ccmu.edu.cn
FU Natural Science Foundation of ChinaNational Natural Science Foundation
   of China (NSFC) [81673449, 91629303]; Beijing Natural Science Foundation
   Program and Scientific Research Key Program of Beijing Municipal
   Commission of EducationBeijing Natural Science Foundation
   [KZ201710025020, KZ201810025033]
FX This work was supported by Natural Science Foundation of China
   (81673449, 91629303) and Beijing Natural Science Foundation Program and
   Scientific Research Key Program of Beijing Municipal Commission of
   Education (KZ201710025020, KZ201810025033).
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NR 32
TC 17
Z9 18
U1 1
U2 7
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 0143-3334
EI 1460-2180
J9 CARCINOGENESIS
JI Carcinogenesis
PD JUL
PY 2018
VL 39
IS 7
BP 889
EP 899
DI 10.1093/carcin/bgy057
PG 11
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA IB1GD
UT WOS:000470012000001
PM 29757351
OA Bronze
DA 2022-04-25
ER

PT J
AU Mao, XH
   Zhang, X
   Zheng, XW
   Chen, YW
   Xuan, ZX
   Huang, P
AF Mao, Xiaohong
   Zhang, Xin
   Zheng, Xiaowei
   Chen, Yongwu
   Xuan, Zixue
   Huang, Ping
TI Curcumin suppresses LGR5(+) colorectal cancer stem cells by inducing
   autophagy and via repressing TFAP2A-mediated ECM pathway
SO JOURNAL OF NATURAL MEDICINES
LA English
DT Article
DE Colorectal cancer; Curcumin; Cancer stem cells; Autophagy; LGR5; TFAP2A
AB Colorectal cancer stem cells (CSCs) have the potential for self-renewal, proliferation, and differentiation. And LGR5 is a stem cell marker gene of colorectal cancer. Curcumin can suppress oncogenicity of many cancer cells, yet the effect and mechanism of curcumin in LGR5(+) colorectal cancer stem cells (CSCs) have not been studied. In this study, we studied the effect of curcumin on LGR5(+) colorectal CSCs using the experiments of tumorsphere formation, cell viability and cell apoptosis. Then autophagy analysis, RNA-Seq, and real-time PCR were used to identify the mechanism responsible for the inhibition of LGR5(+) colorectal CSCs. Our results showed that curcumin inhibited tumorsphere formation, decreased cell viability in a dose-dependent manner, and also promoted apoptosis of LGR5(+) colorectal CSCs. Next, we found curcumin induced autophagy of LGR5(+) colorectal CSCs. When LGR5(+) colorectal CSCs were co-treated with curcumin and the autophagy inhibitor (hydroxychloroquine), curcumin-induced cell proliferation inhibition decreased. In addition, we also found that curcumin inhibited the extracellular matrix (ECM)-receptor interaction pathway via the downregulation of the following genes: GP1BB, COL9A3, COMP, AGRN, ITGB4, LAMA5, COL2A1, ITGB6, ITGA1, and TNC. Further, these genes were transcriptionally regulated by TFAP2A, and the high expression of TFAP2A was associated with poor prognosis in colorectal cancer. In conclusion, curcumin suppressed LGR5(+) colorectal CSCs, potentially by inducing autophagy and repressing the oncogenic TFAP2A-mediated ECM pathway. Graphic abstract
C1 [Mao, Xiaohong; Xuan, Zixue; Huang, Ping] Hangzhou Med Coll, Dept Pharm, Zhejiang Prov Peoples Hosp, Peoples Hosp, Hangzhou 310014, Peoples R China.
   [Zhang, Xin] Hangzhou Med Coll, Dept Pathol, Zhejiang Prov Peoples Hosp, Peoples Hosp, Hangzhou 310014, Peoples R China.
   [Zheng, Xiaowei] Zhejiang Canc Hosp, Dept Pharm, Hangzhou 310022, Peoples R China.
   [Chen, Yongwu] Univ Sci & Technol China, Dept Pharm, Div Life Sci & Med, Affiliated Hosp 1, Hefei 230036, Peoples R China.
RP Xuan, ZX; Huang, P (corresponding author), Hangzhou Med Coll, Dept Pharm, Zhejiang Prov Peoples Hosp, Peoples Hosp, Hangzhou 310014, Peoples R China.
EM xuanzixue0222@163.com; huangping_zry@163.com
OI Xuan, Zi-xue/0000-0002-6296-4062
FU Natural Science Foundation of Zhejiang ProvinceNatural Science
   Foundation of Zhejiang Province [LY19H280007, LQ17H310002]; Zhejiang
   Medical Technology Plan Project [2017ZD003, 2019KY027]
FX This study was supported by Natural Science Foundation of Zhejiang
   Province (Grant Nos. LY19H280007 and LQ17H310002) and Zhejiang Medical
   Technology Plan Project (Grant Nos. 2017ZD003 and 2019KY027).
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NR 38
TC 2
Z9 2
U1 1
U2 3
PU SPRINGER JAPAN KK
PI TOKYO
PA SHIROYAMA TRUST TOWER 5F, 4-3-1 TORANOMON, MINATO-KU, TOKYO, 105-6005,
   JAPAN
SN 1340-3443
EI 1861-0293
J9 J NAT MED-TOKYO
JI J. Nat. Med.
PD JUN
PY 2021
VL 75
IS 3
BP 590
EP 601
DI 10.1007/s11418-021-01505-1
EA MAR 2021
PG 12
WC Chemistry, Medicinal; Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA SJ7GX
UT WOS:000628459300001
PM 33713277
OA Green Published, hybrid
DA 2022-04-25
ER

PT J
AU Yu, DH
   Zhang, X
   Wang, H
   Zhang, L
   Chen, H
   Hu, M
   Dong, Z
   Zhu, G
   Qian, Z
   Fan, J
   Su, X
   Xu, Y
   Zheng, L
   Dong, H
   Yin, X
   Ji, Q
   Ji, J
AF Yu, D-H
   Zhang, X.
   Wang, H.
   Zhang, L.
   Chen, H.
   Hu, M.
   Dong, Z.
   Zhu, G.
   Qian, Z.
   Fan, J.
   Su, X.
   Xu, Y.
   Zheng, L.
   Dong, H.
   Yin, X.
   Ji, Q.
   Ji, J.
TI The essential role of TNIK gene amplification in gastric cancer growth
SO ONCOGENESIS
LA English
DT Article
DE gastric cancer; TNIK; Wnt
ID NCK-INTERACTING KINASE; SIGNAL-TRANSDUCTION; WNT; CYTOSKELETON;
   APOPTOSIS; AUTOPHAGY; PATHWAY
AB Traf2- and Nck-interacting kinase (TNIK) is one of the germinal center kinase family members involved in cytoskeleton organization and neuronal dendrite extension. Emerging evidence supports that TNIK is essential for activation of WNT signaling pathway in colon cancer growth. To search for novel genetic aberrations that drive carcinogenesis, we performed microarray-based comparative hybridization assay for gene copy number variations in primary tumor samples. Our data showed that TNIK gene was amplified in 7% (8/106) of Chinese gastric cancer patients. Theses amplifications were confirmed by fluorescence in situ hybridization analysis. PAMC82 human gastric cancer and T47D human breast cancer cell lines with TNIK amplification were identified to further understand the function of TNIK gene amplification. RNA-interference-mediated silencing of TNIK resulted in significant inhibition of cell growth and induction of cell death in TNIK-amplified, but not in TNIK-non-amplified, cell lines tested. This selective sensitivity to the TNIK inhibition was also observed under the effect of a small-molecule TNIK inhibitor. Furthermore, our data indicated that TNIK's role in gastric cancer growth was not dependent on Wnt signaling but rather was involved in AKT activation and cell autophagy. Together, our results suggest that TNIK is a novel therapeutic target in gastric cancer and TNIK amplification can be potentially used for patient selection.
C1 [Yu, D-H; Zhang, X.; Wang, H.; Hu, M.; Dong, Z.; Zhu, G.; Qian, Z.; Fan, J.; Su, X.; Xu, Y.; Zheng, L.; Dong, H.; Yin, X.; Ji, Q.] AstraZeneca, Innovat Ctr China, Shanghai, Peoples R China.
   [Wang, H.] Fudan Univ, Sch Life Sci, Shanghai 200433, Peoples R China.
   [Zhang, L.; Ji, J.] Peking Univ Canc Hosp & Inst, Dept Surg, Key Lab Carcinogenesis & Translat Res, Minist Educ, Beijing 10042, Peoples R China.
   [Chen, H.] Shanghai Jiao Tong Univ, Sch Med, Renji Hosp, Dept Gen Surg, Shanghai 200030, Peoples R China.
RP Yu, DH (corresponding author), Astrazeneca, Biosci, 199 Liangjing Rd,Zhangjiang High Tech Pk, Shangha 201203, Peoples R China.
EM yudehua@yahoo.com; jiafuj@gmail.com
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NR 17
TC 20
Z9 20
U1 2
U2 6
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 2157-9024
J9 ONCOGENESIS
JI Oncogenesis
PD FEB
PY 2014
VL 3
AR e89
DI 10.1038/oncsis.2014.2
PG 8
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA AZ8CU
UT WOS:000348443300005
PM 24566388
OA Green Published, gold
DA 2022-04-25
ER

PT J
AU Yang, JW
   Zhang, QH
   Liu, T
AF Yang, Jing-wen
   Zhang, Qing-huai
   Liu, Tong
TI Autophagy facilitates anticancer effect of 5-fluorouracil in HCT-116
   cells
SO JOURNAL OF CANCER RESEARCH AND THERAPEUTICS
LA English
DT Article
DE Apoptosis; autophagy; chemotherapy; p53
ID CANCER; CHEMOTHERAPY; INHIBITION; PUERARIN; PATHWAY
AB Aim of Study: The roles of autophagy performed in chemotherapy-induced cell death or proliferation inhibition were still in debate. In this study, we aimed to disclose the function of autophagy in chemotherapy of HCT-116 colon cells. Materials and Methods: Pharmacological and genetic methods were applied to induce and inhibit autophagy and elucidate the roles of autophagy performed in chemotherapy-induced proliferation inhibition and apoptosis. Autophagy was assessed by microtubule-associated protein light chain 3 (LC3) expression and monodansylcadaverine (MDC) staining. Results: After treatment with 5-fluorouracil (5-FU), HCT-116 cells showed typical autophagy as stained by MDC. Autophagy inhibitor (3-methyladenine [3-MA]) or inducer (rapamycin) was applied in combination with 5-FU, respectively. As evidenced by our data, 3-MA inhibited while rapamycin facilitated 5-FU-induced apoptosis and proliferation inhibition of HCT-116 cells. Consistently, 3-MA inhibited, while rapamycin facilitated 5-FU-induced expressions of Beclin1 and LC3B. Moreover, 3-MA inhibited while rapamycin facilitated 5-FU-induced p53 protein expression. Using genetic method, Beclin1 overexpression increased while Beclin1 knockdown decreased 5-FU-induced cell proliferation inhibition and apoptosis. Especially, Beclin1 overexpression increased while Beclin1 knockdown decreased 5-FU-induced p53 expression. Conclusion: Our study provides both of pharmacological and genetic evidence to support that autophagy facilitates anticancer effect of the chemotherapeutic agent. The associated application of autophagy inducer with 5-FU would be beneficial for the chemotherapy in HCT-116 cancer cells.
C1 [Yang, Jing-wen; Zhang, Qing-huai] Tianjin Union Med Ctr, Dept Anorectal Surg, Tianjin, Peoples R China.
   [Liu, Tong] Tianjin Med Univ, Gen Hosp, Dept Gen Surg, Inst Gen Surg, Tianjin, Peoples R China.
RP Liu, T (corresponding author), 154 Anshan Rd, Tianjin 300070, Peoples R China.
EM tongliu12@163.com
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NR 21
TC 10
Z9 11
U1 0
U2 5
PU WOLTERS KLUWER MEDKNOW PUBLICATIONS
PI MUMBAI
PA WOLTERS KLUWER INDIA PVT LTD , A-202, 2ND FLR, QUBE, C T S  NO 1498A-2
   VILLAGE MAROL, ANDHERI EAST, MUMBAI, 400059, INDIA
SN 0973-1482
EI 1998-4138
J9 J CANCER RES THER
JI J. Canc. Res. Ther.
PD DEC
PY 2018
VL 14
SU 5
BP S1141
EP S1147
DI 10.4103/0973-1482.204898
PG 7
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA HE5TR
UT WOS:000453452300035
PM 30539860
OA gold
DA 2022-04-25
ER

PT J
AU Kaluderovic, GN
   Mijatovic, SA
   Zmejkovski, BB
   Bulatovic, MZ
   Gomez-Ruiz, S
   Mojic, MK
   Steinborn, D
   Miljkovic, DM
   Schmidt, H
   Stosic-Grujicic, SD
   Sabo, TJ
   Maksimovic-Ivanic, DD
AF Kaluderovic, Goran N.
   Mijatovic, Sanja A.
   Zmejkovski, Bojana B.
   Bulatovic, Mirna Z.
   Gomez-Ruiz, Santiago
   Mojic, Marija K.
   Steinborn, Dirk
   Miljkovic, Djordje M.
   Schmidt, Harry
   Stosic-Grujicic, Stanislava D.
   Sabo, Tibor J.
   Maksimovic-Ivanic, Danijela D.
TI Platinum(II/IV) complexes containing ethylenediamine-N,N
   '-di-2/3-propionate ester ligands induced caspase-dependent apoptosis in
   cisplatin-resistant colon cancer cells
SO METALLOMICS
LA English
DT Article
ID VITRO ANTITUMORAL ACTIVITY; IN-VITRO; STEREOSPECIFIC LIGANDS; ANTICANCER
   ACTIVITY; MECHANISMS; CRYSTAL; INHIBITOR; COMPOUND; TOXICITY; TARGET
AB Several new R(2)eddp (R = i-Pr, i-Bu; eddp = ethylenediamine-N,N'-di-3-propionate) esters and corresponding platinum(II) and platinum(IV) complexes of the general formula [PtCln(R(2)edda-type)] (n = 2, 4) were synthesized and characterized by spectroscopic methods (IR, H-1 and C-13 NMR) and elemental analysis. The crystal structure of platinum(IV) complex [PtCl4{(c-Pe)(2)eddip}] (3a) was resolved and is given herein. Ligand precursors, platinum(II), and platinum(IV) complexes were tested against eight tumor cell lines (CT26CL25, HTC116, SW620, PC3, LNCaP, U251, A375, and B16). Selectivity in the action of those compounds between tumor and two normal primary cells (fibroblasts and keratinocytes) are discussed. A structure-activity relationship of these compounds is discussed. Furthermore, cell cycle distribution, induction of necrosis, apoptosis, autophagy, anoikis, caspase activation, ROS, and RNS are presented on the cisplatin-resistant colon carcinoma HCT116 cell line.
C1 [Kaluderovic, Goran N.; Zmejkovski, Bojana B.; Steinborn, Dirk; Schmidt, Harry] Univ Halle Wittenberg, Inst Chem, D-06120 Halle, Germany.
   [Mijatovic, Sanja A.; Bulatovic, Mirna Z.; Mojic, Marija K.; Miljkovic, Djordje M.; Stosic-Grujicic, Stanislava D.; Maksimovic-Ivanic, Danijela D.] Univ Belgrade, Inst Biol Res Sinisa Stankovic, Belgrade 11060, Serbia.
   [Zmejkovski, Bojana B.] Univ Belgrade, Inst Chem Technol & Met, Dept Chem, Belgrade 11000, Serbia.
   [Gomez-Ruiz, Santiago] Univ Rey Juan Carlos, ESCET, Dept Quim Inorgan & Analit, Madrid 28933, Spain.
   [Sabo, Tibor J.] Univ Belgrade, Fac Chem, Belgrade 11000, Serbia.
RP Kaluderovic, GN (corresponding author), Univ Halle Wittenberg, Inst Chem, Kurt Mothes Str 2, D-06120 Halle, Germany.
EM goran.kaluderovic@chemie.uni-halle.de; nelamax@yahoo.com
RI Mojić, Marija/E-8729-2015; Miljković, Đorđe/F-1378-2015; Gómez-Ruiz,
   Santiago/E-4863-2012; Kaluderovic, Goran/AAR-7347-2021; Sabo,
   Tibor/Q-6063-2016; Kaluđerović, Goran/E-6310-2013; Stosic-Grujicic,
   Stanislava/E-6828-2015; Maksimović-Ivanić, Danijela/E-7246-2015;
   Bulatović, Mirna/L-6826-2015; Mijatović, Sanja/E-7662-2015
OI Mojić, Marija/0000-0002-4906-9880; Miljković, Đorđe/0000-0002-5613-9306;
   Gómez-Ruiz, Santiago/0000-0001-9538-8359; Kaluderovic,
   Goran/0000-0001-5168-1000; Sabo, Tibor/0000-0002-9866-327X; Kaluđerović,
   Goran/0000-0001-5168-1000; Stosic-Grujicic,
   Stanislava/0000-0002-9845-3299; Maksimović-Ivanić,
   Danijela/0000-0002-8006-5079; Bulatović, Mirna/0000-0002-5472-6144;
   Mijatović, Sanja/0000-0001-9509-9098
FU Alexander von Humboldt FoundationAlexander von Humboldt Foundation;
   Ministry of Science and Technological Development of the Republic of
   SerbiaMinistry of Education, Science & Technological Development, Serbia
   [172035, 173013]
FX GNK acknowledges financial support from the Alexander von Humboldt
   Foundation. The authors are grateful to the Ministry of Science and
   Technological Development of the Republic of Serbia for financial
   support (Grant Nos. 172035 and 173013). We would also like to thank Mrs
   Heidrun Felgner for language corrections of the manuscript.
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NR 42
TC 28
Z9 28
U1 0
U2 23
PU ROYAL SOC CHEMISTRY
PI CAMBRIDGE
PA THOMAS GRAHAM HOUSE, SCIENCE PARK, MILTON RD, CAMBRIDGE CB4 0WF, CAMBS,
   ENGLAND
SN 1756-5901
EI 1756-591X
J9 METALLOMICS
JI Metallomics
PY 2012
VL 4
IS 9
BP 979
EP 987
DI 10.1039/c2mt20058a
PG 9
WC Biochemistry & Molecular Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology
GA 994AR
UT WOS:000307903700013
PM 22820831
DA 2022-04-25
ER

PT J
AU Chiacchiera, F
   Simone, C
AF Chiacchiera, Fulvio
   Simone, Cristiano
TI The AMPK-FoxO3A axis as a target for cancer treatment
SO CELL CYCLE
LA English
DT Review
DE AMPK; FoxO3A; cancer; signal-dependent transcription; antitumor therapy;
   cell metabolism; calorie restriction
ID FOXO TRANSCRIPTION FACTORS; ACTIVATED PROTEIN-KINASE;
   PEUTZ-JEGHERS-SYNDROME; LIFE-SPAN; GENE-EXPRESSION; PROMOTES
   TUMORIGENESIS; DEPENDENT REGULATION; CALORIC RESTRICTION;
   CELL-PROLIFERATION; LKB1-AMPK PATHWAY
AB FoxO proteins are an evolutionarily conserved subfamily of transcription factors involved in tumor suppression, regulation of energy metabolism and development in several tissues, and are mainly regulated by phosphorylation-dependent nuclear/cytoplasmic shuttling. The transcriptional activity of FoxO3A, one of the four members of the family, is further modulated by AMPK, one of the key regulators of cellular metabolism, which basically shifts cell machinery from energy-consuming to energy-producing pathways.
   We recently demonstrated that the AMPK/FoxO3A energy sensor pathway is still inducible in human cancer cells in response to metabolic stress, as it becomes activated in colorectal and ovarian cancer cells in response to the inhibition of p38 alpha. Activation of the FoxO3A transcriptional program initially induces autophagy as an attempt to retain energy to survive, whereas under persistent stress conditions it triggers autophagic cell death.
   In this review, we focus on the connections between AMPK and FoxO3A, describing their central role as modulators of fundamental processes such as stress resistance, cell metabolism, autophagy and cell death, and highlighting the therapeutic potential of pharmacological modulation of the AMPK-FoxO3A axis.
C1 [Chiacchiera, Fulvio; Simone, Cristiano] Consorzio Mario Negri Sud, Lab Signal Dependent Transcript, DTP, Chieti, Italy.
RP Simone, C (corresponding author), Consorzio Mario Negri Sud, Lab Signal Dependent Transcript, DTP, Chieti, Italy.
EM simone@negrisud.it
RI Chiacchiera, Fulvio/K-6740-2016; Chiacchiera, Fulvio/ABD-6137-2020;
   SIMONE, Cristiano/K-3452-2018
OI Chiacchiera, Fulvio/0000-0003-3830-2090; SIMONE,
   Cristiano/0000-0002-2628-7658
FU FIRC (Italian Foundation for Cancer Research)Fondazione AIRC per la
   ricerca sul cancro; Italian Association for Cancer Research
   (AIRC)Fondazione AIRC per la ricerca sul cancro
FX We thank Dr. Francesco Paolo Jori for his helpful discussion during the
   preparation of the manuscript and editorial assistance. Dr. Chiacchiera
   is supported by FIRC (Italian Foundation for Cancer Research)
   fellowships. This work was partially supported by a 'My First Grant'
   from the Italian Association for Cancer Research (AIRC).
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NR 61
TC 126
Z9 128
U1 2
U2 22
PU TAYLOR & FRANCIS INC
PI PHILADELPHIA
PA 530 WALNUT STREET, STE 850, PHILADELPHIA, PA 19106 USA
SN 1538-4101
EI 1551-4005
J9 CELL CYCLE
JI Cell Cycle
PD MAR 15
PY 2010
VL 9
IS 6
BP 1091
EP 1096
DI 10.4161/cc.9.6.11035
PG 6
WC Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Cell Biology
GA 569XT
UT WOS:000275636900015
PM 20190568
OA Bronze, Green Published
DA 2022-04-25
ER

PT J
AU Qiu, SL
   Xiao, ZC
   Piao, CM
   Xian, YL
   Jia, LX
   Qi, YF
   Han, JH
   Zhang, YY
   Du, J
AF Qiu, Shu-Lan
   Xiao, Zhi-Cheng
   Piao, Chun-Mei
   Xian, Ying-Lin
   Jia, Li-Xin
   Qi, Yong-Fen
   Han, Jia-Huai
   Zhang, You-yi
   Du, Jie
TI AMP-activated Protein Kinase alpha 2 Protects against Liver Injury from
   Metastasized Tumors via Reduced Glucose Deprivation-induced Oxidative
   Stress
SO JOURNAL OF BIOLOGICAL CHEMISTRY
LA English
DT Article
DE AMP-activated kinase (AMPK); Glucose; Metastasis; Oxidative Stress;
   Tumor
ID REACTIVE OXYGEN; CELL-DEATH; TNF-ALPHA; ENERGY; MITOCHONDRIA; AUTOPHAGY;
   CANCER; PHOSPHORYLATION; STARVATION; APOPTOSIS
AB Background: AMPK senses energetic changes and regulates glucose metabolism. Results: AMPK 2 deficiency aggravated the glucose deprivation and necrosis of the hepatocytes via increased ROS production and decreased mitophagy. Conclusion: AMPK 2 is essential for attenuation of liver injury during tumor metastasis. Significance: This is the first time to reveal the mechanism by which glucose/energy competition induced tissue damage in tumor.
   It is well known that tumors damage affected tissues; however, the specific mechanism underlying such damage remains elusive. AMP-activated protein kinase (AMPK) senses energetic changes and regulates glucose metabolism. In this study, we examined the mechanisms by which AMPK promotes metabolic adaptation in the tumor-bearing liver using a murine model of colon cancer liver metastasis. Knock-out of AMPK 2 significantly enhanced tumor-induced glucose deprivation in the liver and increased the extent of liver injury and hepatocyte death. Mechanistically, we observed that AMPK 2 deficiency resulted in elevated reactive oxygen species, reduced mitophagy, and increased cell death in response to tumors or glucose deprivation in vitro. These results imply that AMPK 2 is essential for attenuation of liver injury during tumor metastasis via hepatic glucose deprivation and mitophagy-mediated inhibition of reactive oxygen species production. Therefore, AMPK 2 might represent an important therapeutic target for colon cancer metastasis-induced liver injury.
C1 [Qiu, Shu-Lan; Xiao, Zhi-Cheng; Piao, Chun-Mei; Xian, Ying-Lin; Jia, Li-Xin; Du, Jie] Capital Med Univ, Beijing Anzhen Hosp, Beijing Inst Heart Lung & Blood Vessel Dis, Minist Educ,Key Lab Remodeling Related Cardiovasc, Beijing 100029, Peoples R China.
   [Qi, Yong-Fen; Zhang, You-yi] Peking Univ, Hlth Sci Ctr, Sch Basic Med Sci, Lab Cardiovasc Bioact Mol, Beijing 100191, Peoples R China.
   [Han, Jia-Huai] Xiamen Univ, Sch Biol Sci, Xiamen 361005, Peoples R China.
RP Du, J (corresponding author), Capital Med Univ, Inst Heart Lung & Blood Vessel Dis, Beijing Anzhen Hosp, Beijing 100029, Peoples R China.
EM jdu@bcm.edu
RI Han, J/G-4671-2010
FU Chinese Ministry of Science and TechnologyMinistry of Science and
   Technology, China [2009CB522205, 2012AA02A201]; National Natural Science
   Foundation of ChinaNational Natural Science Foundation of China (NSFC)
   [81230006, 31090363, 81000871]
FX This work was supported by Chinese Ministry of Science and Technology
   Grants 2009CB522205 and 2012AA02A201 and National Natural Science
   Foundation of China Grants 81230006, 31090363, and 81000871.
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NR 52
TC 17
Z9 20
U1 4
U2 13
PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3996 USA
EI 1083-351X
J9 J BIOL CHEM
JI J. Biol. Chem.
PD MAR 28
PY 2014
VL 289
IS 13
BP 9449
EP 9459
DI 10.1074/jbc.M113.543447
PG 11
WC Biochemistry & Molecular Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology
GA AD7UJ
UT WOS:000333472100060
PM 24515110
OA Green Published, hybrid
DA 2022-04-25
ER

PT J
AU Che, N
   Yang, ZT
   Liu, XZ
   Li, MX
   Feng, Y
   Zhang, CY
   Li, C
   Cui, Y
   Xuan, YH
AF Che, Nan
   Yang, Zhaoting
   Liu, Xingzhe
   Li, Mengxuan
   Feng, Ying
   Zhang, Chengye
   Li, Chao
   Cui, Yan
   Xuan, Yanhua
TI Suppression of LETM1 inhibits the proliferation and stemness of
   colorectal cancer cells through reactive oxygen species-induced
   autophagy
SO JOURNAL OF CELLULAR AND MOLECULAR MEDICINE
LA English
DT Article
DE autophagy; colorectal cancer; LETM1; reactive oxygen species
ID NEGATIVE BREAST-CANCER; ROS; APOPTOSIS; INVASION; DAMAGE
AB Leucine zipper-EF-hand-containing transmembrane protein 1 (LETM1) is a mitochondrial inner membrane protein that is highly expressed in various cancers. Although LETM1 is known to be associated with poor prognosis in colorectal cancer (CRC), its roles in autophagic cell death in CRC have not been explored. In this study, we examined the mechanisms through which LETM1 mediates autophagy in CRC. Our results showed that LETM1 was highly expressed in CRC tissues and that down-regulation of LETM1 inhibited cell proliferation and induced S-phase arrest. LETM1 silencing also suppressed cancer stem cell-like properties and induced autophagy in CRC cells. Additionally, the autophagy inhibitor 3-methyladenine reversed the inhibitory effects of LETM1 silencing on proliferation and stemness, whereas the autophagy activator rapamycin had the opposite effects. Mechanistically, suppression of LETM1 increased the levels of reactive oxygen species (ROS) and mitochondrial ROS by regulation of SOD2, which in turn activated AMP-activated protein kinase (AMPK)/mammalian target of rapamycin (mTOR), initiated autophagy, and inhibited proliferation and stemness. Our findings suggest that silencing LETM1 induced autophagy in CRC cells by triggering ROS-mediated AMPK/mTOR signalling, thus blocking CRC progression, which will enhance our understanding of the molecular mechanism of LETM1 in CRC.
C1 [Che, Nan; Yang, Zhaoting; Liu, Xingzhe; Feng, Ying; Xuan, Yanhua] Yanbian Univ, Dept Pathol, Coll Med, Yanji, Peoples R China.
   [Che, Nan; Yang, Zhaoting; Liu, Xingzhe; Li, Mengxuan; Feng, Ying; Zhang, Chengye; Li, Chao; Xuan, Yanhua] Yanbian Univ, Inst Regenerat Med, Coll Med, Yanji, Peoples R China.
   [Cui, Yan] Yanbian Univ, Dept Oncol, Affiliated Hosp, Yanji, Peoples R China.
RP Cui, Y (corresponding author), Yanbian Univ, Dept Oncol, Affiliated Hosp, 1827 Juzi Rd, Yanji 133002, Peoples R China.; Xuan, YH (corresponding author), Yanbian Univ, Dept Pathol, Coll Med, 977 Gongyuan Rd, Yanji 133002, Peoples R China.
EM 13514336939@163.com; xuanyh1@ybu.edu.cn
FU National Natural Science Foundation of ChinaNational Natural Science
   Foundation of China (NSFC) [81760531]
FX National Natural Science Foundation of China, Grant/Award Number:
   81760531
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NR 42
TC 4
Z9 4
U1 3
U2 5
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1582-1838
EI 1582-4934
J9 J CELL MOL MED
JI J. Cell. Mol. Med.
PD FEB
PY 2021
VL 25
IS 4
BP 2110
EP 2120
DI 10.1111/jcmm.16169
EA DEC 2020
PG 11
WC Cell Biology; Medicine, Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Cell Biology; Research & Experimental Medicine
GA QG9KQ
UT WOS:000598053800001
PM 33314691
OA gold, Green Published
DA 2022-04-25
ER

PT J
AU Schutz, CA
   Staedler, D
   Crosbie-Staunton, K
   Movia, D
   Bernasconi, CC
   Kenzaoui, BH
   Prina-Mello, A
   Juillerat-Jeanneret, L
AF Schuetz, Catherine A.
   Staedler, Davide
   Crosbie-Staunton, Kieran
   Movia, Dania
   Bernasconi, Catherine Chapuis
   Kenzaoui, Blanka Halamoda
   Prina-Mello, Adriele
   Juillerat-Jeanneret, Lucienne
TI Differential stress reaction of human colon cells to
   oleic-acid-stabilized and unstabilized ultrasmall iron oxide
   nanoparticles
SO INTERNATIONAL JOURNAL OF NANOMEDICINE
LA English
DT Article
DE oleic acid; ultrasmall iron oxide nanoparticles; human colon cells;
   lipid vacuoles; stress reaction; heat shock proteins
ID SUPERPARAMAGNETIC NANOPARTICLES; SURFACE-CHEMISTRY; OXIDATIVE STRESS;
   DELIVERY VECTORS; CONTRAST AGENTS; CANCER-CELLS; CYTOTOXICITY;
   GENOTOXICITY; INHIBITION; METABOLISM
AB Therapeutic engineered nanoparticles (NPs), including ultrasmall superparamagnetic iron oxide (USPIO) NPs, may accumulate in the lower digestive tract following ingestion or injection. In order to evaluate the reaction of human colon cells to USPIO NPs, the effects of non-stabilized USPIO NPs (NS-USPIO NPs), oleic-acid-stabilized USPIO NPs (OA-USPIO NPs), and free oleic acid (OA) were compared in human HT29 and CaCo2 colon epithelial cancer cells. First the biophysical characteristics of NS-USPIO NPs and OA-USPIO NPs in water, in cell culture medium supplemented with fetal calf serum, and in cell culture medium preconditioned by HT29 and CaCo2 cells were determined. Then, stress responses of the cells were evaluated following exposure to NS-USPIO NPs, OA-USPIO NPs, and free OA. No modification of the cytoskeletal actin network was observed. Cell response to stress, including markers of apoptosis and DNA repair, oxidative stress and degradative/autophagic stress, induction of heat shock protein, or lipid metabolism was determined in cells exposed to the two NPs. Induction of an autophagic response was observed in the two cell lines for both NPs but not free OA, while the other stress responses were cell-and NP-specific. The formation of lipid vacuoles/droplets was demonstrated in HT29 and CaCo2 cells exposed to OA-USPIO NPs but not to NS-USPIO NPs, and to a much lower level in cells exposed to equimolar concentrations of free OA. Therefore, the induction of lipid vacuoles in colon cells exposed to OA utilized as a stabilizer for USPIO NPs is higly amplified compared to free OA, and is not observed in the absence of this lipid in NS-USPIO NPs.
C1 [Schuetz, Catherine A.; Bernasconi, Catherine Chapuis; Kenzaoui, Blanka Halamoda; Prina-Mello, Adriele; Juillerat-Jeanneret, Lucienne] CHU Vaudois, UNIL, CH-1015 Lausanne, Switzerland.
   [Staedler, Davide] Ecole Polytech Fed Lausanne, Inst Chem Sci & Engn, CH-1015 Lausanne, Switzerland.
   [Crosbie-Staunton, Kieran; Prina-Mello, Adriele] Trinity Coll Dublin, Sch Med, Dublin, Ireland.
   [Movia, Dania; Prina-Mello, Adriele] Trinity Coll Dublin, CRANN, Dublin, Ireland.
RP Juillerat-Jeanneret, L (corresponding author), Univ Inst Pathol, Rue Bugnon 25, CH-1011 Lausanne, Switzerland.
EM prinamea@tcd.ie; lucienne.juillerat@chuv.ch
RI Movia, Dania/T-6552-2018; Prina-Mello, Adriele/C-6458-2011
OI Movia, Dania/0000-0001-6412-8132; Prina-Mello,
   Adriele/0000-0002-4371-2214
FU European CommissionEuropean CommissionEuropean Commission Joint Research
   Centre [NMP4-CA-2008-21853, HEALTH-2007-201335, NMP4-LA-2010-246479,
   NMP4-LA-2011-262943, NMP6-LA-2013-310584]
FX The authors want to thank the TCD CRANN Advanced Microscopy Laboratory,
   and in particular Dr Valerie Gerard, for the preparation of the TEM
   images of the received NPs and Seher Guney-Ayra for technical
   assistance. This work was partially supported by the European Commission
   7th Framework Projects NanoImpactNet (NMP4-CA-2008-21853), NanoTEST
   (HEALTH-2007-201335), NAM-DIATREAM (NMP4-LA-2010-246479), MULTIFUN
   (NMP4-LA-2011-262943), and NANoREG (NMP6-LA-2013-310584).
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NR 37
TC 15
Z9 15
U1 0
U2 17
PU DOVE MEDICAL PRESS LTD
PI ALBANY
PA PO BOX 300-008, ALBANY, AUCKLAND 0752, NEW ZEALAND
SN 1178-2013
J9 INT J NANOMED
JI Int. J. Nanomed.
PY 2014
VL 9
BP 3481
EP 3498
DI 10.2147/IJN.S65082
PG 18
WC Nanoscience & Nanotechnology; Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Science & Technology - Other Topics; Pharmacology & Pharmacy
GA AM4UR
UT WOS:000339851900001
PM 25092978
OA Green Published, gold, Green Submitted
DA 2022-04-25
ER

PT J
AU Lu, CM
   Chen, JF
   Xu, HG
   Zhou, XZ
   He, QQ
   Li, YL
   Jiang, GQ
   Shan, YX
   Xue, BX
   Zhao, RX
   Wang, Y
   Werle, KD
   Cui, RT
   Liang, JY
   Xu, ZX
AF Lu, Changming
   Chen, Jianfeng
   Xu, Hua-Guo
   Zhou, Xianzheng
   He, Qiongqiong
   Li, Yu-Lin
   Jiang, Guoqing
   Shan, Yuxi
   Xue, Boxin
   Zhao, Rui-Xun
   Wang, Yong
   Werle, Kaitlin D.
   Cui, Rutao
   Liang, Jiyong
   Xu, Zhi-Xiang
TI MIR106B and MIR93 Prevent Removal of Bacteria From Epithelial Cells by
   Disrupting ATG16L1-Mediated Autophagy
SO GASTROENTEROLOGY
LA English
DT Article
DE Inflammatory Bowel Disease; microRNA; Cell Biology; Infection
ID INFLAMMATORY-BOWEL-DISEASE; GENOME-WIDE ASSOCIATION; CROHNS-DISEASE;
   C-MYC; ANTIGEN PRESENTATION; SUSCEPTIBILITY LOCI; MAMMALIAN AUTOPHAGY;
   IMPAIRED AUTOPHAGY; EXPRESSION; ATG16L1
AB BACKGROUND & AIMS: Variants in genes that regulate autophagy have been associated with Crohn's disease (CD). Defects in autophagy-mediated removal of pathogenic microbes could contribute to the pathogenesis of CD. We investigated the role of the microRNAs (miRs) MIR106B and MIR93 in induction of autophagy and bacterial clearance in human cell lines and the correlation between MIR106B and autophagy-related gene 16L1 (ATG16L1) expression in tissues from patients with CD. METHODS: We studied the ability of MIR106B and MIR93 to regulate ATG transcripts in human cancer cell lines (HCT116, SW480, HeLa, and U2OS) using luciferase report assays and bioinformatics analyses; MIR106B and MIR93 mimics and antagonists were transfected into cells to modify levels of miRs. Cells were infected with LF82, a CD-associated adherent-invasive strain of Escherichia coli, and monitored by confocal microscopy and for colony-forming units. Colon tissues from 41 healthy subjects (controls), 22 patients with active CD, 16 patients with inactive CD, and 7 patients with chronic inflammation were assessed for levels of MIR106B and ATG16L1 by in situ hybridization and immunohistochemistry. RESULTS: Silencing Dicer1, an essential processor of miRs, increased levels of ATG protein and formation of autophagosomes in cells, indicating that miRs regulate autophagy. Luciferase reporter assays indicated that MIR106B and MIR93 targeted ATG16L1 messenger RNA. MIR106B and MIR93 reduced levels of ATG16L1 and autophagy; these increased after expression of ectopic ATG16L1. In contrast, MIR106B and MIR93 antagonists increased formation of autophagosomes. Levels of MIR106B were increased in intestinal epithelia from patients with active CD, whereas levels of ATG16L1 were reduced compared with controls. Levels of c-Myc were also increased in intestinal epithelia of patients with active CD compared with controls. These alterations could impair removal of CD-associated bacteria by autophagy. CONCLUSIONS: In human cell lines, MIR106B and MIR93 reduce levels of ATG16L1 and autophagy and prevent autophagy-dependent eradication of intracellular bacteria. This process also appears to be altered in colon tissues from patients with active CD.
C1 [Lu, Changming; Chen, Jianfeng; Xu, Hua-Guo; Zhao, Rui-Xun; Wang, Yong; Werle, Kaitlin D.; Xu, Zhi-Xiang] Univ Alabama Birmingham, Ctr Comprehens Canc, Div Hematol & Oncol, Birmingham, AL 35205 USA.
   [Zhou, Xianzheng] Univ Minnesota, Dept Pediat, Minneapolis, MN 55455 USA.
   [Zhou, Xianzheng] New York Med Coll, Dept Pediat, Valhalla, NY 10595 USA.
   [Zhou, Xianzheng] New York Med Coll, Dept Microbiol & Immunol, Valhalla, NY 10595 USA.
   [Zhou, Xianzheng] New York Med Coll, Dept Cell Biol & Anat, Valhalla, NY 10595 USA.
   [He, Qiongqiong] Cent S Univ, Xiangya Sch Med, Dept Pathol, Changsha, Hunan, Peoples R China.
   [Li, Yu-Lin] Jilin Univ, Norman Bethune Coll Med, Minist Educ, Key Lab Pathobiol, Changchun 130023, Jilin, Peoples R China.
   [Jiang, Guoqing; Shan, Yuxi; Xue, Boxin] Soochow Univ, Affiliated Hosp 2, Dept Surg, Suzhou, Jiangsu, Peoples R China.
   [Cui, Rutao] Boston Univ, Sch Med, Dept Dermatol, Boston, MA 02118 USA.
   [Liang, Jiyong] Univ Texas MD Anderson Canc Ctr, Dept Syst Biol, Houston, TX 77030 USA.
RP Xu, ZX (corresponding author), Univ Alabama Birmingham, Ctr Comprehens Canc, Div Hematol & Oncol, Wallace Tumor Inst Bldg,Room 520D,1824 6th Ave So, Birmingham, AL 35205 USA.
EM zhixiangxu@uabmc.edu
FU National Cancer InstituteUnited States Department of Health & Human
   ServicesNational Institutes of Health (NIH) - USANIH National Cancer
   Institute (NCI) [R01CA133053, P50CA098252]; National Institute of
   Allergy and Infectious DiseasesUnited States Department of Health &
   Human ServicesNational Institutes of Health (NIH) - USANIH National
   Institute of Allergy & Infectious Diseases (NIAID) [R21AI092220];
   NATIONAL CANCER INSTITUTEUnited States Department of Health & Human
   ServicesNational Institutes of Health (NIH) - USANIH National Cancer
   Institute (NCI) [P30CA016672, R01CA133053, P50CA098252] Funding Source:
   NIH RePORTER; NATIONAL CENTER FOR RESEARCH RESOURCESUnited States
   Department of Health & Human ServicesNational Institutes of Health (NIH)
   - USANIH National Center for Research Resources (NCRR) [P20RR021905]
   Funding Source: NIH RePORTER; NATIONAL INSTITUTE OF ALLERGY AND
   INFECTIOUS DISEASESUnited States Department of Health & Human
   ServicesNational Institutes of Health (NIH) - USANIH National Institute
   of Allergy & Infectious Diseases (NIAID) [R21AI092220] Funding Source:
   NIH RePORTER
FX Supported by National Cancer Institute grant R01CA133053, the National
   Cancer Institute Cervical Cancer SPORE Career Development Award and
   Pilot Award P50CA098252 (to Z.-X.X.), and National Institute of Allergy
   and Infectious Diseases grant R21AI092220 (to X.Z.).
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TC 79
Z9 83
U1 1
U2 25
PU W B SAUNDERS CO-ELSEVIER INC
PI PHILADELPHIA
PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA
SN 0016-5085
EI 1528-0012
J9 GASTROENTEROLOGY
JI Gastroenterology
PD JAN
PY 2014
VL 146
IS 1
BP 188
EP 199
DI 10.1053/j.gastro.2013.09.006
PG 12
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA 276GF
UT WOS:000328736000033
PM 24036151
OA Green Accepted
DA 2022-04-25
ER

PT J
AU Lee, JJ
   Park, IH
   Rhee, WJ
   Kim, HS
   Shin, JS
AF Lee, Je-Jung
   Park, In Ho
   Rhee, Woo Joong
   Kim, Hee Sue
   Shin, Jeon-Soo
TI HMGB1 modulates the balance between senescence and apoptosis in response
   to genotoxic stress
SO FASEB JOURNAL
LA English
DT Article
DE cancer; metastasis; cell fate; doxorubicin; camptothecin
ID CELLULAR SENESCENCE; SECRETORY PHENOTYPE; CANCER CELLS; PROTEIN;
   TUMORIGENESIS; SUPPRESSION; AUTOPHAGY; RELEASE; COMPLEX; P53
AB High mobility group box-1 (HMGB1) is involved in various diseases and is associated with the resistance of many types of human cancers to chemotherapy; however, its role in cancer metastasis remains unexplored. This study examined the HMGB1 status of both highly and poorly metastatic cancer cells in response to genotoxic stress. The weakly and highly metastatic mouse melanoma cell lines (B16 vs. B16-F10), human melanoma cell lines (SK-MEL-28 vs. SK-MEL-24), colon cancer cell lines (DLD-1 vs. LS174T), and wild-type (WT) vs. HMGB1 knockout (KO) mouse embryonic fibroblasts (MEFs) were treated with doxorubicin (Dox) and camptothecin (CPT), and then cellular morphology, senescence-associated beta-galactosidase staining, lactate dehydrogenase release, and caspase-3 activation were used to assess cell fate. To investigate the role of HMGB1 in p21 expression, HMGB1 and p21 expressions were examined by Western blotting, and the HMGB1-mediated p21 promoter luciferase assay was performed after small interfering RNA or overexpression of HMGB1 prior to Dox treatment. Although highly metastatic mouse melanoma B16-F10 cells preferred senescence, with persistent HMGB1 expression, poorly metastatic B16 cells entered apoptosis, with decreasing HMGB1 levels via cleavage under Dox treatment. Similarly, more metastatic human melanoma SK-MEL-24 and human colon cancer LS174T cells underwent senescence, whereas fewer metastatic melanoma SK-MEL-28 and DLD-1 cells exhibited apoptosis under Dox stimulation. In senescent B16-F10, SK-MEL-24, and LS174T cells treated with Dox, p21 levels were increased by persistent HMGB1 expression. Furthermore, HMGB1 depletion caused a senescence-apoptosis shift with p21 down-regulation in B16-F10 cells, and HMGB1 overexpression switched from apoptosis to senescence concomitantly with increased p21 expression in B16 cells after Dox treatment. The same effects were observed in both cell pairs of mouse melanoma and human colon cancer cells treated with CPT, another genotoxic stressor. Indeed, although WT MEF entered senescence accompanied by p21 increase, HMGB1 KO underwent apoptosis with p21 decrease by Dox treatment. In our cell model system, we demonstrated that highly metastatic cancer cells preferentially enter senescence, whereas apoptosis predominates in weakly metastatic cancer cells under genotoxic stress, which depends on the presence or absence of HMGB1, suggesting that the HMGB1-p21 axis is required for genotoxic stress-induced senescence. These findings suggest that HMGB1 modulation of cancers with different metastatic status could be a strategy for selectively enforcing tumor suppression.-Lee, J.-J., Park, I. H., Rhee, W. J., Kim, H. S., Shin, J.-S. HMGB1 modulates the balance between senescence and apoptosis in response to genotoxic stress.
C1 [Lee, Je-Jung; Rhee, Woo Joong; Kim, Hee Sue; Shin, Jeon-Soo] Yonsei Univ, Coll Med, Dept Microbiol, 50-1 Yonsei Ro, Seoul 03722, South Korea.
   [Lee, Je-Jung; Park, In Ho; Shin, Jeon-Soo] Yonsei Univ, Coll Med, Inst Immunol & Immunol Dis, Seoul, South Korea.
   [Park, In Ho; Shin, Jeon-Soo] Yonsei Univ, Coll Med, Severance Biomed Sci Inst, Seoul, South Korea.
   [Rhee, Woo Joong; Shin, Jeon-Soo] Inst for Basic Sci Korea, Ctr Nanomed, Seoul, South Korea.
RP Shin, JS (corresponding author), Yonsei Univ, Coll Med, Dept Microbiol, 50-1 Yonsei Ro, Seoul 03722, South Korea.
EM jsshin6203@yuhs.ac
OI Rhee, Woo Joong/0000-0001-9690-0553; Shin, Jeon-Soo/0000-0002-8294-3234;
   Park, In Ho/0000-0003-2190-5469
FU National Research Foundation of Korea (NRF) - Korean government
   [2014R1A4A1008625, 2017R1A2B3006704, 2017R1D1A1B03028551,
   2019R1I1A1A01041284, 2019R1A6A1A03032869]; Research Center Program of
   the Institute for Basic Science (IBS) in Korea [IBS-R026-D1]; Brain
   Korea 21 PLUS Project for Medical Science
FX This work was supported by grants from the National Research Foundation
   of Korea (NRF) funded by the Korean government (2014R1A4A1008625,
   2017R1A2B3006704, 2017R1D1A1B03028551, 2019R1I1A1A01041284, and
   2019R1A6A1A03032869), the Research Center Program of the Institute for
   Basic Science (IBS) in Korea (IBS-R026-D1), and the Brain Korea 21 PLUS
   Project for Medical Science. The authors declare no conflicts of
   interest.
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TC 17
Z9 18
U1 2
U2 7
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0892-6638
EI 1530-6860
J9 FASEB J
JI Faseb J.
PD OCT
PY 2019
VL 33
IS 10
BP 10942
EP 10953
DI 10.1096/fj.201900288R
PG 12
WC Biochemistry & Molecular Biology; Biology; Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
   Topics; Cell Biology
GA JC3GG
UT WOS:000489166300030
PM 31284735
DA 2022-04-25
ER

PT J
AU Mansilla, S
   Llovera, L
   Portugal, J
AF Mansilla, Sylvia
   Llovera, Laia
   Portugal, Jose
TI Chemotherapeutic Targeting of Cell Death Pathways
SO ANTI-CANCER AGENTS IN MEDICINAL CHEMISTRY
LA English
DT Article
DE Apoptosis; Autophagy; Chemotherapy; Mitotic catastrophe; Necrosis;
   Senescence
ID SMALL-MOLECULE INHIBITORS; SENESCENCE-LIKE PHENOTYPE; COLON-CARCINOMA
   CELLS; 2 DISTINCT MODES; MITOTIC CATASTROPHE; CANCER-THERAPY;
   DNA-DAMAGE; TUMOR-CELLS; CHECKPOINT ABROGATION; PROLIFERATION ARREST
AB Cell death plays an important role in cancer growth and progression, as well as in the efficiency of chemotherapy. Although apoptosis is commonly regarded as the principal mechanism of programmed cell death, it has been increasingly reported that several anti-cancer agents do not only induce apoptosis but other forms of cell death such as necrosis, autophagy and mitotic catastrophe, as well as the state of permanent loss of proliferative capacity known as senescence. A deeper understanding of what we know about chemotherapy-induced death is rather relevant considering the emerging knowledge of non-apoptotic cell death signaling pathways, and the fact that many tumors have the apoptosis pathway seriously compromised. In this review we examine the effects that various anti-cancer agents have on pathways involved in the different cell death outcomes. Novel and specific anti-cancer agents directed toward members of the cell death signaling pathways are being developed and currently being tested in clinical trials. If we precisely activate or inhibit molecules that mediate the diversity of cell death outcomes, we might succeed in more effective and less toxic chemotherapy.
C1 [Mansilla, Sylvia; Llovera, Laia; Portugal, Jose] CSIC, Inst Biol Mol Barcelona, E-08028 Barcelona, Spain.
RP Portugal, J (corresponding author), CSIC, Inst Biol Mol Barcelona, Parc Cient Barcelona,Baldiri Reixac 10, E-08028 Barcelona, Spain.
EM jpmbmc@ibmb.csic.es
RI Portugal, José/K-4504-2014
OI Portugal, José/0000-0002-1923-9666; Llovera Nadal,
   Laia/0000-0002-5836-593X; Mansilla, Sylvia/0000-0003-0181-1721
FU Spanish Ministry of Science and InnovationSpanish Government
   [BFU2010-15518]; European CommunityEuropean Commission
FX This work was supported by grant BFU2010-15518 from the Spanish Ministry
   of Science and Innovation, and the FEDER program of the European
   Community, and it was performed within the framework of the Xarxa de
   Referencia en Biotecnologia of the Generalitat de Catalunya. We
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NR 139
TC 33
Z9 34
U1 1
U2 10
PU BENTHAM SCIENCE PUBL LTD
PI SHARJAH
PA EXECUTIVE STE Y-2, PO BOX 7917, SAIF ZONE, 1200 BR SHARJAH, U ARAB
   EMIRATES
SN 1871-5206
EI 1875-5992
J9 ANTI-CANCER AGENT ME
JI Anti-Cancer Agents Med. Chem.
PD MAR
PY 2012
VL 12
IS 3
BP 226
EP 238
DI 10.2174/187152012800228805
PG 13
WC Oncology; Chemistry, Medicinal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Pharmacology & Pharmacy
GA 936TR
UT WOS:000303613400009
PM 22263795
DA 2022-04-25
ER

PT J
AU Hrabakova, R
   Kollareddy, M
   Tyleckova, J
   Halada, P
   Hajduch, M
   Gadher, SJ
   Kovarova, H
AF Hrabakova, Rita
   Kollareddy, Madhu
   Tyleckova, Jirina
   Halada, Petr
   Hajduch, Marian
   Gadher, Suresh Jivan
   Kovarova, Hana
TI Cancer Cell Resistance to Aurora Kinase Inhibitors: Identification of
   Novel Targets for Cancer Therapy
SO JOURNAL OF PROTEOME RESEARCH
LA English
DT Article
DE Aurora kinase inhibitors; resistance; p5.3; apoptosis; autophagy;
   platelet-activating factor acetylhydrolase; Ran; serine
   hydroxymethyltransferase; serpin BS; calretinin
ID DRUG-RESISTANCE; BREAST-CANCER; P53; CHEMOTHERAPY; EXPRESSION;
   CHEMORESISTANCE; CARCINOMA; PATHWAY; ACTIVATION; PROTEOMICS
AB Drug resistance is the major obstacle to successful cancer therapy. Our study focuses on resistance to Aurora kinase inhibitors tested as anti-cancer drugs in clinical trials. We have used 2D electrophoresis in the pH ranges of 4-7 and 6-11 followed by protein identification using MALDI-TOF/TOF to compare the protein composition of HCT116 inhibitors or resistant toward these drugs. The analysis also colon cancer cells either sensitive to CYC116 and ZM447439 included p53(+/+) and p53(-/-) phenotypes of HCT116 cells. Our findings demonstrate that platelet-activating factor acetylhydrolase and GTP-binding nuclear protein Ran contribute to the development of resistance to ZM447439 only where resistance is related to p53. On the other hand, serine hydroxymethyltransferase was found to promote the tumor growth in cells resistant to CYC116 without the influence of p53. Computer modeling of interaction networks highlighted a direct link of the p53-independent mechanism of resistance to CYC116 with autophagy. Importantly, serine hydroxymethyltransferase, serpin B5, and calretinin represent the target proteins that may help overcome resistance in combination therapies. In addition, serpin B5 and calretinin appear to be candidate biomarkers that may be accessible in patients for monitoring of cancer therapy with ease.
C1 [Hrabakova, Rita; Tyleckova, Jirina; Kovarova, Hana] AS CR, Vvi, Inst Anim Physiol & Genet, Lab Biochem & Mol Biol Germ Cells, Libechov 27721, Czech Republic.
   [Kollareddy, Madhu; Hajduch, Marian] Palacky Univ, Inst Mol & Translat Med, Expt Med Lab, Olomouc 77515, Czech Republic.
   [Kollareddy, Madhu; Hajduch, Marian] Univ Hosp, Fac Med & Dent, Olomouc 77515, Czech Republic.
   [Halada, Petr] AS CR, Vvi, Inst Microbiol, Lab Mol Struct Characterisat, Prague 14220, Czech Republic.
   [Gadher, Suresh Jivan] Life Technol, Frederick, MD 21704 USA.
RP Kovarova, H (corresponding author), AS CR, Vvi, Inst Anim Physiol & Genet, Lab Biochem & Mol Biol Germ Cells, Rumburska 89, Libechov 27721, Czech Republic.
EM kovarova@iapg.cas.cz
RI Hajduch, Marian/J-4015-2014; Sucha, Rita/ABA-9387-2021; Kovarova,
   Hana/G-7135-2014; Hrabakova, Rita/G-7136-2014; Halada, Petr/H-3330-2014;
   Dzubak, Petr/D-2175-2013
OI Hajduch, Marian/0000-0002-4834-908X; Sucha, Rita/0000-0002-2808-4870;
   Halada, Petr/0000-0002-7229-3450; Kollareddy, Madhu/0000-0001-7412-096X;
   Dzubak, Petr/0000-0002-3098-5969
FU Ministry of Education, Youth and SportsMinistry of Education, Youth &
   Sports - Czech Republic [LC07017]; Operational Program Research and
   Development for InnovationsEuropean Commission [CZ.1.05/2.1.00/01.0030];
    [RVO67985904];  [RVO61388971]
FX We greatly acknowledge Jaroslava Supolikova for skillful technical
   assistance. This work was supported in part by the Ministry of
   Education, Youth and Sports (Grant LC07017) and by Institutional
   Research Projects RVO67985904 (IAPG, AS CR, v.v.i.) and RVO61388971
   (IMIC, AS CR, v.v.i.). An infrastructural part of this project was
   supported from the Operational Program Research and Development for
   Innovations (CZ.1.05/2.1.00/01.0030).
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NR 60
TC 18
Z9 18
U1 0
U2 30
PU AMER CHEMICAL SOC
PI WASHINGTON
PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA
SN 1535-3893
EI 1535-3907
J9 J PROTEOME RES
JI J. Proteome Res.
PD JAN
PY 2013
VL 12
IS 1
BP 455
EP 469
DI 10.1021/pr300819m
PG 15
WC Biochemical Research Methods
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology
GA 065NX
UT WOS:000313156300046
PM 23151231
DA 2022-04-25
ER

PT J
AU Aredia, F
   Scovassi, AI
AF Aredia, Francesca
   Scovassi, Anna Ivana
TI A new function for miRNAs as regulators of autophagy
SO FUTURE MEDICINAL CHEMISTRY
LA English
DT Review
DE antagomir; autophagy; biomarker; cancer; miRNA; oncomiR; tumor
   suppressor miRNA
ID CANCER STEM-CELLS; TUMOR SUPPRESSIVE ROLES; COLORECTAL-CANCER;
   HEPATOCELLULAR-CARCINOMA; DOWN-REGULATION; CIRCULATING MICRORNAS;
   PROMOTES AUTOPHAGY; SIGNALING NETWORKS; HUMAN GLIOBLASTOMA; SMALL
   MOLECULES
AB Autophagy is a self-digestive process regulated by an intricate network of factors able either to ensure the prosurvival function of autophagy or to convert it in a death pathway. Recently, the involvement of miRNAs in the regulation of autophagy networks has been reported. This review will summarize the main features of these small noncoding endogenous RNAs, focusing on their relevance in cancer and finally addressing their impact on autophagy.
C1 [Aredia, Francesca; Scovassi, Anna Ivana] CNR, Ist Genet Mol, Via Abbiategrasso 207, I-27100 Pavia, Italy.
RP Scovassi, AI (corresponding author), CNR, Ist Genet Mol, Via Abbiategrasso 207, I-27100 Pavia, Italy.
EM scovassi@igm.cnr.it
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NR 128
TC 16
Z9 19
U1 4
U2 21
PU FUTURE SCI LTD
PI LONDON
PA UNITED HOUSE, 2 ALBERT PL, LONDON, N3 1QB, ENGLAND
SN 1756-8919
EI 1756-8927
J9 FUTURE MED CHEM
JI Future Med. Chem.
PD JAN
PY 2017
VL 9
IS 1
BP 25
EP 36
DI 10.4155/fmc-2016-0173
PG 12
WC Chemistry, Medicinal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA EH6FM
UT WOS:000391868200003
PM 27957876
DA 2022-04-25
ER

PT J
AU Chaudhary, P
   Ha, E
   Vo, TTL
   Seo, JH
AF Chaudhary, Prerna
   Ha, Eunyoung
   Tam Thuy Lu Vo
   Seo, Ji Hae
TI Diverse roles of arrest defective 1 in cancer development
SO ARCHIVES OF PHARMACAL RESEARCH
LA English
DT Review
DE ARD1; Acetyltransferase; Acetylation; Tumorigenesis
ID HEPATOCELLULAR-CARCINOMA; POOR-PROGNOSIS; PROTEIN; ACETYLATION; ARD1;
   EXPRESSION; CONTRIBUTES; METASTASIS; REGULATOR; APOPTOSIS
AB Arrest defective 1 is an acetyltransferase that acetylates N-terminal amino acid or internal lysine residues of its target proteins. By acetylating its target proteins, ARD1 plays roles in many cellular activities, including proliferation, differentiation, autophagy, and apoptosis. In recent years, a number of investigations have emerged reporting the dysregulated expression of ARD1 in different types of cancer, including lung, liver, pancreas, breast, prostate, and colon cancer. Furthermore, the expression level of ARD1 in cancer tissues has been correlated with the progression and metastasis of the cancer and the survival of cancer patients. Consequently, mechanistic studies have revealed that ARD1-mediated protein acetylation plays an important role in modulating several cellular events that are important for cancer development, such as cell cycle progression, cell death, and migration. On the basis of this evidence, targeting of ARD1 has been proposed as a promising avenue for the development of novel cancer therapeutics. This review summarizes the biological functions of ARD1 in different types of cancer and provides a deep insight into the biochemical activities of ARD1 during tumor progression.
C1 [Chaudhary, Prerna; Ha, Eunyoung; Tam Thuy Lu Vo; Seo, Ji Hae] Keimyung Univ, Sch Med, Dept Biochem, Daegu 42601, South Korea.
RP Seo, JH (corresponding author), Keimyung Univ, Sch Med, Dept Biochem, Daegu 42601, South Korea.
EM seojh@kmu.ac.kr
FU National Research Foundation of KoreaNational Research Foundation of
   Korea [NRF-2016R1A6A1A03011325, NRF-2016R1D1A1B03935560,
   NRF-2019R1C1C1005855] Funding Source: Medline
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TC 7
Z9 7
U1 1
U2 2
PU PHARMACEUTICAL SOC KOREA
PI SEOUL
PA 1489-3 SUHCHO-DONG, SUHCHO-KU, SEOUL 137-071, SOUTH KOREA
SN 0253-6269
EI 1976-3786
J9 ARCH PHARM RES
JI Arch. Pharm. Res.
PD DEC
PY 2019
VL 42
IS 12
BP 1040
EP 1051
DI 10.1007/s12272-019-01195-0
PG 12
WC Chemistry, Medicinal; Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA JW3CI
UT WOS:000502933000002
PM 31813105
DA 2022-04-25
ER

PT J
AU Fu, YY
   Hong, L
   Xu, JC
   Zhong, GP
   Gu, Q
   Gu, QQ
   Guan, YP
   Zheng, XP
   Dai, Q
   Luo, X
   Liu, C
   Huang, ZY
   Yin, XM
   Liu, PQ
   Li, M
AF Fu, Yuanyuan
   Hong, Liang
   Xu, Jiecheng
   Zhong, Guoping
   Gu, Qiong
   Gu, Qianqian
   Guan, Yanping
   Zheng, Xueping
   Dai, Qi
   Luo, Xia
   Liu, Cui
   Huang, Zhiying
   Yin, Xiao-Ming
   Liu, Peiqing
   Li, Min
TI Discovery of a small molecule targeting autophagy via ATG4B inhibition
   and cell death of colorectal cancer cells in vitro and in vivo
SO AUTOPHAGY
LA English
DT Article
DE Anti-tumor; ATG4B; autophagy; cell death; colorectal cancer;
   delipidation; FRET assay; xenografts
ID PROTEIN; DERIVATIVES; MODULATION; ASSAY; LC3
AB Human Atg4 homologs are cysteine proteases, which play key roles in the macroautophagy/autophagy process by cleaving Atg8 homologs for conjugation to lipid membranes and for deconjugation of Atg8 homologs from membranes. Expression of ATG4B is significantly increased in colorectal cancer cells compared to normal cells, suggesting that ATG4B may be important for cancer biology. Inhibition of ATG4B may reduce the autophagy activity, thereby sensitizing cancer cells to therapeutic agents. Thus, developing specific and potent ATG4B inhibitors for research as well as for potential therapeutic uses is highly needed. In this study, we integrated in silico screening and in vitro assays to discover a potent ATG4B inhibitor, named S130, from a noncommercial library. This chemical binds to ATG4B with strong affinity and specifically suppresses the activity of ATG4B but not other proteases. S130 did not cause the impairment of autophagosome fusion, nor did it result in the dysfunction of lysosomes. Instead, S130 might attenuate the delipidation of LC3-II on the autolysosomes to suppress the recycling of LC3-I, which normally occurs after LC3-II cleavage by ATG4B. Intriguingly, S130 induced cell death, which was accompanied with autophagy stress and could be further exacerbated by nutrient deprivation. Such cytotoxicity could be partially reversed by enhancing ATG4B activity. Finally, we found that S130 was distributed in tumor tissues in vivo and was also effective in arresting the growth of colorectal cancer cells. Thus, this study indicates that ATG4B is a potential anticancer target and S130 might be a novel small-molecule candidate for future cancer therapy.
C1 [Fu, Yuanyuan; Hong, Liang; Xu, Jiecheng; Zhong, Guoping; Gu, Qiong; Gu, Qianqian; Guan, Yanping; Zheng, Xueping; Dai, Qi; Luo, Xia; Liu, Cui; Huang, Zhiying; Liu, Peiqing; Li, Min] Sun Yat Sen Univ, Sch Pharmaceut Sci, Guangdong Prov Key Lab New Drug Design & Evaluat, Natl & Local United Engn Lab Druggabil & New Drug, Guangzhou, Guangdong, Peoples R China.
   [Yin, Xiao-Ming] Indiana Univ Sch Med, Dept Pathol & Lab Med, Indianapolis, IN 46202 USA.
RP Liu, PQ; Li, M (corresponding author), Sun Yat Sen Univ, Sch Pharmaceut Sci, Guangzhou 510006, Guangdong, Peoples R China.
EM liupq@mail.sysu.edu.cn; limin65@mail.sysu.edu.cn
RI 管, 宴萍/AAL-5308-2020; gu, qiong/N-1653-2017; Xu, Jun/AAI-7544-2020
OI Xu, Jun/0000-0002-1075-0337; Liu, Peiqing/0000-0003-4388-2173; Gu,
   Qiong/0000-0001-6011-3697; li, min/0000-0002-5657-8675; Peiqing,
   Liu/0000-0002-3378-4863
FU National Natural Science Foundation of ChinaNational Natural Science
   Foundation of China (NSFC) [31671437]; National Science and Technology
   Major Project of the Ministry of Science and Technology of China
   [2018ZX09735010]; Natural Science Foundation of Guangdong Province,
   ChinaNational Natural Science Foundation of Guangdong Province
   [2016A030313335]; 111 projectMinistry of Education, China - 111 Project
   [B16047]; Guangdong Provincial Key Laboratory of Construction Foundation
   [2017B030314030]
FX This work was supported in part by the National Natural Science
   Foundation of China (31671437), the National Science and Technology
   Major Project of the Ministry of Science and Technology of China
   (2018ZX09735010), the Natural Science Foundation of Guangdong Province,
   China (2016A030313335), the 111 project (B16047), and the Guangdong
   Provincial Key Laboratory of Construction Foundation (2017B030314030).
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NR 42
TC 46
Z9 48
U1 3
U2 79
PU TAYLOR & FRANCIS INC
PI PHILADELPHIA
PA 530 WALNUT STREET, STE 850, PHILADELPHIA, PA 19106 USA
SN 1554-8627
EI 1554-8635
J9 AUTOPHAGY
JI Autophagy
PD FEB 1
PY 2019
VL 15
IS 2
BP 295
EP 311
DI 10.1080/15548627.2018.1517073
PG 17
WC Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Cell Biology
GA HF2SP
UT WOS:000454087000008
PM 30176161
OA Green Published, Bronze
DA 2022-04-25
ER

PT J
AU Yan, T
   Seo, Y
   Schupp, JE
   Zeng, XH
   Desai, AB
   Kinsella, TJ
AF Yan, T
   Seo, Y
   Schupp, JE
   Zeng, XH
   Desai, AB
   Kinsella, TJ
TI Methoxyamine potentiates iododeoxyuridine-induced radiosensitization by
   altering cell cycle kinetics and enhancing senescence
SO MOLECULAR CANCER THERAPEUTICS
LA English
DT Article
ID BASE EXCISION-REPAIR; STRAND-BREAK REPAIR; HALOGENATED PYRIMIDINE;
   DNA-DAMAGE; TUMOR SUPPRESSION; COLON-CANCER; RADIATION; PATHWAYS;
   SUBSTITUTION; ENHANCEMENT
AB We previously reported that methoxyamine (an inhibitor of base excision repair) potentiates iododeoxyuridine (IUdR)induced radiosensitization in human tumor cells. In this study, we investigated the potential mechanisms of this enhanced cell death. Human colorectal carcinoma RKO cells were exposed to IUdR (3 mu mol/L) and/or methoxyamine (3 mmol/L) for 48 hours before ionizing radiation (5 Gy). We found that IUdR/methoxyamine altered cell cycle kinetics and led to an increased G(1) population but a decreased S population before ionizing radiation. Immediately following ionizing radiation (up to 6 hours), IUdR/methoxyamine-pretreated cells showed a stringent Gi-S checkpoint but an insufficient G(2)-M checkpoint, whereas a prolonged G(1) arrest, containing 2CG1 and 4CG1 cells, was found at later time:; up to 72 hours. Levels of cell cycle-specific markers [p21, p27, cyclin A, cyclin B1, and pcdc2(Y15)] and DIVA damage signaling proteins [gamma H2AX, pChk1(S317), and pChk2(T68)] supported these altered cell cycle kinetics. Interestingly, we found that IUdR/methoxyamine pretreatment reduced ionizing radiation-induced apoptosis. Additionally, the extent of cell death through necrosis or autophagy seemed similar in all (IUDR +/- methoxyamine + ionizing radiation) treatment groups. However, a larger population of senescence-activated beta-galactosidase-positive cells was seen in IUdR/methoxyamine/ionizing radiation-treated cells, which was correlated with the increased activation of the senescence factors p53 and pRb. These data indicate that Ili methoxyamine pretreatment enhanced the effects of ionizing radiation by causing a prolonged G(1) cell cycle arrest and by promoting stress-induced premature senescence. Thus, senescence, a novel ionizing radiation induced tumor suppression pathway, may be effectively targeted by IUdR/methoxyamine pretreatment, resulting in an improved therapeutic gain for ionizing radiation.
C1 Univ Hosp Cleveland, Ireland Canc Ctr, Dept Radiat Oncol, Cleveland, OH 44106 USA.
   Case Western Reserve Univ, Sch Med, Cleveland, OH 44106 USA.
RP Kinsella, TJ (corresponding author), Univ Hosp Cleveland, Ireland Canc Ctr, Dept Radiat Oncol, LTR 6068,11100 Euclid Ave, Cleveland, OH 44106 USA.
EM timothy.kinsella@uhhs.com
FU NATIONAL CANCER INSTITUTEUnited States Department of Health & Human
   ServicesNational Institutes of Health (NIH) - USANIH National Cancer
   Institute (NCI) [R01CA050595] Funding Source: NIH RePORTER; NCI NIH
   HHSUnited States Department of Health & Human ServicesNational
   Institutes of Health (NIH) - USANIH National Cancer Institute (NCI)
   [CA112963, CA50595] Funding Source: Medline
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NR 33
TC 22
Z9 23
U1 0
U2 3
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 1535-7163
EI 1538-8514
J9 MOL CANCER THER
JI Mol. Cancer Ther.
PD APR
PY 2006
VL 5
IS 4
BP 893
EP 902
DI 10.1158/1535-7163.MCT-05-0364
PG 10
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA 041LU
UT WOS:000237458500012
PM 16648559
DA 2022-04-25
ER

PT J
AU Chaachouay, H
   Fehrenbacher, B
   Toulany, M
   Schaller, M
   Multhoff, G
   Rodemann, HP
AF Chaachouay, Hassan
   Fehrenbacher, Birgit
   Toulany, Mahrnoud
   Schaller, Martin
   Multhoff, Gabriele
   Rodemann, H. Peter
TI AMPK-independent autophagy promotes radioresistance of human tumor cells
   under clinical relevant hypoxia in vitro
SO RADIOTHERAPY AND ONCOLOGY
LA English
DT Article; Proceedings Paper
CT 14th International Wolfsberg Meeting on Molecular Radiation
   Biology/Oncology
CY JUL 20-22, 2015
CL Wolfsberg, AUSTRIA
SP ESTRO
DE Clinical relevant hypoxia; Autophagy; Ionizing radiation; Solid tumor
   cells
ID RADIATION; SURVIVAL; CONTRIBUTES; EXPRESSION; INDUCTION; RESISTANT;
   BNIP3; ULK1
AB Background and purpose: Blocking of the autophagy-signaling has the potential to improve cancer therapy. In the present study, the role of autophagy for radioresistance of human tumor cells was tested under clinically relevant hypoxia (1% O-2).
   Materials and methods: Non-small cell lung cancer cell lines A549 and H460, head and neck squamous cell carcinoma FaDu, colon carcinoma cell line HCT116 and mouse-embryo-fibroblasts were analyzed under normoxic (21% O-2) and hypoxic (0.01% and 1% O-2) conditions with respect to clonogenic cell survival and hypoxia-induced autophagy. Immunofluorescence and electron microscopy were used to monitor the autophagy process and Western blotting of LC3, AMPK, and BNIP3 was applied to analyze autophagy signaling.
   Results: Clinically relevant hypoxia stimulated autophagy in tumor cells as indicated by enhanced LC3-I to LC3-II conversion. Furthermore, hypoxia stimulated autophagy was approved by Immunofluorescence staining and electron-microscopy analysis of autophagosome vacuoles. Preconditioning of tumor cells to moderate-hypoxia increased their radioresistance that was significantly reversed following pretreatment with autophagy inhibitor, chloroquine. Using siRNA against AMPK as well as AMPK deficient cells, autophagy stimulation by 1% O-2 was shown to be AMPK-independent. However, a correlation between the expression of BNIP3 and autophagy-stimulation was observed under this condition.
   Conclusion: Under clinically relevant hypoxia (1% O-2) the stimulation of autophagy mediates resistance of hypoxic tumor cells to ionizing radiation, which is independent of AMPK signaling. (C) 2015 Elsevier Ireland Ltd. All rights reserved.
C1 [Chaachouay, Hassan; Toulany, Mahrnoud; Rodemann, H. Peter] Univ Tubingen, Div Radiobiol & Mol Environm Res, Dept Radiat Oncol, D-72076 Tubingen, Germany.
   [Fehrenbacher, Birgit; Schaller, Martin] Univ Tubingen, Dept Dermatol, D-72076 Tubingen, Germany.
   [Chaachouay, Hassan; Multhoff, Gabriele] Tech Univ Munich, Dept Radiat Oncol, D-80290 Munich, Germany.
   [Chaachouay, Hassan; Multhoff, Gabriele] HMGU CCG Innate Immun Tumor Biol, Munich, Germany.
   [Chaachouay, Hassan] Univ Zurich, Vetsuisse Fac, Sect Radiat Oncol, CH-8006 Zurich, Switzerland.
RP Rodemann, HP (corresponding author), Univ Tubingen, Div Radiobiol & Mol Environm Res, Dept Radiat Oncol, Rontgenweg 11, D-72076 Tubingen, Germany.
EM hans-peter.rodemann@uni-tuebingen.de
RI Multhoff, Gabriele/AAW-9796-2021
OI Multhoff, Gabriele/0000-0002-2616-3137; Chaachouay,
   Hassan/0000-0002-9100-2612
FU Deutsche ForschungsgemeinschaftGerman Research Foundation (DFG) [SFB-773
   TP-B2, Ro 572/7-1, SFB773 TP-Z2]; DFG-Graduate SchoolGerman Research
   Foundation (DFG) [SFB773];  [SFB824/II]
FX This work was supported by the Deutsche Forschungsgemeinschaft by grants
   awarded to HPR (SFB-773 TP-B2 and Ro 572/7-1) and to MS (SFB773 TP-Z2).
   HC received a fellowship of the SFB773 associated DFG-Graduate School
   and GM received funding from the SFB824/II. The support of Dr. Tassula
   Proikas-Cezanne (Institute of Cell Biology, University of Tubingen) and
   Benoit Viollet, PhD (Institut Cochin, INSERM U1016, CNRS UMR 8104,
   Universite Paris Descartes, France) who provided the AMPK proficient and
   deficient MEF is gratefully acknowledged.
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NR 35
TC 20
Z9 22
U1 0
U2 10
PU ELSEVIER IRELAND LTD
PI CLARE
PA ELSEVIER HOUSE, BROOKVALE PLAZA, EAST PARK SHANNON, CO, CLARE, 00000,
   IRELAND
SN 0167-8140
EI 1879-0887
J9 RADIOTHER ONCOL
JI Radiother. Oncol.
PD SEP
PY 2015
VL 116
IS 3
BP 409
EP 416
DI 10.1016/j.radonc.2015.08.012
PG 8
WC Oncology; Radiology, Nuclear Medicine & Medical Imaging
WE Science Citation Index Expanded (SCI-EXPANDED); Conference Proceedings Citation Index - Science (CPCI-S)
SC Oncology; Radiology, Nuclear Medicine & Medical Imaging
GA CU8UN
UT WOS:000363819700013
PM 26318663
DA 2022-04-25
ER

PT J
AU Li, Y
   Li, W
   Hoffman, AR
   Cui, JW
   Hu, JF
AF Li, Yan
   Li, Wei
   Hoffman, Andrew R.
   Cui, Jiuwei
   Hu, Ji-Fan
TI The Nucleus/Mitochondria-Shuttling LncRNAs Function as New Epigenetic
   Regulators of Mitophagy in Cancer
SO FRONTIERS IN CELL AND DEVELOPMENTAL BIOLOGY
LA English
DT Review
DE mitochondria; mitophagy; cancer metabolism; long non-coding RNA; cancer
   stem cells; cancer therapy
ID LONG NONCODING RNAS; HEPATOCELLULAR-CARCINOMA CELL; COLORECTAL-CANCER;
   MITOCHONDRIAL CLEARANCE; DAMAGED MITOCHONDRIA; GLUCOSE-METABOLISM;
   PARKIN ISOFORMS; HIGH EXPRESSION; BNIP3 PROTEIN; TARGET GENE
AB Mitophagy is a specialized autophagic pathway responsible for the selective removal of damaged or dysfunctional mitochondria by targeting them to the autophagosome in order to maintain mitochondria quality. The role of mitophagy in tumorigenesis has been conflicting, with the process both supporting tumor cell survival and promoting cell death. Cancer cells may utilize the mitophagy pathway to augment their metabolic requirements and resistance to cell death, thereby leading to increased cell proliferation and invasiveness. This review highlights major regulatory pathways of mitophagy involved in cancer. In particular, we summarize recent progress regarding how nuclear-encoded long non-coding RNAs (lncRNAs) function as novel epigenetic players in the mitochondria of cancer cells, affecting the malignant behavior of tumors by regulating mitophagy. Finally, we discuss the potential application of regulating mitophagy as a new target for cancer therapy.
C1 [Li, Yan; Li, Wei; Cui, Jiuwei; Hu, Ji-Fan] First Hosp Jilin Univ, Ctr Canc, Key Lab Organ Regenerat & Transplantat, Minist Educ, Changchun, Peoples R China.
   [Li, Yan; Hoffman, Andrew R.; Hu, Ji-Fan] Stanford Univ, VA Palo Alto Hlth Care Syst, Med Sch, Palo Alto, CA 94305 USA.
RP Cui, JW; Hu, JF (corresponding author), First Hosp Jilin Univ, Ctr Canc, Key Lab Organ Regenerat & Transplantat, Minist Educ, Changchun, Peoples R China.; Hu, JF (corresponding author), Stanford Univ, VA Palo Alto Hlth Care Syst, Med Sch, Palo Alto, CA 94305 USA.
EM cuijw@jlu.edu.cn; jifan@stanford.edu
OI Hoffman, Andrew/0000-0002-0145-1917
FU National Key R&D Program of China [2018YFA0106902]; National Natural
   Science Foundation of ChinaNational Natural Science Foundation of China
   (NSFC) [82050003, 81900701, 31430021, 81874052, 81672275, 31871297,
   81670143, 32000431]; Key Project of Chinese Ministry of
   EducationMinistry of Education, China [311015]; National Basic Research
   Program of China (973 Program)National Basic Research Program of China
   [2015CB943303]; Nation Key Research and Development Program of China
   grant [2016YFC13038000]; Research on Chronic Non-communicable Diseases
   Prevention and Control of National Ministry of Science and Technology
   [2016YFC1303804]; National Health Development Planning Commission Major
   Disease Prevention and Control of Science and Technology Plan of Action,
   Cancer Prevention and Control [ZX-07-C2016004]; Natural Science
   Foundation of Jilin Province [20200801046GH, 20150101176JC,
   20180101117JC, 20130413010GH]; Provincial Science Fund of Jilin Province
   Development and Reform Commission [2014N147, 2017C022]; 10th Youth Fund
   of First Hospital of Jilin University [JDYY 102019034]; California
   Institute of Regenerative Medicine (CIRM)California Institute for
   Regenerative Medicine [RT2-01942]; Biomedical Research Service of the
   Department of Veterans AffairsUS Department of Veterans Affairs
   [BX002905]
FX This work was supported by the National Key R&D Program of China
   (2018YFA0106902), the National Natural Science Foundation of China
   (82050003, 81900701, 31430021, 81874052, 81672275, 31871297, 81670143,
   81900701, and 32000431), the Key Project of Chinese Ministry of
   Education grant (311015), the National Basic Research Program of China
   (973 Program; 2015CB943303), the Nation Key Research and Development
   Program of China grant (2016YFC13038000), Research on Chronic
   Non-communicable Diseases Prevention and Control of National Ministry of
   Science and Technology (2016YFC1303804), the National Health Development
   Planning Commission Major Disease Prevention and Control of Science and
   Technology Plan of Action, Cancer Prevention and Control
   (ZX-07-C2016004), the Natural Science Foundation of Jilin Province
   (20200801046GH, 20150101176JC, 20180101117JC, and 20130413010GH), the
   Provincial Science Fund of Jilin Province Development and Reform
   Commission (2014N147 and 2017C022), the 10th Youth Fund of First
   Hospital of Jilin University (JDYY 102019034), California Institute of
   Regenerative Medicine (CIRM) grant (RT2-01942), and the Biomedical
   Research Service of the Department of Veterans Affairs (BX002905).
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NR 153
TC 1
Z9 1
U1 4
U2 5
PU FRONTIERS MEDIA SA
PI LAUSANNE
PA AVENUE DU TRIBUNAL FEDERAL 34, LAUSANNE, CH-1015, SWITZERLAND
SN 2296-634X
J9 FRONT CELL DEV BIOL
JI Front. Cell. Dev. Biol.
PD SEP 8
PY 2021
VL 9
AR 699621
DI 10.3389/fcell.2021.699621
PG 14
WC Cell Biology; Developmental Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Cell Biology; Developmental Biology
GA US7SG
UT WOS:000697626300001
PM 34568319
OA gold, Green Published
DA 2022-04-25
ER

PT J
AU Rovito, D
   Giordano, C
   Vizza, D
   Plastina, P
   Barone, I
   Casaburi, I
   Lanzino, M
   De Amicis, F
   Sisci, D
   Mauro, L
   Aquila, S
   Catalano, S
   Bonofiglio, D
   Ando, S
AF Rovito, Daniela
   Giordano, Cinzia
   Vizza, Donatella
   Plastina, Pierluigi
   Barone, Ines
   Casaburi, Ivan
   Lanzino, Marilena
   De Amicis, Francesca
   Sisci, Diego
   Mauro, Loredana
   Aquila, Saveria
   Catalano, Stefania
   Bonofiglio, Daniela
   Ando, Sebastiano
TI Omega-3 PUFA ethanolamides DHEA and EPEA induce autophagy through PPAR
   gamma activation in MCF-7 breast cancer cells
SO JOURNAL OF CELLULAR PHYSIOLOGY
LA English
DT Article
ID POLYUNSATURATED FATTY-ACIDS; EICOSAPENTAENOIC ACID; RECEPTOR-GAMMA;
   GENE-EXPRESSION; N-ACYLETHANOLAMINES; COLON-CANCER; OMEGA-3-FATTY-ACIDS;
   APOPTOSIS; BINDING; BCL-2
AB The omega-3 long chain polyunsaturated fatty acids, docosahexaenoic acid (DHA), and eicosapentaenoic acid (EPA), elicit anti-proliferative effects in cancer cell lines and in animal models. Dietary DHA and EPA can be converted to their ethanolamide derivatives, docosahexaenoyl ethanolamine (DHEA), and eicosapentaenoyl ethanolamine (EPEA), respectively; however, few studies are reported on their anti-cancer activities. Here, we demonstrated that DHEA and EPEA were able to reduce cell viability in MCF-7 breast cancer cells whereas they did not elicit any effects in MCF-10A non-tumorigenic breast epithelial cells. Since DHA and EPA are ligands of Peroxisome Proliferator-Activated Receptor gamma (PPAR), we sought to determine whether PPAR may also mediate DHEA and EPEA actions. In MCF-7 cells, both compounds enhanced PPAR expression, stimulated a PPAR response element-dependent transcription as confirmed by the increased expression of its target gene PTEN, resulting in the inhibition of AKT-mTOR pathways. Besides, DHEA and EPEA treatment induced phosphorylation of Bcl-2 promoting its dissociation from beclin-1 which resulted in autophagy induction. We also observed an increase of beclin-1 and microtubule-associated protein 1 light chain 3 expression along with an enhanced autophagosomes formation as revealed by mono-dansyl-cadaverine staining. Finally, we demonstrated the involvement of PPAR in DHEA- and EPEA-induced autophagy by using siRNA technology and a selective inhibitor. In summary, our data show that the two omega-3 ethanolamides exert anti-proliferative effects by inducing autophagy in breast cancer cells highlighting their potential use as breast cancer preventive and/or therapeutic agents. J. Cell. Physiol. 228: 13141322, 2013. (c) 2012 Wiley Periodicals, Inc.
C1 [Rovito, Daniela; Vizza, Donatella; Casaburi, Ivan; Lanzino, Marilena; De Amicis, Francesca; Sisci, Diego; Aquila, Saveria; Catalano, Stefania; Bonofiglio, Daniela] Univ Calabria, Dept Pharmacobiol, Arcavacata Di Rende, CS, Italy.
   [Giordano, Cinzia; Barone, Ines; Ando, Sebastiano] Univ Calabria, Ctr Sanit, Arcavacata Di Rende, CS, Italy.
   [Plastina, Pierluigi] Univ Calabria, Dept Pharmaceut Sci, Arcavacata Di Rende, CS, Italy.
   [Barone, Ines; Mauro, Loredana; Ando, Sebastiano] Univ Calabria, Arcavacata Di Rende, CS, Italy.
RP Ando, S (corresponding author), Univ Calabria, Dept Cell Biol, I-87036 Cosenza, Italy.
EM daniela.bonofiglio@tin.it; sebastiano.ando@unical.it
RI /AAD-9701-2019; Bonofiglio, Daniela/AAV-8371-2020
OI /0000-0001-6577-1541; Lanzino, Marilena/0000-0002-6362-5396; Rovito,
   Daniela/0000-0001-5390-5477; BONOFIGLIO, Daniela/0000-0002-4142-0496;
   GIORDANO, Cinzia/0000-0003-4969-0607; CATALANO,
   Stefania/0000-0002-6352-9628; AQUILA, Saveria/0000-0003-4738-6927; De
   Amicis, Francesca/0000-0001-7079-1037; BARONE, Ines/0000-0002-9769-1615
FU Associazione Italiana Ricerca sul Cancro (AIRC)Fondazione AIRC per la
   ricerca sul cancro [IG 11595]; Reintegration AIRC/Marie Curie
   International Fellowship; AIRC MFAGFondazione AIRC per la ricerca sul
   cancro [6180]; MURSTMinistry of Education, Universities and Research
   (MIUR); Lilli Funaro Foundation; FSE (Fondo Sociale Europeo); Calabria
   RegionRegione Calabria
FX Contract grant sponsor: Associazione Italiana Ricerca sul Cancro (AIRC)
   IG 11595.; Contract grant sponsor: Reintegration AIRC/Marie Curie
   International Fellowship.; Contract grant sponsor: AIRC MFAG 6180.;
   Contract grant sponsor: MURST and Ex 60%.; Contract grant sponsor: Lilli
   Funaro Foundation.; Contract grant sponsor: FSE (Fondo Sociale Europeo)
   and Calabria Region.
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NR 49
TC 89
Z9 92
U1 1
U2 103
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0021-9541
EI 1097-4652
J9 J CELL PHYSIOL
JI J. Cell. Physiol.
PD JUN
PY 2013
VL 228
IS 6
BP 1314
EP 1322
DI 10.1002/jcp.24288
PG 9
WC Cell Biology; Physiology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Cell Biology; Physiology
GA 096OL
UT WOS:000315414000021
PM 23168911
DA 2022-04-25
ER

PT J
AU Du, RN
   Zhao, PW
   Wu, SK
   Gao, YX
   Wu, RN
   Yang, ML
   Song, WY
   Gao, HN
AF Du, Rina
   Zhao, Pengwei
   Wu, Shikui
   Gao, Yaoxing
   Wu, Rina
   Yang, Minli
   Song, Wanying
   Gao, Haining
TI Sendeng-4 Suppressed Melanoma Growth by Induction of Autophagy and
   Apoptosis
SO EVIDENCE-BASED COMPLEMENTARY AND ALTERNATIVE MEDICINE
LA English
DT Article
ID BECLIN-1; LC3; CANCER
AB Sendeng-4 is a traditional Chinese medicine that has been successfully applied to anti-inflammatory diseases in clinical practice. Monomers within Sendeng-4 showed promising antitumor activity against lung cancer, colon cancer, and cutaneous cancer. However, potency of Sendeng-4 in melanoma has not been explored. This study aims to explore the potential application of Sendeng-4 in melanoma treatment. In the present study, we systemically investigate the possibility of Sendeng-4 for treatment of melanoma cancer in vitro by proliferation assay, colony formation, flow cell cytometry, RNA-seq, western blot, and fluorescence-based assay. Our data demonstrated that Sendeng-4 suppresses the proliferation and colony formation capacity of melanoma cells and induces cell cycle block at G2/M phase and eventually cell death. Mechanistically, transcriptome sequencing demonstrates that the PI3K-AKT pathway was significantly inactivated upon Sendeng-4 exposure, which was confirmed by western blot showing decreased phosphorylation of AKT. In addition, decreased BCL-2 expression and increased BAX expression were observed, suggesting programmed cell death via apoptosis. Moreover, LC3-II production as well as autophagosomes formation was observed as demonstrated by western blot and immunofluorescence, indicating elevated autophagy network by Sendeng-4 stimulation. Collectively, we concluded that Sendeng-4 might be used as an anticancer drug for melanoma.
C1 [Du, Rina] Inner Mongolian Int Mongolian Hosp, Wulanchabudong St, Hohhot 010090, Peoples R China.
   [Zhao, Pengwei; Song, Wanying; Gao, Haining] Inner Mongolia Med Univ, Sch Basic Med Sci, Lab Microbiol & Immunol, Xinhua St, Hohhot 010059, Peoples R China.
   [Wu, Shikui; Wu, Rina] Inner Mongolia Med Univ, Coll Pharm, Jinshan St, Hohhot 010010, Peoples R China.
   [Gao, Yaoxing] Inner Mongolia Med Univ, Affiliated Hosp, Tongdao St, Hohhot 010010, Peoples R China.
   [Yang, Minli] Inner Mongolia Baihanxumu Biotechnol Co LTD, Jinshan St, Hohhot 010010, Peoples R China.
RP Zhao, PW (corresponding author), Inner Mongolia Med Univ, Sch Basic Med Sci, Lab Microbiol & Immunol, Xinhua St, Hohhot 010059, Peoples R China.; Gao, YX (corresponding author), Inner Mongolia Med Univ, Affiliated Hosp, Tongdao St, Hohhot 010010, Peoples R China.
EM rina_du@163.com; pengwzhao@126.com; shikuiwu@yahoo.com;
   gaoyaoxing1506@163.com; wurinawu506@hotmail.com; 895758757@qq.com;
   swy7990@126.com; 1766768147@qq.com
OI zhao, pengwei/0000-0002-2526-5705
FU Inner Mongolia Major Science and Technology Projects
FX This work was supported by Inner Mongolia Major Science and Technology
   Projects (Study of Mongolian medicine Sendeng-4 and development of its
   related nanocosmeceutical products).
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NR 39
TC 0
Z9 0
U1 3
U2 3
PU HINDAWI LTD
PI LONDON
PA ADAM HOUSE, 3RD FLR, 1 FITZROY SQ, LONDON, W1T 5HF, ENGLAND
SN 1741-427X
EI 1741-4288
J9 EVID-BASED COMPL ALT
JI Evid.-based Complement Altern. Med.
PD AUG 24
PY 2021
VL 2021
AR 5519973
DI 10.1155/2021/5519973
PG 10
WC Integrative & Complementary Medicine
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Integrative & Complementary Medicine
GA UL9DZ
UT WOS:000692944700001
PM 34475961
OA Green Published, gold
DA 2022-04-25
ER

PT J
AU Wang, GY
   Zhang, T
   Sun, W
   Wang, HS
   Yin, F
   Wang, ZY
   Zuo, DQ
   Sun, MX
   Zhou, ZF
   Lin, BH
   Xu, J
   Hua, YQ
   Li, HQ
   Cai, ZD
AF Wang, Gangyang
   Zhang, Tao
   Sun, Wei
   Wang, Hongsheng
   Yin, Fei
   Wang, Zhuoying
   Zuo, Dongqing
   Sun, Mengxiong
   Zhou, Zifei
   Lin, Binhui
   Xu, Jing
   Hua, Yingqi
   Li, Haoqing
   Cai, Zhengdong
TI Arsenic sulfide induces apoptosis and autophagy through the activation
   of ROS/JNK and suppression of Akt/mTOR signaling pathways in
   osteosarcoma
SO FREE RADICAL BIOLOGY AND MEDICINE
LA English
DT Article
DE Arsenic sulfide; Apoptosis; Autophagy; Osteosarcoma; Call cycle
ID ACUTE PROMYELOCYTIC LEUKEMIA; ROS-MEDIATED MECHANISMS; IN-VITRO;
   CELL-CYCLE; CANCER-CELLS; MOLECULAR-MECHANISMS; MITOTIC ARREST;
   TETRA-SULFIDE; GROWTH; DEATH
AB Osteosarcoma is a common primary malignant bone tumor, the cure rate of which has stagnated over the past 25-30 years. Arsenic sulfide (As2S2), the main active ingredient of the traditional Chinese medicine realgar, has been proved to have antitumor efficacy in several tumor types including acute promyelocytic leukemia, gastric cancer and colon cancer. Here, we investigated the efficacy and mechanism of As2S2 in osteosarcoma both in vitro and in vivo. In this study, we demonstrated that As2S2 potently suppressed cell proliferation by inducing G2/M phase arrest in various osteosarcoma cell lines. Also, treatment with As2S2 induced apoptosis and autophagy in osteosarcoma cells. The apoptosis induction was related to PARP cleavage and activation of caspase-3, -8, -9. As2S2 was demonstrated to induce autophagy as evidenced by formation of autophagokme and accumulation of LC3H. Further studies showed that As2S2-induced apoptosis and autophagy could be significantly attenuated by ROS scavenger and JNK inhibitor. Moreover, we found that As2S2 inhibited Akt/mTOR signaling pathway, and suppressing Akt and mTOR kinases activity can increase As2S2-induced apoptosis and autophagy. Finally, As2S2 in vivo suppressed tumor growth with few side effects. In summary, our results revealed that As2S2 induced G2/M phase arrest, apoptosis, and autophagy via activing ROS/JNK and blocking Altt/mTOR signaling pathway in human osteosarcoma cells. Arsenic sulfide may be a potential clinical antitumor drugs targeting osteosarcoma.
C1 [Wang, Gangyang; Zhang, Tao; Sun, Wei; Wang, Hongsheng; Yin, Fei; Wang, Zhuoying; Zuo, Dongqing; Sun, Mengxiong; Zhou, Zifei; Lin, Binhui; Xu, Jing; Hua, Yingqi; Li, Haoqing; Cai, Zhengdong] Shanghai Jiao Tong Univ, Dept Orthopaed, Shanghai Bone Tumor Inst, Shanghai Gen Hosp,Sch Med, Shanghai, Peoples R China.
   [Wang, Hongsheng] Tongji Univ, Yangpu Hosp, Dept Orthopaed, Sch Med, Shanghai, Peoples R China.
   [Zuo, Dongqing] Tongji Univ, Shanghai Peoples Hosp 10, Dept Orthopaed, Sch Med, Shanghai, Peoples R China.
   [Zhou, Zifei] Tongji Univ, Shanghai East Hosp, Dept Orthopaed, Shanghai, Peoples R China.
   [Wang, Gangyang; Zhang, Tao; Sun, Wei; Wang, Hongsheng; Yin, Fei; Wang, Zhuoying; Zuo, Dongqing; Sun, Mengxiong; Zhou, Zifei; Lin, Binhui; Xu, Jing; Hua, Yingqi; Li, Haoqing; Cai, Zhengdong] Shanghai Jiao Tong Univ, Shanghai Gen Hosp, Sch Med, 100 Haining Rd Shanghai, Shanghai, Peoples R China.
RP Hua, YQ; Li, HQ; Cai, ZD (corresponding author), Shanghai Jiao Tong Univ, Dept Orthopaed, Shanghai Bone Tumor Inst, Shanghai Gen Hosp,Sch Med, Shanghai, Peoples R China.
EM gangyang_wang@163.com; zhangtaoabc@2008.sina.com; viv-sun@163.com;
   wanghs1231@gmail.com; yinfeicat@163.com; wyz135@163.com;
   zuozuo198@163.com; sunmensiong@126.com; zhouzf@yeah.net;
   nylbh7581@163.com; piao_hay@163.com; hua_yingqi@163.com;
   lihaoqing@medmail.com; czd856@vip.163.com
FU National Natural Science FoundationNational Natural Science Foundation
   of China (NSFC) [81502604]; Shanghai Science and Technology
   CommissionShanghai Science & Technology CommitteeScience & Technology
   Commission of Shanghai Municipality (STCSM) [14140904000]; School of
   Medicine, Shanghai Jiao Tong University [81450110092]; Shanghai Hospital
   Development Center [SHDC12013107]
FX This work was supported by the National Natural Science Foundation (No.
   81502604); Shanghai Science and Technology Commission (No. 14140904000);
   School of Medicine, Shanghai Jiao Tong University (No. 81450110092) and
   Research Grant from Shanghai Hospital Development Center (No.
   SHDC12013107).
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NR 61
TC 88
Z9 94
U1 8
U2 81
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA STE 800, 230 PARK AVE, NEW YORK, NY 10169 USA
SN 0891-5849
EI 1873-4596
J9 FREE RADICAL BIO MED
JI Free Radic. Biol. Med.
PD MAY
PY 2017
VL 106
BP 24
EP 37
DI 10.1016/j.freeradbiomed.2017.02.015
PG 14
WC Biochemistry & Molecular Biology; Endocrinology & Metabolism
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Endocrinology & Metabolism
GA EU0TN
UT WOS:000400724500003
PM 28188923
DA 2022-04-25
ER

PT J
AU McAllister, SD
   Soroceanu, L
   Desprez, PY
AF McAllister, Sean D.
   Soroceanu, Liliana
   Desprez, Pierre-Yves
TI The Antitumor Activity of Plant-Derived Non-Psychoactive Cannabinoids
SO JOURNAL OF NEUROIMMUNE PHARMACOLOGY
LA English
DT Review
DE Cannabinoid; Cannabidiol; Cancer; Reactive oxygen species
ID CANNABIDIOL-INDUCED APOPTOSIS; CANCER-CELL INVASION; ENDOCANNABINOID
   SYSTEM; POSSIBLE INVOLVEMENT; TUMOR-GROWTH; INHIBITION;
   DELTA-9-TETRAHYDROCANNABINOL; THERAPY; TETRAHYDROCANNABINOL; AUTOPHAGY
AB As a therapeutic agent, most people are familiar with the palliative effects of the primary psychoactive constituent of Cannabis sativa (CS), Delta(9)-tetrahydrocannabinol (THC), a molecule active at both the cannabinoid 1 (CB1) and cannabinoid 2 (CB2) receptor subtypes. Through the activation primarily of CB1 receptors in the central nervous system, THC can reduce nausea, emesis and pain in cancer patients undergoing chemotherapy. During the last decade, however, several studies have now shown that CB1 and CB2 receptor agonists can act as direct antitumor agents in a variety of aggressive cancers. In addition to THC, there are many other cannabinoids found in CS, and a majority produces little to no psychoactivity due to the inability to activate cannabinoid receptors. For example, the second most abundant cannabinoid in CS is the non-psychoactive cannabidiol (CBD). Using animal models, CBD has been shown to inhibit the progression of many types of cancer including glioblastoma (GBM), breast, lung, prostate and colon cancer. This review will center on mechanisms by which CBD, and other plant-derived cannabinoids inefficient at activating cannabinoid receptors, inhibit tumor cell viability, invasion, metastasis, angiogenesis, and the stem-like potential of cancer cells. We will also discuss the ability of non-psychoactive cannabinoids to induce autophagy and apoptotic-mediated cancer cell death, and enhance the activity of first-line agents commonly used in cancer treatment.
C1 [McAllister, Sean D.; Soroceanu, Liliana; Desprez, Pierre-Yves] Calif Pacific Med Ctr, Res Inst, San Francisco, CA 94107 USA.
RP McAllister, SD (corresponding author), Calif Pacific Med Ctr, Res Inst, 475 Brannan St,Suite 220, San Francisco, CA 94107 USA.
EM mcallis@cpmcri.org
FU NATIONAL CANCER INSTITUTEUnited States Department of Health & Human
   ServicesNational Institutes of Health (NIH) - USANIH National Cancer
   Institute (NCI) [R01CA135281] Funding Source: NIH RePORTER; NCI NIH
   HHSUnited States Department of Health & Human ServicesNational
   Institutes of Health (NIH) - USANIH National Cancer Institute (NCI) [R01
   CA135281] Funding Source: Medline
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NR 101
TC 53
Z9 56
U1 0
U2 88
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 1557-1890
EI 1557-1904
J9 J NEUROIMMUNE PHARM
JI J. Neuroimmune Pharm.
PD JUN
PY 2015
VL 10
IS 2
BP 255
EP 267
DI 10.1007/s11481-015-9608-y
PG 13
WC Neurosciences; Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Neurosciences & Neurology; Pharmacology & Pharmacy
GA CK5WF
UT WOS:000356296100007
PM 25916739
OA Green Accepted
DA 2022-04-25
ER

PT J
AU Zhang, W
   Li, QY
   Song, C
   Lao, LF
AF Zhang, Wei
   Li, Qianyi
   Song, Chao
   Lao, Lifeng
TI Knockdown of autophagy-related protein 6, Beclin-1, decreases cell
   growth, invasion, and metastasis and has a positive effect on
   chemotherapy-induced cytotoxicity in osteosarcoma cells
SO TUMOR BIOLOGY
LA English
DT Article
DE Autophagy; Beclin-1; Proliferation; Invasion; Chemoresistance
ID CANCER-THERAPY; APOPTOSIS; DEATH; INHIBITION; ACTIVATION;
   MATRIX-METALLOPROTEINASE-9; CHEMOSENSITIVITY; RESISTANCE; INDUCTION;
   MIGRATION
AB Beclin-1, a well-known key regulator of autophagy, has been implicated in many disorders, including cancer, aging, and degenerative diseases. Previous studies demonstrated that Beclin-1 participated in tumorgenesis and was highly expressed in colorectal cancer cells, primary duodenal adenocarcinoma, and hepatocellular carcinoma cells, and overexpression of Beclin-1 could induce autophagic cell death in leukemia cells. However, the exact effects and molecular mechanisms of Beclin-1-mediated autophagy in osteosarcoma are still unknown up to now. Here, we evaluated the role of Beclin-1 in human osteosarcoma cell lines in vivo and in vitro. In order to characterize the endogenous expression of Beclin-1 in osteosarcoma cell lines, we performed real-time PCR and Western blot analysis. We further analyzed the level of Beclin-1 in osteosarcoma cells after chemotherapy and investigated the impact of autophagy inhibition on chemotherapy-induced cytotoxicity. We used the small interfering RNA (siRNA) directed against Beclin-1 to infect the osteosarcoma cell line with relatively high Belcin-1 expression. Furthermore, we determine the functional relevance of Beclin-1 knockdown to osteosarcoma cell growth, migration, and invasion, and investigate the expression levels of matrix metallopeptidase-2 (MMP-2), MMP-9, phosphoinositide 3-kinase p85 alpha (PI3Kp85 alpha), and phosphorylated AKT (p-AKT). As a result, HOS osteosarcoma cells exhibited higher Beclin-1 expression. Anticancer agents including doxorubicin, cisplatin, and methotrexate each induced Beclin-1 up-regulation in human osteosarcoma cells, and siRNA-mediated knockdown of Beclin-1 suppressed cell proliferation, migration, and invasion indicated by 3-(4,5-dimethylthiazolyl-2)-2,5-diphenylthetrazolium bromide, would healing, and transwell assays. Cell apoptosis induced by anticancer agents was markedly increased. Knockdown of Beclin-1 or inhibition of autophagy by 3-methyladenine (an inhibitor of autophagy and PI3K) rendered them significantly more sensitive to chemotherapy. Addition of the pan-caspase inhibitor ZVAD-FMK partly reversed the cisplatin-induced cell death. When Beclin-1 expression was inhibited, the expression of PI3Kp85 alpha, p-AKT, and MMP-9 was downregulated in HOS cells. In addition, the tumor volumes in subcutaneous nude mouse models in Beclin-1-deleted HOS cells were significantly smaller than those of control group. These results suggested that knockdown of Beclin-1 by siRNA exerts inhibitory effects on growth and migration of osteosarcoma cells possibly via blockade of the PI3K/AKT signaling. Beclin-1 knockdown rendered them significantly more sensitive to chemotherapy through activating apoptosis pathway. The results of this study suggest that Beclin-1 plays an important role in proliferation and tumor progression in osteosarcoma and inhibition autophagy can increase the efficacy of anticancer agent therapy.
C1 [Zhang, Wei; Li, Qianyi; Song, Chao; Lao, Lifeng] Shanghai Jiao Tong Univ, Dept Orthopaed Surg, Renji Hosp, Sch Med, Shanghai 200127, Peoples R China.
RP Lao, LF (corresponding author), Shanghai Jiao Tong Univ, Dept Orthopaed Surg, Renji Hosp, Sch Med, Shanghai 200127, Peoples R China.
EM WZhangDoctor@163.com; QLi667@126.com; CSongspine@163.com;
   laolifeng@gmail.com
FU National Natural Science Foundation of Youth Program [81101394];
   Shanghai Special Fund for Outstanding Young Teachers in Universities
   [JDY10080]; Shanghai Renji Hospital Fund for Outstanding Youth
   [RJPY10-010]; Shanghai Fund for Young Physician Development [20141051]
FX This work was supported by the grants from the National Natural Science
   Foundation of Youth Program (No. 81101394), Shanghai Special Fund for
   Outstanding Young Teachers in Universities (No. JDY10080), Shanghai
   Renji Hospital Fund for Outstanding Youth (No. RJPY10-010), and Shanghai
   Fund for Young Physician Development (No. 20141051).
CR Bao LJ, 2014, INT J CLIN EXP PATHO, V7, P1502
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NR 31
TC 25
Z9 29
U1 2
U2 12
PU SAGE PUBLICATIONS LTD
PI LONDON
PA 1 OLIVERS YARD, 55 CITY ROAD, LONDON EC1Y 1SP, ENGLAND
SN 1010-4283
EI 1423-0380
J9 TUMOR BIOL
JI Tumor Biol.
PD APR
PY 2015
VL 36
IS 4
BP 2531
EP 2539
DI 10.1007/s13277-014-2868-y
PG 9
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA CF9LJ
UT WOS:000352885900038
PM 25427639
DA 2022-04-25
ER

PT J
AU Papademetrio, DL
   Lompardia, SL
   Simunovich, T
   Costantino, S
   Mihalez, CY
   Cavaliere, V
   Alvarez, E
AF Laura Papademetrio, Daniela
   Laura Lompardia, Silvina
   Simunovich, Tania
   Costantino, Susana
   Yamila Mihalez, Cintia
   Cavaliere, Victoria
   Alvarez, Elida
TI Inhibition of Survival Pathways MAPK and NF-kB Triggers Apoptosis in
   Pancreatic Ductal Adenocarcinoma Cells via Suppression of Autophagy
SO TARGETED ONCOLOGY
LA English
DT Article
ID FACTOR-KAPPA-B; GENE-EXPRESSION; SIGNALING PATHWAYS; CANCER-TREATMENT;
   LUNG-CANCER; ACTIVATION; INDUCTION; PROTEINS; COLON; RAS/RAF/MEK/ERK
AB Background Pancreatic ductal adenocarcinoma (PDAC) is an aggressive disease with a survival rate of 4-6 months from diagnosis. PDAC is the fourth leading cause of cancer-related death in the Western world, with a mortality rate of 10 cases per 100,000 population. Chemotherapy constitutes only a palliative strategy, with limited effects on life expectancy.
   Aims To investigate the biological response of PDAC to mitogen-activated protein kinase (MAPK) and NF-kappaB (NF-kB) inhibitors and the role of autophagy in the modulation of these signaling pathways in order to address the challenge of developing improved medical protocols for patients with PDAC.
   Methods Two ATCC cell lines, MIAPaCa-2 and PANC-1, were used as PDAC models. Cells were exposed to inhibitors of MAPK or NF-kB survival pathways alone or after autophagy inhibition. Several aspects were analyzed, as follows: cell proliferation, by [H-3] TdR incorporation; cell death, by TUNEL assay, regulation of autophagy by LC3-II expression level and modulation of pro-and anti-apoptotic proteins by Western blot.
   Results We demonstrated that the inhibition of the MAPK and NF-kB survival pathways with U0126 and caffeic acid phenethyl ester (CAPE), respectively, produced strong inhibition of pancreatic tumor cell growth without inducing apoptotic death. Interestingly, U0126 and CAPE induced apoptosis after autophagy inhibition in a caspase-dependent manner in MIA PaCa-2 cells and in a caspase-independent manner in PANC-1 cells.
   Conclusions Here we present evidence that allows us to consider a combined therapy regimen comprising an autophagy inhibitor and a MAPK or NF-kB pathway inhibitor as a possible treatment strategy for pancreatic cancer.
C1 [Laura Papademetrio, Daniela; Laura Lompardia, Silvina; Simunovich, Tania; Costantino, Susana; Yamila Mihalez, Cintia; Cavaliere, Victoria; Alvarez, Elida] Univ Buenos Aires, Fac Farm & Bioquim, Catedra Inmunol, Junin 956,4 Piso, RA-1113 Buenos Aires, Buenos Aires, Argentina.
   [Laura Papademetrio, Daniela; Laura Lompardia, Silvina; Costantino, Susana; Yamila Mihalez, Cintia; Alvarez, Elida] Consejo Nacl Invest Cient & Tecn, IDEHU, RA-1033 Buenos Aires, Buenos Aires, Argentina.
RP Papademetrio, DL; Alvarez, E (corresponding author), Univ Buenos Aires, Fac Farm & Bioquim, Catedra Inmunol, Junin 956,4 Piso, RA-1113 Buenos Aires, Buenos Aires, Argentina.; Papademetrio, DL; Alvarez, E (corresponding author), Consejo Nacl Invest Cient & Tecn, IDEHU, RA-1033 Buenos Aires, Buenos Aires, Argentina.
EM dpapademetrio@ffyb.uba.ar; elialv@ffyb.uba.ar
RI Lompardía, Silvina/AAF-7230-2021
OI Lompardia, Silvina/0000-0002-8499-5417; Papademetrio,
   Daniela/0000-0002-3419-5614
FU Universidad de Buenos AiresUniversity of Buenos Aires; Consejo Nacional
   de Investigaciones Cientificas y Tecnicas (CONICET)Consejo Nacional de
   Investigaciones Cientificas y Tecnicas (CONICET)
FX This study was funded by Universidad de Buenos Aires and Consejo
   Nacional de Investigaciones Cientificas y Tecnicas (CONICET).
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NR 65
TC 42
Z9 44
U1 1
U2 36
PU SPRINGER
PI DORDRECHT
PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS
SN 1776-2596
EI 1776-260X
J9 TARGET ONCOL
JI Target. Oncol.
PD APR
PY 2016
VL 11
IS 2
BP 183
EP 195
DI 10.1007/s11523-015-0388-3
PG 13
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA DI7QA
UT WOS:000373695200007
PM 26373299
DA 2022-04-25
ER

PT J
AU Dumas, JF
   Brisson, L
   Chevalier, S
   Maheo, K
   Fromont, G
   Moussata, D
   Besson, P
   Roger, S
AF Dumas, Jean-Francois
   Brisson, Lucie
   Chevalier, Stephan
   Maheo, Karine
   Fromont, Gaelle
   Moussata, Driffa
   Besson, Pierre
   Roger, Sebastien
TI Metabolic reprogramming in cancer cells, consequences on pH and tumour
   progression: Integrated therapeutic perspectives with dietary lipids as
   adjuvant to anticancer treatment
SO SEMINARS IN CANCER BIOLOGY
LA English
DT Review
DE Cancer cell metabolism; pH; Cancer cell invasiveness; Resistance to
   treatments; N-3 polyunsaturated fatty acids
ID POLYUNSATURATED FATTY-ACIDS; GATED SODIUM-CHANNELS;
   EPITHELIAL-MESENCHYMAL TRANSITION; NA+/H+ EXCHANGER NHE1; TRANSCRIPTION
   FACTOR SNAIL; BREAST-CANCER; COLON-CANCER; DOCOSAHEXAENOIC ACID;
   OXIDATIVE STRESS; EXTRACELLULAR PH
AB While tumours arise from acquired mutations in oncogenes or tumour-suppressor genes, it is clearly established that cancers are metabolic diseases characterized by metabolic alterations in tumour cells, and also non-tumour cells of the host organism resulting in tumour cachexia and patient weakness. In this review, we aimed at delineating details by which metabolic alterations in cancer cells, characterized by mitochondrial bioenergetics deregulations and the preference for aerobic glycolysis, are critical parameters controlling the aggressive progression of tumours. In particular, metabolic alteration in cancer cells are coupled to the modulation of intracellular and extracellular pH, epithelial-to-mesenchymal transition and associated increased invasiveness, autophagy, and the development of anticancer treatment resistance. Finally, based on mechanistic, pre-clinical and clinical studies, we proposed the adjuvant supplementation of dietary n-3 polyunsaturated fatty acids for a complementary holistic treatment of the cancer disease. (C) 2017 Elsevier Ltd. All rights reserved.
C1 [Dumas, Jean-Francois; Brisson, Lucie; Chevalier, Stephan; Maheo, Karine; Fromont, Gaelle; Moussata, Driffa; Besson, Pierre; Roger, Sebastien] Univ Francois Rabelais Tours, INSERM, Nutr Croissance & Canc UMR1069, 10 Blvd Tonnelle, F-37032 Tours, France.
   [Dumas, Jean-Francois; Chevalier, Stephan; Maheo, Karine; Besson, Pierre] Univ Francois Rabelais Tours, UFR Sci Pharmaceut, Ave Monge, F-37200 Tours, France.
   [Fromont, Gaelle] CHU Tours, Serv Anat & Cytol Pathol, F-37044 Tours 9, France.
   [Moussata, Driffa] CHU Tours, Serv Hepatogastroenterol & Cancerol Digest, F-37044 Tours 9, France.
   [Roger, Sebastien] Univ Francois Rabelais Tours, UFR Sci & Tech, Dept Physiol Anim, Ave Monge, F-37200 Tours, France.
   [Roger, Sebastien] Inst Univ France, 1 Rue Descartes, F-75231 Paris, France.
RP Roger, S (corresponding author), Univ Francois Rabelais Tours, INSERM, UMR 1069, 10 Blvd Tonnelle, F-37032 Tours, France.
EM sebastien.roger@univ-tours.fr
RI Maheo, Karine/AAC-3259-2022; fromont, gaelle/N-8708-2016; Dumas,
   Jean-François/AAN-5035-2020; Brisson, Lucie/R-1179-2016; Dumas,
   Jean-François/S-7486-2017
OI Dumas, Jean-François/0000-0002-2293-6606; Brisson,
   Lucie/0000-0001-7811-1382; Dumas, Jean-François/0000-0002-2293-6606;
   Roger, Sebastien/0000-0002-9852-5248
FU Ministere de la Recherche et des Technologies; InsermInstitut National
   de la Sante et de la Recherche Medicale (Inserm)European Commission;
   Ligue Nationale Contre le Cancer - Interregion Grand-Ouest; Region
   Centre-Val de LoireRegion Centre-Val de Loire; Centre
   Hospitalo-Universitaire of Tours; Association CANCEN; Studium;
   Canceropole Grand-Ouest; Institut Universitaire de France (IUF)
FX We thank all our colleagues from the Inserm UMR1069 for all constructive
   discussion and Catherine Le Roy for secretary and administrative
   assistance. The work performed at the Inserm UMR1069 was supported by
   the "Ministere de la Recherche et des Technologies", the Inserm, the
   "Ligue Nationale Contre le Cancer - Interregion Grand-Ouest", the Region
   Centre-Val de Loire (grant "NaVMetarget", project "ARD2020
   Biomedicaments), the Centre Hospitalo-Universitaire of Tours, the
   "Association CANCEN", the "Studium" and the "Canceropole Grand-Ouest".
   SR is supported by the Institut Universitaire de France (IUF).
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NR 314
TC 23
Z9 23
U1 0
U2 22
PU ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD
PI LONDON
PA 24-28 OVAL RD, LONDON NW1 7DX, ENGLAND
SN 1044-579X
EI 1096-3650
J9 SEMIN CANCER BIOL
JI Semin. Cancer Biol.
PD APR
PY 2017
VL 43
BP 90
EP 110
DI 10.1016/j.semcancer.2017.03.004
PG 21
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA EU8UZ
UT WOS:000401315300010
PM 28323020
OA Green Submitted
DA 2022-04-25
ER

PT J
AU Gil, J
   Ramsey, D
   Szmida, E
   Leszczynski, P
   Pawlowski, P
   Bebenek, M
   Sasiadek, MM
AF Gil, Justyna
   Ramsey, David
   Szmida, Elzbieta
   Leszczynski, Przemyslaw
   Pawlowski, Pawel
   Bebenek, Marek
   Sasiadek, Maria M.
TI The BAX gene as a candidate for negative autophagy-related genes
   regulator on mRNA levels in colorectal cancer
SO MEDICAL ONCOLOGY
LA English
DT Article
DE Autophagy; Apoptosis; Colorectal cancer; Relative expression
ID DOWN-REGULATION; EXPRESSION; PROTEIN; TUMOR; APOPTOSIS; BECLIN-1;
   MECHANISMS; METASTASIS; PCR
AB Autophagy is a catabolic process, which is involved in the maintenance of intracellular homeostasis by degrading redundant molecules and organelles. Autophagy begins with the formation of a double-membrane phago-phore, followed by its enclosure, thus leading to the appearance of an autophagosome which fuses with lysosome. This process is highly conserved, precisely orchestrated and regulated by autophagy-related genes. Recently, autophagy has been widely studied in different types of cancers, including colorectal cancer. As it has been revealed, autophagy plays two opposite roles in tumorigenesis, as a tumor suppressor and a tumor enhancer/activator, and therefore is called a double-edge sword. Recently, interaction between autophagy and apoptosis has been found. Therefore, we aimed to study the mRNA levels of genes engaged in autophagy and apoptosis in colorectal cancer tissues. Colorectal cancer and adjacent healthy tissues were obtained from 73 patients diagnosed with primary colorectal cancer. Real-time PCR analysis employing Universal Probe Library was used to assess the expression of the seven following selected genes: BECN1, UVRAG, ULK1, ATG13, Bif-1, BCL2 and BAX. For all but one of the tested genes, a decrease in expression was observed. An increase in expression was observed for BAX. BAX expression decreases consistently from early to more advanced stages. High expression of BAX was strongly associated with negative UVRAG expression. The high expression of the BAX gene seems to be a negative regulator of autophagy in colorectal cancer cells. The relative downregulation of autophagy-related genes was observed in colorectal cancer samples.
C1 [Gil, Justyna; Szmida, Elzbieta; Pawlowski, Pawel; Sasiadek, Maria M.] Wroclaw Med Univ, Dept Genet, PL-50368 Wroclaw, Poland.
   [Ramsey, David] Wroclaw Univ Technol, Dept Operat Res, PL-50372 Wroclaw, Poland.
   [Leszczynski, Przemyslaw] Wroclaw Med Univ, Dept Biol & Med Parasitol, PL-50345 Wroclaw, Poland.
   [Bebenek, Marek] Lower Silesian Oncol Ctr, Dept Surg Oncol 1, PL-53413 Wroclaw, Poland.
RP Gil, J (corresponding author), Wroclaw Med Univ, Dept Genet, PL-50368 Wroclaw, Poland.
EM justyna.gil@umed.wroc.pl
RI /L-5618-2019
OI /0000-0003-0991-7686; Bebenek, Marek/0000-0001-7716-5960; Szmida,
   Elzbieta/0000-0003-3108-0165; Sasiadek, Maria/0000-0002-7599-7074;
   Leszczynski, Przemyslaw/0000-0002-4181-4997
FU National Science Centre (Poland) [DEC-2012/07/D/NZ5/04305]
FX This work was financed from the funds of the National Science Centre
   (Poland) decision number DEC-2012/07/D/NZ5/04305.
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NR 38
TC 18
Z9 19
U1 0
U2 0
PU HUMANA PRESS INC
PI TOTOWA
PA 999 RIVERVIEW DRIVE SUITE 208, TOTOWA, NJ 07512 USA
SN 1357-0560
EI 1559-131X
J9 MED ONCOL
JI Med. Oncol.
PD FEB
PY 2017
VL 34
IS 2
AR 16
DI 10.1007/s12032-016-0869-y
PG 7
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA EK1MF
UT WOS:000393689000002
PM 28035578
OA hybrid, Green Published
DA 2022-04-25
ER

PT J
AU Malarz, K
   Mularski, J
   Kuczak, M
   Mrozek-Wilczkiewicz, A
   Musiol, R
AF Malarz, Katarzyna
   Mularski, Jacek
   Kuczak, Michal
   Mrozek-Wilczkiewicz, Anna
   Musiol, Robert
TI Novel Benzenesulfonate Scaffolds with a High Anticancer Activity and
   G2/M Cell Cycle Arrest
SO CANCERS
LA English
DT Article
DE styrylquinazoline; sulfonic derivatives; anticancer activity; cell cycle
   inhibition; G2; M phase; apoptosis; autophagy
AB Simple Summary
   Sulfonate derivatives have limited application in pharmacology. Only few examples of small-molecule alkylating agents used as DNA poisons are known. This is the first report presenting strong anticancer activity of aromatic sulfonates based on quinazolines. The screening revealed that compounds expressed good submicromolar activity exceeding imatinib against a panel of cancer cell lines, including leukemia, colon, pancreatic cancers and glioblastoma, and minimal effect on proliferation of non-cancer cells. This activity corresponds with strong cell cycle arrest and mitotic inhibition similar or higher than that of paclitaxel. Further investigation revealed a more multitargeted mechanism of action. This structure may be an effective, novel scaffold for drug design.
   Sulfonates, unlike their derivatives, sulphonamides, have rarely been investigated for their anticancer activity. Unlike the well-known sulphonamides, esters are mainly used as convenient intermediates in a synthesis. Here, we present the first in-depth investigation of quinazoline sulfonates. A small series of derivatives were synthesized and tested for their anticancer activity. Based on their structural similarity, these compounds resemble tyrosine kinase inhibitors and the p53 reactivator CP-31398. Their biological activity profile, however, was more related to sulphonamides because there was a strong cell cycle arrest in the G2/M phase. Further investigation revealed a multitargeted mechanism of the action that corresponded to the p53 protein status in the cell. Although the compounds expressed a high submicromolar activity against leukemia and colon cancers, pancreatic cancer and glioblastoma were also susceptible. Apoptosis and autophagy were confirmed as the cell death modes that corresponded with the inhibition of metabolic activity and the activation of the p53-dependent and p53-independent pathways. Namely, there was a strong activation of the p62 protein and GADD44. Other proteins such as cdc2 were also expressed at a higher level. Moreover, the classical caspase-dependent pathway in leukemia was observed at a lower concentration, which again confirmed a multitargeted mechanism. It can therefore be concluded that the sulfonates of quinazolines can be regarded as promising scaffolds for developing anticancer agents.
C1 [Malarz, Katarzyna; Kuczak, Michal; Mrozek-Wilczkiewicz, Anna] Univ Silesia Katowice, A Chelkowski Inst Phys, 75 Pulku Piechoty 1a, PL-41500 Chorzow, Poland.
   [Malarz, Katarzyna; Kuczak, Michal; Mrozek-Wilczkiewicz, Anna] Univ Silesia Katowice, Silesian Ctr Educ & Interdisciplinary Res, 75 Pulku Piechoty 1a, PL-41500 Chorzow, Poland.
   [Mularski, Jacek; Kuczak, Michal; Musiol, Robert] Univ Silesia Katowice, Inst Chem, 75 Pulku Piechoty 1a, PL-41500 Chorzow, Poland.
RP Malarz, K (corresponding author), Univ Silesia Katowice, A Chelkowski Inst Phys, 75 Pulku Piechoty 1a, PL-41500 Chorzow, Poland.; Malarz, K (corresponding author), Univ Silesia Katowice, Silesian Ctr Educ & Interdisciplinary Res, 75 Pulku Piechoty 1a, PL-41500 Chorzow, Poland.; Musiol, R (corresponding author), Univ Silesia Katowice, Inst Chem, 75 Pulku Piechoty 1a, PL-41500 Chorzow, Poland.
EM katarzyna.malarz@us.edu.pl; jacek.mularski@us.edu.pl; mkuczak@us.edu.pl;
   anna.mrozek-wilczkiewicz@us.edu.pl; robert.musiol@us.edu.pl
OI K, Michal/0000-0002-7577-3011; Mularski, Jacek/0000-0002-1502-0421;
   Musiol, Robert/0000-0002-6219-7369; Malarz,
   Katarzyna/0000-0003-4283-3126
FU National Science CentreNational Science Centre, Poland
   [2019/35/B/NZ5/04208]
FX This work was financed by the National Science Centre grant
   2019/35/B/NZ5/04208 (K.M.).
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NR 80
TC 3
Z9 3
U1 2
U2 6
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 2072-6694
J9 CANCERS
JI Cancers
PD APR
PY 2021
VL 13
IS 8
AR 1790
DI 10.3390/cancers13081790
PG 24
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA RS8GA
UT WOS:000644010200001
PM 33918637
OA Green Published, gold
DA 2022-04-25
ER

PT J
AU Olsen, I
   Yilmaz, O
AF Olsen, Ingar
   Yilmaz, Ozlem
TI Possible role of Porphyromonas gingivalis in orodigestive cancers
SO JOURNAL OF ORAL MICROBIOLOGY
LA English
DT Review
DE Porphyromonas gingivalis; orodigestive cancers; oral cavity; esophagus;
   colon; pancreas; precancerous lesions; experimental models; direct
   relationship
ID SQUAMOUS-CELL CARCINOMA; PEPTIDYLARGININE DEIMINASE TYPE-4;
   NUCLEOSIDE-DIPHOSPHATE-KINASE; ORAL-CANCER; PERIODONTAL-DISEASE;
   EPITHELIAL-CELLS; POLYMICROBIAL SYNERGY; GENE-EXPRESSION; NECK-CANCER;
   RISK
AB There is increasing evidence for an association between periodontitis/tooth loss and oral, gastrointestinal, and pancreatic cancers. Periodontal disease, which is characterized by chronic inflammation and microbial dysbiosis, is a significant risk factor for orodigestive carcinogenesis. Porphyromonas gingivalis is proposed as a keystone pathogen in chronic periodontitis causing both dysbiosis and discordant immune response. The present review focuses on the growing recognition of a relationship between P. gingivalis and orodigestive cancers. Porphyromonas gingivalis has been recovered in abundance from oral squamous cell carcinoma (OSCC). Recently established tumorigenesis models have indicated a direct relationship between P. gingivalis and carcinogenesis. The bacterium upregulates specific receptors on OSCC cells and keratinocytes, induces epithelial-to-mesenchymal (EMT) transition of normal oral epithelial cells and activates metalloproteinase-9 and interleukin-8 in cultures of the carcinoma cells. In addition, P. gingivalis accelerates cell cycling and suppresses apoptosis in cultures of primary oral epithelial cells. In oral cancer cells, the cell cycle is arrested and there is no effect on apoptosis, but macro autophagy is increased. Porphyromonas gingivalis promotes distant metastasis and chemoresistance to anti-cancer agents and accelerates proliferation of oral tumor cells by affecting gene expression of defensins, by peptidyl-arginine deiminase and noncanonical activation of beta-catenin. The pathogen also converts ethanol to the carcinogenic intermediate acetaldehyde. In addition, P. gingivalis can be implicated in precancerous gastric and colon lesions, esophageal squamous cell carcinoma, head and neck (larynx, throat, lip, mouth and salivary glands) carcinoma, and pancreatic cancer. The fact that distant organs can be involved clearly emphasizes that P. gingivalis has systemic tumorigenic effects in addition to the local effects in its native territory, the oral cavity. Although coinfection with other bacteria, viruses, and fungi occurs in periodontitis, P. gingivalis relates to cancer even in absence of periodontitis. Thus, there may be a direct relationship between P. gingivalis and orodigestive cancers.
C1 [Olsen, Ingar] Univ Oslo, Fac Dent, Dept Oral Biol, POB 1052 Blindern, N-0316 Oslo, Norway.
   [Yilmaz, Ozlem] Med Univ South Carolina, Dept Oral Hlth Sci, Charleston, SC 29425 USA.
RP Olsen, I (corresponding author), Univ Oslo, Fac Dent, Dept Oral Biol, POB 1052 Blindern, N-0316 Oslo, Norway.
EM ingaro@odont.uio.no
RI Yilmaz, Ozlem/ABG-5367-2021
OI Yilmaz, Ozlem/0000-0003-3487-7217
FU NIDCRUnited States Department of Health & Human ServicesNational
   Institutes of Health (NIH) - USANIH National Institute of Dental &
   Craniofacial Research (NIDCR) [R01DE016593]; NATIONAL INSTITUTE OF
   DENTAL & CRANIOFACIAL RESEARCHUnited States Department of Health & Human
   ServicesNational Institutes of Health (NIH) - USANIH National Institute
   of Dental & Craniofacial Research (NIDCR) [R01DE016593] Funding Source:
   NIH RePORTER
FX This work was supported by the NIDCR [grant number R01DE016593 to OY].
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NR 112
TC 49
Z9 52
U1 7
U2 30
PU TAYLOR & FRANCIS LTD
PI ABINGDON
PA 2-4 PARK SQUARE, MILTON PARK, ABINGDON OR14 4RN, OXON, ENGLAND
SN 2000-2297
J9 J ORAL MICROBIOL
JI J. Oral Microbiology
PD JAN 1
PY 2019
VL 11
IS 1
DI 10.1080/20002297.2018.1563410
PG 12
WC Microbiology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Microbiology
GA HH1OL
UT WOS:000455489400001
PM 30671195
OA Green Published, gold
DA 2022-04-25
ER

PT J
AU Hou, XY
   Yang, CL
   Zhang, LJ
   Hu, TT
   Sun, D
   Cao, H
   Yang, F
   Guo, G
   Gong, CY
   Zhang, XN
   Tong, AP
   Li, R
   Zheng, Y
AF Hou, Xueyan
   Yang, Chengli
   Zhang, Lijing
   Hu, Tingting
   Sun, Dan
   Cao, Hua
   Yang, Fan
   Guo, Gang
   Gong, Changyang
   Zhang, Xiaoning
   Tong, Aiping
   Li, Rui
   Zheng, Yu
TI Killing colon cancer cells through PCD pathways by a novel hyaluronic
   acid-modified shell-core nanoparticle loaded with RIP3 in combination
   with chloroquine
SO BIOMATERIALS
LA English
DT Article
DE Hyaluronic acid-modified shell-core; nanoparticle; mRIP3; Chloroquine;
   Necroptosis; Autophagy; Lysosomal membrane permeabilization; (LMP)
ID POLYMER HYBRID NANOPARTICLES; NEGATIVE BREAST-CANCER; PLGA
   NANOPARTICLES; GENE DELIVERY; AUTOPHAGY; TUMOR; APOPTOSIS; DEATH; DRUG;
   INHIBITION
AB Due to extensive apoptosis defects and multidrug resistance, there is great interest regarding nonapoptotic programmed cell death (PCD) pathways, such as lysosomal-mediated programmed cell death (LM-PCD), necroptosis and autophagy. Because there is an intricate effector network among these PCD pathways, it is expected that they may act synergistically in cancer therapy. In this study, chloroquine (CQ) was found to significantly upregulate receptor-interacting protein kinase 3 (RIP3) expression, and RIP3 were involved in CQ-related autophagy. Overexpressed-eGFP-RIP3 co-localized with the selective autophagy receptor p62. mRIP3 overexpression in combination with CQ markedly increased the inhibition rate relative to that observed in the CQ-treatment group. Several experiments, including Hoechst staining, transmission electron microscopy (TEM) observation, the high-mobility group box 1 (HMGB1) release assay, Annexin V/PI staining and immunoblotting of proteins included in PCD pathways, verified that mRIP3 overexpression in combination with CQ induced lysosomal membrane permeabilization (LMP) and necroptosis of cancer cells, leading to cancer cell death. For tumor-targeted delivery, hyaluronic acid (HA)-modified, lipid-coated PLGA nanoparticles loaded with mRlP3-pDNA were prepared and characterized using a particle sizer, differential scanning calorimetry (DSC) and TEM. The nanoparticles exhibited ideal biocompatibility and good tumor-targeting efficiency, and the tumor inhibition rate of HA-Lip-PEI-mRIP3-PLGA-NPs CQ was 80.2% in the CT26 mouse model. In this study, we attempted to treat tumors by inducing several alternative PCD pathways to shed light on the combination therapy of alternative PCD inducers. (C) 2017 Elsevier Ltd. All rights reserved.
C1 [Hou, Xueyan; Hu, Tingting; Cao, Hua; Guo, Gang; Gong, Changyang; Tong, Aiping; Li, Rui; Zheng, Yu] Sichuan Univ, West China Hosp, State Key Lab Biotherapy, Collaborat Innovat Ctr Biotherapy, 17,Sect 3,Ren Min Nan Rd, Chengdu 610041, Sichuan, Peoples R China.
   [Yang, Chengli] Zunyi Med Univ, Dept Clin Pharm, Sch Pharm, 6 Xuefu Xi Rd, Zunyi 563006, Guizhou, Peoples R China.
   [Zhang, Lijing] Zhengzhou Univ, Med Res Ctr, Affiliated Hosp 1, 1 Jianshe East Rd, Zhengzhou 450052, Henan, Peoples R China.
   [Sun, Dan] Sichuan Univ, Coll Life Sci, Chengdu 610041, Sichuan, Peoples R China.
   [Yang, Fan] Sichuan Univ, West China Univ Hosp 2, Dept Gynecol, Chengdu 610041, Peoples R China.
   [Zhang, Xiaoning] Tsinghua Univ, Sch Med, Lab Pharmaceut, 30 Shuangqing Rd, Beijing 100084, Peoples R China.
RP Zheng, Y (corresponding author), Sichuan Univ, West China Hosp, State Key Lab Biotherapy, Collaborat Innovat Ctr Biotherapy, 17,Sect 3,Ren Min Nan Rd, Chengdu 610041, Sichuan, Peoples R China.
EM zhengyu82@scu.edu.cn
RI 孙, 丹/AAJ-6568-2020
FU National Natural Science Foundation of ChinaNational Natural Science
   Foundation of China (NSFC) [81001012]; China Postdoctoral Science
   FoundationChina Postdoctoral Science Foundation [2014T70877,
   2013M542421]
FX The mRIP3-pDNA is a gift from Dr. Jiahuai Han (Key Laboratory of the
   Ministry of Education for Cell Biology and Tumor Cell Engineering,
   School of Life Sciences, Xiamen University, Xiamen, Fujian 361005,
   China). This work was supported by the National Natural Science
   Foundation of China (81001012), the China Postdoctoral Science
   Foundation (2014T70877, 2013M542421).
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NR 83
TC 35
Z9 37
U1 13
U2 184
PU ELSEVIER SCI LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND
SN 0142-9612
EI 1878-5905
J9 BIOMATERIALS
JI Biomaterials
PD APR
PY 2017
VL 124
BP 195
EP 210
DI 10.1016/j.biomaterials.2016.12.032
PG 16
WC Engineering, Biomedical; Materials Science, Biomaterials
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Engineering; Materials Science
GA EN4CS
UT WOS:000395956000016
PM 28199887
DA 2022-04-25
ER

PT J
AU Hsieh, YY
   Chou, CJ
   Lo, HL
   Yang, PM
AF Hsieh, Y-Y
   Chou, C-J
   Lo, H-L
   Yang, P-M
TI Repositioning of a cyclin-dependent kinase inhibitor GW8510 as a
   ribonucleotide reductase M2 inhibitor to treat human colorectal cancer
SO CELL DEATH DISCOVERY
LA English
DT Article
AB Colorectal cancer (CRC) is the second leading cause of cancer-related death in males and females in the world. It is of immediate importance to develop novel therapeutics. Human ribonucleotide reductase (RRM1/RRM2) has an essential role in converting ribonucleoside diphosphate to 2'-deoxyribonucleoside diphosphate to maintain the homeostasis of nucleotide pools. RRM2 is a prognostic biomarker and predicts poor survival of CRC. In addition, increased RRM2 activity is associated with malignant transformation and tumor cell growth. Bioinformatics analyses show that RRM2 was overexpressed in CRC and might be an attractive target for treating CRC. Therefore, we attempted to search novel RRM2 inhibitors by using a gene expression signature-based approach, connectivity MAP (CMAP). The result predicted GW8510, a cyclin-dependent kinase inhibitor, as a potential RRM2 inhibitor. Western blot analysis indicated that GW8510 inhibited RRM2 expression through promoting its proteasomal degradation. In addition, GW8510 induced autophagic cell death. In addition, the sensitivities of CRC cells to GW8510 were associated with the levels of RRM2 and endogenous autophagic flux. Taken together, our study indicates that GW8510 could be a potential anti-CRC agent through targeting RRM2.
C1 [Hsieh, Y-Y; Chou, C-J; Lo, H-L; Yang, P-M] Taipei Med Univ, Coll Med Sci & Technol, PhD Program Canc Biol & Drug Discovery, Taipei, Taiwan.
   [Hsieh, Y-Y; Chou, C-J; Lo, H-L; Yang, P-M] Acad Sinica, Taipei, Taiwan.
   [Hsieh, Y-Y] Taipei Meidcal Univ, Shuang Ho Hosp, Div Hematol & Oncol, Taipei, Taiwan.
   [Chou, C-J; Lo, H-L; Yang, P-M] Taipei Med Univ, Coll Med Sci & Technol, Grad Inst Canc Biol & Drug Discovery, Taipei, Taiwan.
RP Yang, PM (corresponding author), Taipei Med Univ, Coll Med Sci & Technol, PhD Program Canc Biol & Drug Discovery, Taipei, Taiwan.; Yang, PM (corresponding author), Acad Sinica, Taipei, Taiwan.; Yang, PM (corresponding author), Taipei Med Univ, Coll Med Sci & Technol, Grad Inst Canc Biol & Drug Discovery, Taipei, Taiwan.
EM yangpm@tmu.edu.tw
RI Yang, Pei-Ming/G-3763-2014
OI Yang, Pei-Ming/0000-0002-4004-2518
FU Taiwan's Ministry of Science and Technology [MOST103-2632-B-038-001,
   MOST104-2320-B-038-005]; Taipei Medical University-Shuang Ho Hospital
   [104TMU-SHH-03]; Research Team of Prevention and Therapy of Colorectal
   Cancer at Taipei Medical University [TMU-T104-01]; Comprehensive Cancer
   Center of Taipei Medical University - Health and welfare surcharge of
   tobacco products [MOHW105-TDU-B-212-134001]
FX This work was supported by research grants from Taiwan's Ministry of
   Science and Technology (MOST103-2632-B-038-001 and
   MOST104-2320-B-038-005), Taipei Medical University-Shuang Ho Hospital
   (104TMU-SHH-03), Research Team of Prevention and Therapy of Colorectal
   Cancer at Taipei Medical University (TMU-T104-01), and Comprehensive
   Cancer Center of Taipei Medical University (MOHW105-TDU-B-212-134001)
   funded by the Health and welfare surcharge of tobacco products.
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U1 0
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PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
EI 2058-7716
J9 CELL DEATH DISCOV
JI Cell Death Discov.
PY 2016
VL 2
AR 16027
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PG 8
WC Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Cell Biology
GA VI2GA
UT WOS:000463076300029
PM 27551518
OA gold, Green Published
DA 2022-04-25
ER

PT J
AU Li, YJ
   Chen, YY
   Huang, HY
   Shi, MM
   Yang, WP
   Kuang, J
   Yan, JQ
AF Li, Yongjian
   Chen, Yunyang
   Huang, Haiyan
   Shi, Minmin
   Yang, Weiping
   Kuang, Jie
   Yan, Jiqi
TI Autophagy mediated by endoplasmic reticulum stress enhances the
   caffeine-induced apoptosis of hepatic stellate cells
SO INTERNATIONAL JOURNAL OF MOLECULAR MEDICINE
LA English
DT Article
DE caffeine; endoplasmic reticulum stress; autophagy; inositol-requiring
   enzyme-1 alpha; liver fibrosis
ID UNFOLDED-PROTEIN RESPONSE; PROMOTES TUMOR-GROWTH; LIVER FIBROSIS;
   MOLECULAR-MECHANISMS; COFFEE CONSUMPTION; COLORECTAL-CANCER; ACTIVATION;
   DISEASE; EXPRESSION; SORAFENIB
AB Caffeine has been identified to have beneficial effects against chronic liver diseases, particularly liver fibrosis. Many studies have reported that caffeine ameliorates liver fibrosis by directly inducing hepatic stellate cell (HSC) apoptosis; however, the molecular mechanisms involved in this process remain unclear. The presents study aimed to detect the underlying mechanisms by which caffeine mediates HSC apoptosis and eliminates activated HSCs. For this purpose, the LX-2 cell line was applied in this study and the cells were exposed to various concentrations of caffeine for the indicated times. The effects of caffeine on cell viability and apoptosis were assessed by Cell Counting Kit-8 assay and flow cytometry, respectively. Autophagy and endoplasmic reticulum (ER) stress were explored by morphological assessment and western blotting. In the present study, caffeine was found to inhibit the viability and increase the apoptosis of the LX-2 cells in dose-and time-dependent manners. ER stress was stimulated by caffeine as demonstrated by increased levels of GRP78/Bip, CHOP and inositol-requiring enzyme 1 (IRE1)-alpha as well as many enlarged ERs detected by electron microscopy. Caffeine induced autophagy as shown by increased p62 and LC3. accumulation and the number of GFP/RFP-LC3 puncta and autophagosomes/autolysosomes. Moreover, IRE1-alpha knockdown decreased the level of autophagic flux, and inhibition of autophagy protected LX-2 cells from apoptotic death. In conclusion, our study showed that the caffeine-enhanced autophagic flux in HSCs was stimulated by ER stress via the IRE1-alpha signaling pathway, which further weakened HSC viability via the induction of apoptosis. These findings provide new insight into the mechanism of caffeine's anti-fibrotic effects.
C1 [Li, Yongjian; Chen, Yunyang; Huang, Haiyan; Yang, Weiping; Kuang, Jie; Yan, Jiqi] Shanghai Jiao Tong Univ, Sch Med, Ruijin Hosp, Dept Gen Surg, 197 Ruijin Er Rd, Shanghai 200025, Peoples R China.
   [Li, Yongjian; Chen, Yunyang; Shi, Minmin; Yang, Weiping; Kuang, Jie; Yan, Jiqi] Shanghai Jiao Tong Univ, Sch Med, Ruijin Hosp, Shanghai Inst Digest Surg, Shanghai 200025, Peoples R China.
   [Chen, Yunyang] Jiangmen Cent Hosp, Dept Hepatobiliary Surg, Jiangmen 529030, Guangdong, Peoples R China.
RP Kuang, J; Yan, JQ (corresponding author), Shanghai Jiao Tong Univ, Sch Med, Ruijin Hosp, Dept Gen Surg, 197 Ruijin Er Rd, Shanghai 200025, Peoples R China.
EM kuangjie823@msn.com; yanjiqi@sohu.com
FU National Natural Science Foundation of ChinaNational Natural Science
   Foundation of China (NSFC) [81070358]
FX This study was supported by the National Natural Science Foundation of
   China (no. 81070358), (http://www.nsfc.gov.cn) to JQY.
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NR 44
TC 23
Z9 27
U1 5
U2 18
PU SPANDIDOS PUBL LTD
PI ATHENS
PA POB 18179, ATHENS, 116 10, GREECE
SN 1107-3756
EI 1791-244X
J9 INT J MOL MED
JI Int. J. Mol. Med.
PD NOV
PY 2017
VL 40
IS 5
BP 1405
EP 1414
DI 10.3892/ijmm.2017.3145
PG 10
WC Medicine, Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Research & Experimental Medicine
GA FK3PS
UT WOS:000413398800011
PM 28949381
OA Green Submitted, hybrid, Green Published
DA 2022-04-25
ER

PT J
AU Gueraud, F
   Atalay, M
   Bresgen, N
   Cipak, A
   Eckl, PM
   Huc, L
   Jouanin, I
   Siems, W
   Uchida, K
AF Gueraud, F.
   Atalay, M.
   Bresgen, N.
   Cipak, A.
   Eckl, P. M.
   Huc, L.
   Jouanin, I.
   Siems, W.
   Uchida, K.
TI Chemistry and biochemistry of lipid peroxidation products
SO FREE RADICAL RESEARCH
LA English
DT Review
DE Lipid peroxidation; alkenals; 4-hydroxy-2-nonenal; glutathione;
   apoptosis; adducts; volatile aldehydes
ID LOW-DENSITY-LIPOPROTEIN; POLYUNSATURATED FATTY-ACIDS;
   GLUTATHIONE-S-TRANSFERASE; PROTEIN-DISULFIDE-ISOMERASE; PIGMENT
   EPITHELIAL-CELLS; HEADSPACE GAS-CHROMATOGRAPHY; AMYLOID-BETA-PEPTIDE;
   HEAT-SHOCK PROTEINS; DNA-DAMAGE RESPONSE; COLON-CANCER CELLS
AB Oxidative stress and resulting lipid peroxidation is involved in various and numerous pathological states including inflammation, atherosclerosis, neurodegenerative diseases and cancer. This review is focused on recent advances concerning the formation, metabolism and reactivity towards macromolecules of lipid peroxidation breakdown products, some of which being considered as 'second messengers' of oxidative stress. This review relates also new advances regarding apoptosis induction, survival/proliferation processes and autophagy regulated by 4-hydroxynonenal, a major product of omega-6 fatty acid peroxidation, in relationship with detoxication mechanisms. The use of these lipid peroxidation products as oxidative stress/lipid peroxidation biomarkers is also addressed.
C1 [Gueraud, F.; Huc, L.; Jouanin, I.] INRA, UMR1089 Xenobiot, F-31027 Toulouse 3, France.
   [Atalay, M.] Univ Eastern Finland, Inst Biomed, Kuopio, Finland.
   [Bresgen, N.; Eckl, P. M.] Salzburg Univ, Dept Cell Biol, A-5020 Salzburg, Austria.
   [Cipak, A.] Rudjer Boskovic Inst, Zagreb, Croatia.
   [Siems, W.] KortexMed Res, Inst Physiotherapy & Gerontol, Bad Harzburg, Germany.
   [Uchida, K.] Nagoya Univ, Grad Sch Bioagr Sci, Nagoya, Aichi 4648601, Japan.
RP Gueraud, F (corresponding author), INRA, UMR1089 Xenobiot, BP93173, F-31027 Toulouse 3, France.
EM fgueraud@toulouse.inra.fr
RI Huc, Laurence/J-1888-2014
OI Huc, Laurence/0000-0002-0336-7559; Uchida, Koji/0000-0003-3894-5299;
   Eckl, Peter/0000-0002-3842-1746; Gueraud, Francoise/0000-0001-5455-1244
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NR 298
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Z9 343
U1 12
U2 114
PU TAYLOR & FRANCIS LTD
PI ABINGDON
PA 2-4 PARK SQUARE, MILTON PARK, ABINGDON OR14 4RN, OXON, ENGLAND
SN 1071-5762
EI 1029-2470
J9 FREE RADICAL RES
JI Free Radic. Res.
PD OCT
PY 2010
VL 44
IS 10
SI SI
BP 1098
EP 1124
DI 10.3109/10715762.2010.498477
PG 27
WC Biochemistry & Molecular Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology
GA 654BP
UT WOS:000282143400002
PM 20836659
OA Green Published
DA 2022-04-25
ER

PT J
AU Gijon, M
   Metheringham, RL
   Toss, MS
   Paston, SJ
   Durrant, LG
AF Gijon, Mohamed
   Metheringham, Rachael L.
   Toss, Michael S.
   Paston, Samantha J.
   Durrant, Lindy G.
TI The Clinical and Prognostic Significance of Protein Arginine Deiminases
   2 and 4 in Colorectal Cancer
SO PATHOBIOLOGY
LA English
DT Article; Early Access
DE Protein arginine deiminase 2; Protein arginine deiminase 4;
   Citrullination; Colorectal cancer; Immunohistochemistry
ID MHC CLASS-I; PEPTIDYLARGININE DEIMINASE; CITRULLINATED VIMENTIN;
   RHEUMATOID-ARTHRITIS; HISTONE DEIMINATION; BETA-CATENIN; COLON-CANCER;
   EXPRESSION; CELLS; AUTOPHAGY
AB Introduction: Protein arginine deiminases (PADIs) are a family of enzymes that catalyse the post-translational modification of proteins. Association between PADI expression and clinicopathology, protein expression, and outcome was determined. Methods: PADI2 and PADI4 expression was assessed immunohistochemically in a cohort of colorectal cancer (CRC) patients. Results: CRC tissues expressed variable levels of PADI2 which was mainly localised in the cytoplasm and correlated with patient survival (p = 0.005); high expression increased survival time from 43.5 to 67.6 months. Expression of cytoplasmic PADI2 correlated with the expression of nuclear beta catenin, PADI4, and alpha-enolase. In contrast, expression of nuclear PADI2 correlated with a decrease in survival (p = 0.010), with high expression decreasing survival from 76.4 to 42.9 months. CRC tissues expressed variable levels of PADI4 in both the nucleus and cytoplasm. Expression of cytoplasmic PADI4 correlated with survival (p = 0.001) with high expression increasing survival time from 48.1 to 71.8 months. Expression of cytoplasmic PADI4 correlated with expression of nuclear beta catenin, alpha-enolase (p <= 0.0001, p = 0.002), and the apoptotic related protein, Bcl-2. Expression of nuclear PADI4 also correlated with survival (p = 0.011), with high expression of nuclear PADI4 increasing survival time from 55.4 to 74 months. Expression of nuclear PADI4 correlated with p53, alpha-enolase, and Bcl-2. Multivariate analysis showed that TNM stage, cytoplasmic PADI2, and PADI4 remained independent prognostic factors in CRC. Both PADI2 and PADI4 are good prognostic factors in CRC. Conclusion: High expression of cytoplasmic PADI2, PADI4, and nuclear PADI4 were associated with an increase in overall survival.
C1 [Gijon, Mohamed; Metheringham, Rachael L.; Paston, Samantha J.; Durrant, Lindy G.] Scancell Ltd, Biodiscovery Inst, Univ Pk, Nottingham, England.
   [Durrant, Lindy G.] Univ Nottingham, Biodiscovery Inst, Div Canc & Stem Cells, Univ Pk, Nottingham, England.
   [Toss, Michael S.] Univ Nottingham, Nottingham City Hosp, Nottingham Breast Canc Res Ctr, Sch Med,Div Canc & Stem Cells, Nottingham, England.
RP Durrant, LG (corresponding author), Scancell Ltd, Biodiscovery Inst, Univ Pk, Nottingham, England.; Durrant, LG (corresponding author), Univ Nottingham, Biodiscovery Inst, Div Canc & Stem Cells, Univ Pk, Nottingham, England.
EM lindy.durrant@nottingham.ac.uk
OI Gijon, Mohamed/0000-0002-2444-0727
FU Scancell Ltd.
FX This work was funded by Scancell Ltd.
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NR 55
TC 0
Z9 0
U1 1
U2 1
PU KARGER
PI BASEL
PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND
SN 1015-2008
EI 1423-0291
J9 PATHOBIOLOGY
JI Pathobiology
DI 10.1159/000518414
EA SEP 2021
PG 11
WC Cell Biology; Pathology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Cell Biology; Pathology
GA UT4TM
UT WOS:000698109800001
PM 34569542
DA 2022-04-25
ER

PT S
AU Baghy, K
   Reszegi, A
   Tatrai, P
   Kovalszky, I
AF Baghy, Kornelia
   Reszegi, Andrea
   Tatrai, Peter
   Kovalszky, Ilona
BE Birbrair, A
TI Decorin in the Tumor Microenvironment
SO TUMOR MICROENVIRONMENT: EXTRACELLULAR MATRIX COMPONENTS - PT B
SE Advances in Experimental Medicine and Biology
LA English
DT Article; Book Chapter
DE Decorin; Extracellular matrix; Receptor tyrosine kinase; Autophagy;
   Mitophagy; Inflammation; SLRP; Tumor; Stroma; EGFR; Met; Angiogenesis;
   Cell cycle; Signaling; Growth factor
ID EPIDERMAL-GROWTH-FACTOR; LEUCINE-RICH PROTEOGLYCANS; BREAST-CARCINOMA
   CELLS; HUMAN-COLON CARCINOMA; IMPRINTED GENE PEG3; FACTOR-I RECEPTOR;
   EXTRACELLULAR-MATRIX; CANCER GROWTH; FACTOR-BETA; COLLAGEN
   FIBRILLOGENESIS
AB The tumor microenvironment plays a determining role in cancer development through a plethora of interactions between the extracellular matrix and tumor cells. Decorin is a prototype member of the SLRP family found in a variety of tissues and is expressed in the stroma of various forms of cancer. Decorin has gained recognition for its essential roles in inflammation, fibrotic disorders, and cancer, and due to its antitumor properties, it has been proposed to act as a "guardian from the matrix." Initially identified as a natural inhibitor of transforming growth factor-beta, soluble decorin is emerging as a pan-RTK inhibitor targeting a multitude of RTKs, including EGFR, Met, IGF-IR, VEGFR2, and PDGFR. Besides initiating signaling, decorin/RTK interaction can induce caveosomal internalization and receptor degradation. Decorin also triggers cell cycle arrest and apoptosis and evokes antimetastatic and antiangiogenic processes. In addition, as a novel regulatory mechanism, decorin was shown to induce conserved catabolic processes, such as endothelial cell autophagy and tumor cell mitophagy. Therefore, decorin is a promising candidate for combatting cancer, especially the cancer types heavily dependent on RTK signaling.
C1 [Baghy, Kornelia; Reszegi, Andrea; Kovalszky, Ilona] Semmelweis Univ, Dept Pathol & Expt Canc Res 1, Budapest, Hungary.
   [Tatrai, Peter] Solvo Biotechnol, Budapest, Hungary.
RP Baghy, K (corresponding author), Semmelweis Univ, Dept Pathol & Expt Canc Res 1, Budapest, Hungary.
EM baghy.kornelia@med.semmelweis-univ.hu; tatrai@solvo.com;
   koval@korb1.sote.hu
RI Kovalszky, Ilona/ABH-2832-2020; Baghy, Kornélia/ABH-2549-2020; Tatrai,
   Peter/AAR-6014-2020
OI Kovalszky, Ilona/0000-0002-0179-3378; Baghy,
   Kornélia/0000-0002-5323-2775; Tatrai, Peter/0000-0001-9726-1992;
   Reszegi, Andrea/0000-0001-6902-7883
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NR 188
TC 7
Z9 7
U1 2
U2 2
PU SPRINGER INTERNATIONAL PUBLISHING AG
PI CHAM
PA GEWERBESTRASSE 11, CHAM, CH-6330, SWITZERLAND
SN 0065-2598
EI 2214-8019
BN 978-3-030-48457-6; 978-3-030-48456-9
J9 ADV EXP MED BIOL
JI Adv.Exp.Med.Biol.
PY 2020
VL 1272
BP 17
EP 38
DI 10.1007/978-3-030-48457-6_2
D2 10.1007/ 978-3-030-48457-6
PG 22
WC Biochemistry & Molecular Biology; Oncology
WE Book Citation Index – Science (BKCI-S); Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Oncology
GA BP9DW
UT WOS:000569017500003
PM 32845500
DA 2022-04-25
ER

PT J
AU Chiang, JH
   Tsai, FJ
   Hsu, YM
   Yin, MC
   Chiu, HY
   Yang, JS
AF Chiang, Jo-Hua
   Tsai, Fuu-Jen
   Hsu, Yuan-Man
   Yin, Mei-Chin
   Chiu, Hong-Yi
   Yang, Jai-Sing
TI Sensitivity of allyl isothiocyanate to induce apoptosis via ER stress
   and the mitochondrial pathway upon ROS production in colorectal
   adenocarcinoma cells
SO ONCOLOGY REPORTS
LA English
DT Article
DE allyl isothiocyanate; colon cancer cells; apoptosis; ER stress;
   mitochondria; ROS production
ID ENDOPLASMIC-RETICULUM STRESS; PHASE ARREST; IN-VITRO; CANCER;
   PROLIFERATION; INHIBITION; ANGIOGENESIS; DYSFUNCTION; METASTASIS;
   AUTOPHAGY
AB Allyl isothiocyanate (AITC), a bioactive phytochemical compound that is a constituent of dietary cruciferous vegetables, possesses promising chemopreventive and anticancer effects. However, reports of AITC exerting antitumor effects on apoptosis induction of colorectal cancer (CRC) cells in vitro are not well elucidated. The present study focused on the functional mechanism of the endoplasmic reticulum (ER) stress-based apoptotic machinery induced by AITC in human colorectal cancer HT-29 cells. Our results indicated that AITC decreased cell growth and number, reduced viability, and facilitated morphological changes of apoptotic cell death. DNA analysis by flow cytometry showed G2/M phase arrest, and alterations in the modulated protein levels caused by AITC were detected via western blot analysis. AITC also triggered vital intrinsic apoptotic factors (caspase-9/caspase-3 activity), disrupted mitochondrial membrane potential, and stimulated mitochondrial-related apoptotic molecules (e.g., cytochrome c, apoptotic protease activating factor 1, apoptosis-inducing factor, and endonuclease G). Additionally, AITC prompted induced cytosolic Ca2+ release and Ca2+-dependent ER stress-related signals, such as calpain 1, activating transcription factor 6 alpha, glucose-regulated proteins 78 and 94, growth arrest- and DNA damage-inducible protein 153 (GADD153), and caspase-4. The level of reactive oxygen species (ROS) production was found to induce the hallmark of ER stress GADD153, proapoptotic marker caspase-3, and calpain activity after AITC treatment. Our findings showed for the first time that AITC induced G2/M phase arrest and apoptotic death via ROS-based ER stress and the intrinsic pathway (mitochondrial-dependent) in HT-29 cells. Overall, AITC may exert an epigenetic effect and is a potential bioactive compound for CRC treatment.
C1 [Chiang, Jo-Hua] Chung Jen Jr Coll Nursing Hlth Sci & Management, Dept Nursing, Chiayi 62241, Taiwan.
   [Tsai, Fuu-Jen] China Med Univ Hosp, Dept Med Res, Human Genet Ctr, Taichung 40447, Taiwan.
   [Tsai, Fuu-Jen] China Med Univ Hosp, Dept Med Genet, Taichung 40447, Taiwan.
   [Tsai, Fuu-Jen] China Med Univ, Sch Chinese Med, Taichung 40402, Taiwan.
   [Hsu, Yuan-Man] China Med Univ, Dept Biol Sci & Technol, Taichung 40402, Taiwan.
   [Yin, Mei-Chin] Asia Univ, Dept Food Nutr & Hlth Biotechnol, Taichung 41354, Taiwan.
   [Chiu, Hong-Yi] Buddhist Tzu Chi Med Fdn, Hualien Tzu Chi Hosp, Dept Pharm, Sec 3,707 Chung Yang Rd, Hualien 97002, Taiwan.
   [Chiu, Hong-Yi] Tzu Chi Univ, Sch Med, Master & PhD Program Pharmacol & Toxicol, Hualien 97004, Taiwan.
   [Chiu, Hong-Yi] Tzu Chi Univ Sci & Technol, Gen Educ Ctr, Hualien 97005, Taiwan.
   [Yang, Jai-Sing] China Med Univ, China Med Univ Hosp, Dept Med Res, Taichung 40442, Taiwan.
RP Chiu, HY (corresponding author), Buddhist Tzu Chi Med Fdn, Hualien Tzu Chi Hosp, Dept Pharm, Sec 3,707 Chung Yang Rd, Hualien 97002, Taiwan.; Yang, JS (corresponding author), China Med Univ, China Med Univ Hosp, Dept Med Res, 2 Yude Rd, Taichung 40447, Taiwan.
EM hychiu@tzuchi.com.tw; jaisingyang@gmail.com
RI Hsu, Yuan-Man/K-7074-2015
OI Hsu, Yuan-Man/0000-0002-4575-7475
FU Chung-Jen Junior College of Nursing, Health Sciences and Management
   [105015, 106-003]; Hualien Tzu Chi Hospital [TCRD107-55]; China Medical
   University Hospital [DMR-108-122]
FX This work was financially supported by Chung-Jen Junior College of
   Nursing, Health Sciences and Management (grants nos. 105015 and 106-003)
   and in part by Hualien Tzu Chi Hospital (grant no. TCRD107-55) and China
   Medical University Hospital (grant no. DMR-108-122).
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NR 51
TC 6
Z9 6
U1 0
U2 7
PU SPANDIDOS PUBL LTD
PI ATHENS
PA POB 18179, ATHENS, 116 10, GREECE
SN 1021-335X
EI 1791-2431
J9 ONCOL REP
JI Oncol. Rep.
PD OCT
PY 2020
VL 44
IS 4
BP 1415
EP 1424
DI 10.3892/or.2020.7700
PG 10
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA NO3CL
UT WOS:000569361800012
PM 32700751
OA Green Published, hybrid
DA 2022-04-25
ER

PT J
AU Schonewolf, CA
   Mehta, M
   Schiff, D
   Wu, H
   Haffty, BG
   Karantza, V
   Jabbour, SK
AF Schonewolf, Caitlin A.
   Mehta, Monal
   Schiff, Devora
   Wu, Hao
   Haffty, Bruce G.
   Karantza, Vassiliki
   Jabbour, Salma K.
TI Autophagy inhibition by chloroquine sensitizes HT-29 colorectal cancer
   cells to concurrent chemoradiation
SO WORLD JOURNAL OF GASTROINTESTINAL ONCOLOGY
LA English
DT Article
DE Autophagy; Chloroquine; Radiosensitization; Colorectal cancer
ID HIF-1
AB AIM: To investigate whether the inhibition of autophagy by chloroquine (CQ) sensitizes rectal tumors to radiation therapy (RT) or concurrent chemoradiation (chemoRT).
   METHODS: In vitro, HCT-116 and HT-29 colorectal cancer (CRC) cell lines were treated as following: (1) PBS; (2) CQ; (3) 5-fluorouracil (5-FU); (4) RT; (5) CQ and RT; (6) 5-FU and RT; (7) CQ and 5-FU; and (8) 5-FU and CQ and RT. Each group was then exposed to various doses of radiation (0-8 Gy) depending on the experiment. Cell viability and proliferative capacity were measured by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) and clonogenic assays. Clonogenic survival curves were constructed and compared across treatment groups. Autophagy status was determined by assessing the LC3-II to LC3-I ratio on western blot analysis, autophagosome formation on electron microscopy and identification of a perinuclear punctate pattern with GFP-labeled LC3 on fluorescence microscopy. Cell cycle arrest and cell death were evaluated by FACS and Annexin. analysis. All experiments were performed in triplicate and statistical analysis was performed by the student's t test to compare means between treatment groups.
   RESULTS: RT (2-8 Gy) induced autophagy in HCT-116 and HT-29 CRC cell lines at 4 and 6 h post-radiation, respectively, as measured by increasing LC3-II to LC3-I ratio on western blot. Additionally, electron microscopy demonstrated autophagy induction in HT-29 cells 24 h following irradiation at a dose of 8 Gy. Drug treatment with 5-FU (25 mu mol/L) induced autophagy and the combination of 5-FU and RT demonstrated synergism in autophagy induction. CQ (10 mu mol/L) alone and in combination with RT effectively inhibited autophagy and sensitized both HCT-116 and HT-29 cells to treatment with radiation (8 Gy; P < 0.001 and 0.00001, respectively). Significant decrease in clonogenic survival was seen only in the HT-29 cell line, when CQ was combined with RT at doses of 2 and 8 Gy (P < 0.5 and P = 0.05, respectively). There were no differences in cell cycle progression or Annexin V staining upon CQ addition to RT.
   CONCLUSION: Autophagy inhibition by CQ increases CRC cell sensitivity to concurrent treatment with 5-FU and RT in vitro, suggesting that addition of CQ to chemoRT improves CRC treatment response. (C) 2014 Baishideng Publishing Group Co., Limited. All rights reserved.
C1 [Schonewolf, Caitlin A.; Mehta, Monal; Schiff, Devora; Wu, Hao; Haffty, Bruce G.; Jabbour, Salma K.] Univ Med & Dent New Jersey, Robert Wood Johnson Med Sch, Canc Inst New Jersey, Dept Radiat Oncol, 195 Little Albany St, New Brunswick, NJ 08903 USA.
   [Karantza, Vassiliki] Univ Med & Dent New Jersey, Robert Wood Johnson Med Sch, Canc Inst New Jersey, Dept Med, New Brunswick, NJ 08903 USA.
RP Jabbour, SK (corresponding author), Univ Med & Dent New Jersey, Robert Wood Johnson Med Sch, Canc Inst New Jersey, Dept Radiat Oncol, 195 Little Albany St, New Brunswick, NJ 08903 USA.
EM jabbousk@umdnj.edu
CR Amaravadi RK, 2011, CLIN CANCER RES, V17, P654, DOI 10.1158/1078-0432.CCR-10-2634
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NR 18
TC 49
Z9 52
U1 0
U2 7
PU BAISHIDENG PUBLISHING GROUP INC
PI PLEASANTON
PA 8226 REGENCY DR, PLEASANTON, CA 94588 USA
SN 1948-5204
J9 WORLD J GASTRO ONCOL
JI World J. Gastrointest. Oncol.
PD MAR 15
PY 2014
VL 6
IS 3
BP 74
EP 82
DI 10.4251/wjgo.v6.i3.74
PG 9
WC Oncology; Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Gastroenterology & Hepatology
GA V9A3O
UT WOS:000422130700003
PM 24653797
OA Green Published, hybrid, Green Submitted
DA 2022-04-25
ER

PT J
AU Li, T
   Zhang, SY
   Chen, FS
   Hu, J
   Yuan, S
   Li, CR
   Wang, XT
   Zhang, WH
   Tang, RW
AF Li, Tian
   Zhang, Shiyi
   Chen, Fengsong
   Hu, Jun
   Yuan, Shuai
   Li, Chaoran
   Wang, Xiaoting
   Zhang, Weihong
   Tang, Runwei
TI Formononetin ameliorates the drug resistance of Taxol resistant triple
   negative breast cancer by inhibiting autophagy
SO AMERICAN JOURNAL OF TRANSLATIONAL RESEARCH
LA English
DT Article
DE Formononetin; Taxol; triple negative breast cancer; autophagy;
   miR-199a-3p
ID MECHANISMS; INVASION; GROWTH
AB Characterized by autophagy-associated protein disorders, autophagy participates in Taxol resistance in triple negative breast cancer (TNBC). As an evolutionarily conserved serine/threonine protein kinase with complex signaling pathway, mammalian target of rapamycin (mTOR) can regulate various cellular functions by phosphorylation of its downstream target proteins after activation. A large number of references have demonstrated that mTOR signaling pathway is related to autophagy and apoptosis. Formononetin (FMNT) has anticancer properties against breast, prostate and colon cancers. This study aimed to explore the regulatory effect of FMNT/miR-199a-3p/mTOR pathway on Taxol resistance and autophagy in breast cancer (BC). MiR-199a-3p, mTOR, LC3 and other autophagy related proteins were detected in Taxol sensitive and Taxol resistant TNBC cell lines, which were MDA-MB-231 and MDA-MB-231/Taxol, respectively. Cell viability and toxicity were determined by CCK-8 and MTT assay, respectively. The therapeutic effect of FMNT was evaluated in xenotransplantation model of nude mice. MiR-199a-3p was more highly expressed in MDA-MB-231/Taxol than in MDA-MB-231, while mTOR and p-mTOR decreased in MDA-MB-231/Taxol in comparison with MDA-MB-231, and autophagy activation and drug resistance were enhanced. In MDAMB-231/Taxol cell line, the role of FMNT was verified to inhibit high miR-199a-3p expression. In addition, the combination therapy of FMNT and Taxol was found to be more effective in inhibiting autophagy and drug resistance. Moreover, mTOR was the target of miR-199a-3p, which was confirmed by dual luciferase reporter (DLR) gene assay. Oral administration of FMNT reduced tumor volume after MDA-MB-231/Taxol injection in vivo. Moreover, oral administration of FMNT and Taxol suppressed autophagy and Taxol resistance by restoring mTOR protein level to that of the parent MDA-MB-231, suggesting that miR-199a-3p can severe as a new target to overcome Taxol resistance in TNBC.
C1 [Li, Tian; Yuan, Shuai; Li, Chaoran; Wang, Xiaoting; Zhang, Weihong; Tang, Runwei] Shanghai Univ Tradit Chinese Med, Breast Surg Dept, Baoshan Branch, Shanghai 201900, Peoples R China.
   [Zhang, Shiyi] Guangdong Med Univ, Sch Clin Med 2, Dongguan 523000, Peoples R China.
   [Chen, Fengsong] Nantong Haimen Peoples Hosp, Nantong 226100, Peoples R China.
   [Hu, Jun] Shanghai Univ Tradit Chinese Med, Shanghai 201900, Peoples R China.
RP Zhang, WH; Tang, RW (corresponding author), Shanghai Univ Tradit Chinese Med, Shuguang Hosp, Baoshan Branch, Breast Surg Dept, 181 Youyi Rd, Shanghai 201900, Peoples R China.
EM zwh_08219@163.com; springtrw@sina.cn
FU Shanghai Municipal Health Commission Traditional Chinese Medicine
   Heritage and Technology Innovation Project [ZYCC2019020]; National
   Nature Science Nurturing Project of Baoshan Branch, Shuguang Hospital
   Affiliated to Shanghai University of Traditional Chinese Medicine
   [GZRPYJJ-201702]; Weihong famous TCM inheritance studio
   [BSMZYGZS-201909]; Shanghai Key Specialty Training Project of
   Traditional Chinese Medicine
FX 1. Shanghai Municipal Health Commission Traditional Chinese Medicine
   Heritage and Technology Innovation Project (ZYCC2019020). 2. National
   Nature Science Nurturing Project of Baoshan Branch, Shuguang Hospital
   Affiliated to Shanghai University of Traditional Chinese Medicine
   (GZRPYJJ-201702). 3. Zhang Weihong famous TCM inheritance studio
   (BSMZYGZS-201909). 4. Shanghai Key Specialty Training Project of
   Traditional Chinese Medicine.
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NR 39
TC 4
Z9 4
U1 1
U2 2
PU E-CENTURY PUBLISHING CORP
PI MADISON
PA 40 WHITE OAKS LN, MADISON, WI 53711 USA
SN 1943-8141
J9 AM J TRANSL RES
JI Am. J. Transl. Res.
PY 2021
VL 13
IS 2
BP 497
EP 514
PG 18
WC Oncology; Medicine, Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Research & Experimental Medicine
GA QG3IJ
UT WOS:000617482700005
PM 33594306
DA 2022-04-25
ER

PT J
AU Chi, KH
   Ko, HL
   Yang, KL
   Lee, CY
   Chi, MS
   Kao, SJ
AF Chi, Kwan-Hwa
   Ko, Hui-Ling
   Yang, Kai-Lin
   Lee, Cheng-Yen
   Chi, Mau-Shin
   Kao, Shang-Jyh
TI Addition of rapamycin and hydroxychloroquine to metronomic chemotherapy
   as a second line treatment results in high salvage rates for refractory
   metastatic solid tumors: a pilot safety and effectiveness analysis in a
   small patient cohort
SO ONCOTARGET
LA English
DT Article
DE rapamycin; hydroxychloroquine; metronomic chemotherapy; autophagy
ID ADVANCED BREAST-CANCER; CELL LUNG-CANCER; PHASE-I TRIAL;
   GLIOBLASTOMA-MULTIFORME; HEPATOCELLULAR-CARCINOMA; COMBINED AUTOPHAGY;
   DOUBLE-BLIND; EVEROLIMUS; CYCLOPHOSPHAMIDE; BEVACIZUMAB
AB Autophagy is an important oncotarget that can be modulated during anti-cancer therapy. Enhancing autophagy using chemotherapy and rapamycin (Rapa) treatment and then inhibiting it using hydroxychloroquine (HCQ) could synergistically improve therapy outcome in cancer patients. It is still unclear whether addition of Rapa and HCQ to chemotherapy could be used for reversing drug resistance.
   PATIENTS AND METHODS:
   Twenty-five stage IV cancer patients were identified. They had no clinical response to first-line metronomic chemotherapy; the patients were salvaged by adding an autophagy inducer (Rapa, 2 mg/day) and an autophagosome inhibitor (HCQ, 400 mg/day) to their current metronomic chemotherapy for at least 3 months. Patients included 4 prostate, 4 bladder, 4 lung, 4 breast, 2 colon, and 3 head and neck cancer patients as well as 4 sarcoma patients.
   RESULTS: Chemotherapy was administered for a total of 137 months. The median duration of chemotherapy cycles per patient was 4 months (95% confidence interval, 3-7 months). The overall response rate to this treatment was of 40%, with an 84% disease control rate. The most frequent and clinically significant toxicities were myelotoxicities. Grade >= 3 leucopenia occurred in 6 patients (24%), grade >= 3 thrombocytopenia in 8 (32%), and anemia in 3 (12%). None of them developed febrile neutropenia. Non-hematologic toxicities were fatigue (total 32%, with 1 patient developing grade 3 fatigue), diarrhea (total 20%, 1 patient developed grade 3 fatigue), reversible grade 3 cardiotoxicity (1 patient), and grade V liver toxicity from hepatitis B reactivation (1 patient).
   CONCLUSION: Our results of Rapa, HCQ and chemotherapy triplet combination suggest autophagy is a promising oncotarget and warrants further investigation in phase II studies.
C1 [Chi, Kwan-Hwa; Ko, Hui-Ling; Yang, Kai-Lin; Lee, Cheng-Yen; Chi, Mau-Shin] Shin Kong Wu Ho Su Mem Hosp, Dept Radiat Therapy & Oncol, Taipei, Taiwan.
   [Chi, Kwan-Hwa] Natl Yang Ming Univ, Sch Med, Taipei 112, Taiwan.
   [Chi, Kwan-Hwa] Natl Yang Ming Univ, Inst Biomed Imaging & Radiol Sci, Taipei 112, Taiwan.
   [Kao, Shang-Jyh] Shin Kong Wu Ho Su Mem Hosp, Div Chest Med, Taipei, Taiwan.
RP Chi, KH (corresponding author), Shin Kong Wu Ho Su Mem Hosp, Dept Radiat Therapy & Oncol, Taipei, Taiwan.
EM M006565@ms.skh.org.tw; M001002@ms.skh.org.tw
RI Yang, Kai-Lin/AAG-2047-2020
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NR 48
TC 24
Z9 28
U1 0
U2 4
PU IMPACT JOURNALS LLC
PI ORCHARD PARK
PA 6666 E QUAKER ST, STE 1, ORCHARD PARK, NY 14127 USA
EI 1949-2553
J9 ONCOTARGET
JI Oncotarget
PD JUN 30
PY 2015
VL 6
IS 18
BP 16735
EP 16745
DI 10.18632/oncotarget.3793
PG 11
WC Oncology; Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Cell Biology
GA CO2UL
UT WOS:000359012000094
PM 25944689
OA Green Published, gold, Green Submitted
DA 2022-04-25
ER

PT J
AU Ni, CL
   Li, BL
   Ding, YY
   Wu, Y
   Wang, QY
   Wang, JR
   Cheng, JJ
AF Ni, Chunlei
   Li, Bailiang
   Ding, Yangyue
   Wu, Yue
   Wang, Qiuye
   Wang, Jiarong
   Cheng, Jianjun
TI Anti-Cancer Properties of Coix Seed Oil against HT-29 Colon Cells
   through Regulation of the PI3K/AKT Signaling Pathway
SO FOODS
LA English
DT Article
DE coix seed oil; anti-colon cancer; cell cycle; apoptosis; PI3K/AKT
ID HEPATOCELLULAR-CARCINOMA; APOPTOSIS INDUCTION; CYCLE ARREST; FATTY-ACID;
   INHIBITION; DOXORUBICIN; AUTOPHAGY; CHICKENS; EXTRACT; GROWTH
AB This study aims to observe the effects of coix seed oil (CSO) on HT-29 cells and investigate its possible regulation mechanism of the PI3K/Akt signaling pathway. Fatty acid analysis showed that coix seed oil mainly contains oleic acid (50.54%), linoleic acid (33.76%), palmitic acid (11.74%), and stearic acid (2.45%). Fourier transform infrared results found that the fatty acid functional groups present in the oil matched well with the vegetable oil band. The results from CCK-8 assays showed that CSO dose-dependently and time-dependently inhibited the viability of HT-29 cells in vitro. CSO inhibited cell viability, with IC50 values of 5.30 mg/mL for HT-29 obtained after 24 h treatment. Morphological changes were observed by apoptotic body/cell nucleus DNA (Hoechst 33258) staining using inverted and fluorescence microscopy. Moreover, flow cytometry analysis was used to evaluate the cell cycle and cell apoptosis. It showed that CSO induced cell apoptosis and cycle arrest in the G(2) phase. Quantitative real-time PCR and Western blotting revealed that CSO induced cell apoptosis by downregulating the PI3K/AKT signaling pathway. Additionally, CSO can cause apoptosis in cancer cells by activating caspase-3, up-regulating Bax, and down-regulating Bcl-2. In conclusion, the results revealed that CSO induced G(2) arrest and apoptosis of HT-29 cells by regulating the PI3K/AKT signaling pathway.
C1 [Ni, Chunlei; Li, Bailiang; Ding, Yangyue; Wu, Yue; Wang, Qiuye; Wang, Jiarong; Cheng, Jianjun] Northeast Agr Univ, Coll Food Sci, Harbin 150030, Peoples R China.
RP Cheng, JJ (corresponding author), Northeast Agr Univ, Coll Food Sci, Harbin 150030, Peoples R China.
EM jjcheng@neau.edu.cn
FU National Key Research and Development Program of China
   [2017YFD0401204-5]
FX FundingThis research was funded by the National Key Research and
   Development Program of China, grant number 2017YFD0401204-5.
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NR 57
TC 0
Z9 0
U1 7
U2 7
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 2304-8158
J9 FOODS
JI Foods
PD NOV
PY 2021
VL 10
IS 11
AR 2833
DI 10.3390/foods10112833
PG 16
WC Food Science & Technology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Food Science & Technology
GA XG9XS
UT WOS:000725099200001
PM 34829119
OA Green Published, gold
DA 2022-04-25
ER

PT J
AU Brun, S
   Pascussi, JM
   Gifu, EP
   Bestion, E
   Macek-Jilkova, Z
   Wang, GX
   Bassissi, F
   Mezouar, S
   Courcambeck, J
   Merle, P
   Decaens, T
   Pannequin, J
   Halfon, P
   de Fromentel, CC
AF Brun, Sonia
   Pascussi, Jean-Marc
   Gifu, Elena Patricia
   Bestion, Eloine
   Macek-Jilkova, Zuzana
   Wang, Guanxiong
   Bassissi, Firas
   Mezouar, Soraya
   Courcambeck, Jerome
   Merle, Philippe
   Decaens, Thomas
   Pannequin, Julie
   Halfon, Philippe
   de Fromentel, Claude Caron
TI GNS561, a New Autophagy Inhibitor Active against Cancer Stem Cells in
   Hepatocellular Carcinoma and Hepatic Metastasis from Colorectal Cancer
SO JOURNAL OF CANCER
LA English
DT Article
DE GNS561; cancer stem cell; liver cancer; colorectal cancer; lysosome;
   therapy
ID CHEMORESISTANCE; SALINOMYCIN; RESISTANCE
AB Patients with advanced hepatocellular carcinoma (HCC) or metastatic colorectal cancer (mCRC) have a very poor prognosis due to the lack of efficient treatments. As observed in several other tumors, the effectiveness of treatments is mainly hampered by the presence of a highly tumorigenic sub-population of cancer cells called cancer stem cells (CSCs). Indeed, CSCs are resistant to chemotherapy and radiotherapy and can regenerate the tumor bulk. Hence, innovative drugs that are efficient against both bulk tumor cells and CSCs would likely improve cancer treatment. In this study, we demonstrated that GNS561, a new autophagy inhibitor that induces lysosomal cell death, showed significant activity against not only the whole tumor population but also a sub-population displaying CSC features (high ALDH activity and tumorsphere formation ability) in HCC and in liver mCRC cell lines. These results were confirmed in vivo in HCC from a DEN-induced cirrhotic rat model in which GNS561 decreased tumor growth and reduced the frequency of CSCs (CD90(+)CD45(-)). Thus, GNS561 offers great promise for cancer therapy by exterminating both the tumor bulk and the CSC sub-population. Accordingly, a global phase 1b clinical trial in liver cancers was recently completed.
C1 [Brun, Sonia; Bestion, Eloine; Bassissi, Firas; Mezouar, Soraya; Courcambeck, Jerome; Halfon, Philippe] Genosci Pharma, 10 Rue Iena, F-13006 Marseille, France.
   [Pascussi, Jean-Marc; Pannequin, Julie] Univ Montpellier, IGF, CNRS, INSERM, Montpellier, France.
   [Gifu, Elena Patricia; Wang, Guanxiong; Merle, Philippe; de Fromentel, Claude Caron] Univ Lyon 1 Ctr Leon Berard, CRCL, INSERM, CNRS 5286,U1052, Lyon, France.
   [Bestion, Eloine] Aix Marseille Univ, IHU Mediterranee Infect, AP HM, MEPHI,IRD, Marseille, France.
   [Macek-Jilkova, Zuzana; Decaens, Thomas] Inst Adv Biosci, Res Ctr UGA, INSERM, U1209,CNRS 5309, La Tronche, France.
   [Macek-Jilkova, Zuzana; Decaens, Thomas] Univ Grenoble Alpes, Fac Med, Grenoble, France.
   [Macek-Jilkova, Zuzana; Decaens, Thomas] CHU Grenoble, Clin Univ Hepatogastroenterol, Pole Digidune, Grenoble, France.
   [Merle, Philippe] Hosp Civils Lyon, Hepatol & Gastroenterol Unit, Croix Rousse Hosp, Lyon, France.
RP Brun, S; Halfon, P (corresponding author), Genosci Pharma, 10 Rue Iena, F-13006 Marseille, France.; de Fromentel, CC (corresponding author), CRCL, INSERM, U1052, 151 Cours A Thomas, F-69003 Lyon, France.
EM brun.sonia@hotmail.fr; phalfon@genosciencepharma.com;
   claude.de-fromentel@inserm.fr
RI Macek Jílková, Zuzana/N-4051-2014
OI Macek Jílková, Zuzana/0000-0002-2553-5971
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NR 51
TC 2
Z9 2
U1 0
U2 2
PU IVYSPRING INT PUBL
PI LAKE HAVEN
PA PO BOX 4546, LAKE HAVEN, NSW 2263, AUSTRALIA
SN 1837-9664
J9 J CANCER
JI J. Cancer
PY 2021
VL 12
IS 18
BP 5432
EP 5438
DI 10.7150/jca.58533
PG 7
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA TI4XG
UT WOS:000672805200007
PM 34405006
OA Green Submitted, Green Published, gold
DA 2022-04-25
ER

PT J
AU Su, CC
AF Su, Chin-Cheng
TI Sann-Joong-Kuey-Jian-Tang decreases the protein expression of mammalian
   target of rapamycin but increases microtubule associated protein II
   light chain 3 expression to inhibit human BxPC-3 pancreatic carcinoma
   cells
SO MOLECULAR MEDICINE REPORTS
LA English
DT Article
DE Sann-Joong-Kuey-Jian-Tang; mammalian target of rapamycin; microtubule
   associated protein II light chain 3; autophagy; human pancreatic
   carcinoma BxPC-3 cells
ID TNF-ALPHA; CANCER CELLS; AUTOPHAGY; DEATH; MCL-1; TCTP; BAX
AB Sann-Joong-Kuey-Jian-Tang (SJKJT), a Traditional Chinese Medicinal prescription, has been used for the treatment of lymphadenopathy and solid tumors, and has shown therapeutic potential in a number of human malignant tumor cell lines, such as Hep-G2 hepatocellular carcinoma cells. Previous mechanistic studies demonstrated that SJKJT inhibited the proliferation of BxPC-3 pancreatic carcinoma cells through the extrinsic and intrinsic apoptotic pathways in vitro. SJKJT was also shown to be cytotoxic to colo 205 colon cancer cells by inducing autophagy in vitro. The present study therefore investigated molecular mechanisms of autophagy in human BxPC-3 pancreatic cancer cells treated with SJKJT. The cytotoxic effects of SJKJT on BxPC-3 human pancreatic carcinoma cells were evaluated using an MTT assay. Furthermore, the expression of autophagy-associated proteins, including mammalian target of rapamycin (mTOR), beclin-1, autophagocytosis-associated protein (Atg)3, Atg7, Atg5-Atg12 and microtubule-associated protein II light chain 3 (LC3-II), was assessed using western blot analysis. The results demonstrated that BxPC-3 cells treated with SJKJT exhibited decreased expression levels of mTOR and increased expression of LC3-II protein. In addition, the expression of the beclin-1, Atg3, Atg7 and Atg5-Atg12 proteins was increased during the first 24 h, but decreased from 48 to 72 h. The results showed that SJKJT inhibited the proliferation of human BxPC-3 pancreatic cancer cells in vitro. A possible underlying molecular mechanism may be the induction of autophagy. Further investigation into the therapeutic potential of SJKJT in human pancreatic cancer is required.
C1 [Su, Chin-Cheng] Changhua Christian Hosp, Tumor Res Ctr Integrat Med, Changhua 50006, Taiwan.
   [Su, Chin-Cheng] Changhua Christian Hosp, Comprehens Breast Canc Ctr, Changhua 50006, Taiwan.
   [Su, Chin-Cheng] Changhua Christian Hosp, Dept Surg, Changhua 50006, Taiwan.
   [Su, Chin-Cheng] China Med Univ, Sch Chinese Med, Coll Chinese Med, Taichung 40651, Taiwan.
RP Su, CC (corresponding author), Changhua Christian Hosp, Tumor Res Ctr Integrat Med, 135 Nan Hsiao St, Changhua 50006, Taiwan.
EM succ.maeva@msa.hinet.net
FU Changhua Christian Hospital [100-CCH-ICO-06-1]
FX This study was supported by the Changhua Christian Hospital (grant no.
   100-CCH-ICO-06-1).
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NR 16
TC 2
Z9 2
U1 0
U2 6
PU SPANDIDOS PUBL LTD
PI ATHENS
PA POB 18179, ATHENS, 116 10, GREECE
SN 1791-2997
EI 1791-3004
J9 MOL MED REP
JI Mol. Med. Rep.
PD APR
PY 2015
VL 11
IS 4
BP 3160
EP 3166
DI 10.3892/mmr.2014.3090
PG 7
WC Oncology; Medicine, Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Research & Experimental Medicine
GA CE3FG
UT WOS:000351711100112
PM 25516264
OA Bronze
DA 2022-04-25
ER

PT J
AU Pattingre, S
   De Vries, L
   Bauvy, C
   Chantret, I
   Cluzeaud, F
   Ogier-Denis, E
   Vandewalle, A
   Codogno, P
AF Pattingre, S
   De Vries, L
   Bauvy, C
   Chantret, I
   Cluzeaud, F
   Ogier-Denis, E
   Vandewalle, A
   Codogno, P
TI The g-protein regulator AGS3 controls an early event during
   macroautophagy in human intestinal HT-29 cells
SO JOURNAL OF BIOLOGICAL CHEMISTRY
LA English
DT Article
ID CONTROLS AUTOPHAGIC SEQUESTRATION; ALPHA-INTERACTING PROTEIN;
   HETEROTRIMERIC G-PROTEIN; TETRATRICOPEPTIDE REPEAT;
   SUBCELLULAR-DISTRIBUTION; DISSOCIATION INHIBITOR; RAT HEPATOCYTES; GOLGI
   MEMBRANES; LINE HT-29; VACUOLES
AB AGS3 contains GoLoco or G-protein regulatory motifs in its COOH-terminal half that stabilize the GDP-bound conformation of the alpha-subunit of the trimeric G(i3) protein. The latter is part of a signaling pathway that controls the lysosomal-autophagic catabolism in human colon cancer HT-29 cells. In the present work we show that the mRNA encoding for AGS3 is expressed in human intestinal cell lines (Caco-2 and HT-29) whatever their state of differentiation. Together with the full-length form, minute amounts of the mRNA encoding a NH2-terminal truncated form of AGS3, previously characterized in cardiac tissues, were also detected. Both the endogenous form of AGS3 and a tagged expressed form have a localization compatible with a role in the Galpha(i3)-dependent control of autophagy. Accordingly, expressing its non-Galpha(i3)-interacting NH2-terminal domain or its Galpha(i3)-interacting COOH-terminal domain reversed the stimulatory role of AGS3 on autophagy. On the basis of biochemical and morphometric analysis, we conclude that AGS3 is involved in an early event during the autophagic pathway probably prior to the formation of the autophagosome. These data demonstrate that AGS3 is a novel partner of the Galpha(i3) protein in the control of a major catabolic pathway.
C1 INSERM, U504, F-94807 Villejuif, France.
   Univ Calif San Diego, Dept Mol & Cellular Biol, La Jolla, CA 92093 USA.
   Univ Paris 07, INSERM, U478, F-75018 Paris, France.
RP Codogno, P (corresponding author), INSERM, U504, 16 Ave Paul Vaillant Couturier, F-94807 Villejuif, France.
RI Codogno, Patrice/G-1384-2013; CHANTRET, Isabelle/AAF-7134-2021;
   Ogier-Denis, Eric/E-5030-2016
OI Codogno, Patrice/0000-0002-5492-3180; CHANTRET,
   Isabelle/0000-0002-0896-1274; Pattingre, Sophie/0000-0001-6284-6050;
   Ogier-Denis, Eric/0000-0002-0057-7593
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NR 64
TC 57
Z9 58
U1 0
U2 0
PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3996 USA
SN 0021-9258
J9 J BIOL CHEM
JI J. Biol. Chem.
PD JUN 6
PY 2003
VL 278
IS 23
BP 20995
EP 21002
DI 10.1074/jbc.M300917200
PG 8
WC Biochemistry & Molecular Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology
GA 684WY
UT WOS:000183230500072
PM 12642577
OA hybrid
DA 2022-04-25
ER

PT J
AU Li, L
   Jing, LL
   Wang, JJ
   Xu, WJ
   Gong, XL
   Zhao, YY
   Ma, Y
   Yao, XQ
   Sun, XG
AF Li, Lu
   Jing, Linlin
   Wang, Junjiang
   Xu, Wenjuan
   Gong, Xianling
   Zhao, Yiye
   Ma, Ye
   Yao, Xueqing
   Sun, Xuegang
TI Autophagic flux is essential for the downregulation of D-dopachrome
   tautomerase by atractylenolide I to ameliorate intestinal adenoma
   formation
SO JOURNAL OF CELL COMMUNICATION AND SIGNALING
LA English
DT Article
DE Atractylenolide I; Autophagy; Adenoma; D-dopachrome tautomerase; p53;
   Acetylation; Sirt 1
ID MIGRATION-INHIBITORY FACTOR; COLORECTAL-CANCER; SIRT1; ACTIVATION;
   PHOSPHORYLATION; DEACETYLATION; PATHOGENESIS; HOMOLOG; COMPLEX
AB Colorectal cancer is generally believed to progress through an adenoma - carcinoma sequence. Adenomatous polyposis coli (APC) mutations serve as the initiating event in adenoma formation. The Apc(Min/+) mouse harbors a mutation in the APC gene, which is similar or identical to the mutation found in individuals with familial adenomatous polyposis and 70% of all sporadic CRC cases. Autophagy is a constitutive process required for proper cellular homeostasis. However, its role in intestinal adenoma formation is still controversial. Atractylenolide I (AT1) is a sesquiterpenoid that possesses various clinically relevant properties such as anti-tumor and anti-inflammatory activities. The role of AT1 on adenoma formation was tested in Apc(Min/+) mice and its underlying mechanism in regulating autophagy was documented. D-dopachrome tautomerase (D-DT) was identified as a potential target of AT1 by an proteomics-based approach. The effects of p53 modification on autophgic flux was monitored in p53(-/-) and p53(+/+) HCT116 cells. Small interfering RNA was used to investigate the function of Atg7 and D-DT on autophagy programme induce by AT1. AT1 effectively reduced the formation of adenoma and downregulated the tumorigenic proteins in Apc(Min/+) mice. Importantly, AT1 stimulated autophagic flux through downregulating acetylation of p53. Activation of Sirt1 by AT1 was essential for the deacetylation of p53 and downregulation of D-DT. The lowered expression of COX-2 and -catenin by AT1 were partly recovered by Atg7 knockdown. AT1 activates autophagy machinery to downregulate D-DT and reduce intestinal adenoma formation. This discovery provides evidence in vivo and in vitro that inducing autophagy by natural products maybe a potential therapy to ameliorate colorectal adenoma formation.
C1 [Li, Lu; Gong, Xianling; Ma, Ye; Sun, Xuegang] Southern Med Univ, Sch Tradit Chinese Med, Guangzhou 510515, Guangdong, Peoples R China.
   [Jing, Linlin; Zhao, Yiye; Sun, Xuegang] Southern Med Univ, TCM Integrated Hosp, Guangzhou 510315, Guangdong, Peoples R China.
   [Wang, Junjiang; Yao, Xueqing] Guangdong Gen Hosp, Dept Gastrointestinal Surg, Guangzhou 510120, Guangdong, Peoples R China.
   [Xu, Wenjuan] Binzhou Med Univ, Sch Tradit Chinese Med, Yantai 256600, Shandong, Peoples R China.
   [Gong, Xianling] Guangdong Med Univ, Sch Pharm, Dongguan 523808, Guangdong, Peoples R China.
RP Sun, XG (corresponding author), Southern Med Univ, Sch Tradit Chinese Med, Guangzhou 510515, Guangdong, Peoples R China.; Sun, XG (corresponding author), Southern Med Univ, TCM Integrated Hosp, Guangzhou 510315, Guangdong, Peoples R China.
EM 549812447@qq.com; jll47379@163.com; langyisheng6726582@qq.com;
   xwjycd@163.com; 1290064145@qq.com; 1056882895@qq.com; 915242251@qq.com;
   yjb9211@21cn.com; sxg_smu@126.com
OI SUN, Xuegang/0000-0001-6581-0520
FU National Science Foundation of ChinaNational Natural Science Foundation
   of China (NSFC) [81573848, 81774172, 81472315]; Guangdong Natural
   Science FoundationNational Natural Science Foundation of Guangdong
   Province [2014A030313323]; Planned Science Technology Project of
   Guangzhou [201607010146]; Guangdong Province Bureau of Traditional
   Chinese Medicine Scientific Research Project [20151024, 20161161]
FX Founed by the National Science Foundation of China (81573848, 81774172,
   81472315), Guangdong Natural Science Foundation (2014A030313323),
   Planned Science Technology Project of Guangzhou (201607010146),
   Guangdong Province Bureau of Traditional Chinese Medicine Scientific
   Research Project (No: 20151024, 20161161).
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NR 36
TC 2
Z9 3
U1 2
U2 15
PU SPRINGER
PI DORDRECHT
PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS
SN 1873-9601
EI 1873-961X
J9 J CELL COMMUN SIGNAL
JI J. Cell Commun. Signal
PD DEC
PY 2018
VL 12
IS 4
BP 689
EP 698
DI 10.1007/s12079-018-0454-6
PG 10
WC Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Cell Biology
GA HC7DP
UT WOS:000451961100006
PM 29368299
OA Green Published
DA 2022-04-25
ER

PT J
AU Wu, QH
   Wang, X
   Nepovimova, E
   Miron, A
   Liu, QY
   Wang, Y
   Su, DX
   Yang, HL
   Li, L
   Kuca, K
AF Wu, Qinghua
   Wang, Xu
   Nepovimova, Eugenie
   Miron, Anca
   Liu, Qianying
   Wang, Yun
   Su, Dongxiao
   Yang, Hualin
   Li, Li
   Kuca, Kamil
TI Trichothecenes: immunomodulatory effects, mechanisms, and anti-cancer
   potential
SO ARCHIVES OF TOXICOLOGY
LA English
DT Review
DE T-2 toxin; Deoxynivalenol; Immunomodulation; Anti-cancer; Signaling
   pathway; Autophagy; Immune evasion
ID RESPIRATORY SYNDROME VIRUS; RIBOTOXIC STRESS-RESPONSE; ACTIVATED
   PROTEIN-KINASE; TRAIL-INDUCED APOPTOSIS; STEROID-RECEPTOR COACTIVATOR-3;
   DEOXYNIVALENOL DON MYCOTOXIN; SYSTEMIC-LUPUS-ERYTHEMATOSUS; NATURALLY
   CONTAMINATED FEED; HYPOXIA-INDUCIBLE FACTOR-1; MESSENGER-RNA EXPRESSION
AB Paradoxically, trichothecenes have both immunosuppressive and immunostimulatory effects. The underlying mechanisms have not been fully explored. Early studies show that dose, exposure timing, and the time at which immune function is assessed influence whether trichothecenes act in an immunosuppressive or immunostimulatory fashion. Recent studies suggest that the immunomodulatory function of trichothecenes is also actively shaped by competing cell-survival and death-signaling pathways. Autophagy may also promote trichothecene immunosuppression, although the mechanism may be complicated. Moreover, trichothecenes may generate an "immune evasion" milieu that allows pathogens to escape host and vaccine immune defenses. Some trichothecenes, especially macrocyclic trichothecenes, also potently kill cancer cells. T-2 toxin conjugated with anti-cancer monoclonal antibodies significantly suppresses the growth of thymoma EL-4 cells and colon cancer cells. The type B trichothecene diacetoxyscirpenol specifically inhibits the tumor-promoting factor HIF-1 in cancer cells under hypoxic conditions. Trichothecin markedly inhibits the growth of multiple cancer cells with constitutively activated NF-kappa B. The type D macrocyclic toxin Verrucarin A is also a promising therapeutic candidate for leukemia, breast cancer, prostate cancer, and pancreatic cancer. The anti-cancer activities of trichothecenes have not been comprehensively summarized. Here, we first summarize the data on the immunomodulatory effects of trichothecenes and discuss recent studies that shed light on the underlying cellular and molecular mechanisms. These mechanisms include autophagy and major signaling pathways and their crosstalk. Second, the anti-cancer potential of trichothecenes and the underlying mechanisms will be discussed. We hope that this review will show how trichothecene bioactivities can be exploited to generate therapies against pathogens and cancer.
C1 [Wu, Qinghua; Wang, Yun; Su, Dongxiao; Yang, Hualin; Li, Li] Yangtze Univ, Inst Biomed, Coll Life Sci, Jingzhou 434025, Peoples R China.
   [Wu, Qinghua; Nepovimova, Eugenie; Kuca, Kamil] Univ Hradec Kralove, Dept Chem, Fac Sci, Hradec Kralove, Czech Republic.
   [Wang, Xu; Liu, Qianying] Huazhong Agr Univ, Natl Reference Lab Vet Drug Residues HZAU, Wuhan 430070, Hubei, Peoples R China.
   [Wang, Xu; Liu, Qianying] Huazhong Agr Univ, MAO Key Lab Detect Vet Drug Residues, Wuhan 430070, Hubei, Peoples R China.
   [Miron, Anca] Univ Med & Pharm Grigore T Popa, Dept Pharmacognosy, Fac Pharm, Iasi, Romania.
RP Wu, QH (corresponding author), Yangtze Univ, Inst Biomed, Coll Life Sci, Jingzhou 434025, Peoples R China.; Wu, QH; Kuca, K (corresponding author), Univ Hradec Kralove, Dept Chem, Fac Sci, Hradec Kralove, Czech Republic.
EM wqh212@hotmail.com; kamil.kuca@uhk.cz
RI Nepovimova, Eugenie/AAU-7268-2020; Kuca, Kamil/D-1396-2011
OI Nepovimova, Eugenie/0000-0003-0281-246X; Kuca, Kamil/0000-0001-9664-1109
FU National Natural Science Foundation of ChinaNational Natural Science
   Foundation of China (NSFC) [31602114, 31572575]; Yangtze Fund for Youth
   Teams of Science and Technology Innovation [2016cqt02]; Fundamental
   Research Funds for the Central UniversitiesFundamental Research Funds
   for the Central Universities [2662016PY115]; project of long-term
   development plan UHK
FX This work was supported by the National Natural Science Foundation of
   China (Grant No. 31602114 and 31572575), the Yangtze Fund for Youth
   Teams of Science and Technology Innovation (2016cqt02), the Fundamental
   Research Funds for the Central Universities (2662016PY115), and the
   project of long-term development plan UHK.
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NR 275
TC 60
Z9 61
U1 4
U2 71
PU SPRINGER HEIDELBERG
PI HEIDELBERG
PA TIERGARTENSTRASSE 17, D-69121 HEIDELBERG, GERMANY
SN 0340-5761
EI 1432-0738
J9 ARCH TOXICOL
JI Arch. Toxicol.
PD DEC
PY 2017
VL 91
IS 12
BP 3737
EP 3785
DI 10.1007/s00204-017-2118-3
PG 49
WC Toxicology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Toxicology
GA FP0CJ
UT WOS:000417266400002
PM 29152681
DA 2022-04-25
ER

PT J
AU Sivridis, E
   Koukourakis, MI
   Mendrinos, SE
   Karpouzis, A
   Fiska, A
   Kouskoukis, C
   Giatromanolaki, A
AF Sivridis, Efthimios
   Koukourakis, Michael I.
   Mendrinos, Savvas E.
   Karpouzis, Antonios
   Fiska, Aliki
   Kouskoukis, Constantinos
   Giatromanolaki, Alexandra
TI Beclin-1 and LC3A expression in cutaneous malignant melanomas: a
   biphasic survival pattern for beclin-1
SO MELANOMA RESEARCH
LA English
DT Article
DE autophagy; beclin 1; cutaneous malignant melanoma; hypoxia; light chain
   3A
ID COLORECTAL-CANCER; PROGNOSTIC-SIGNIFICANCE; INDUCED AUTOPHAGY;
   CELL-DEATH; HYPOXIA; PROTEIN; GENE; METASTASIS; TOLERANCE;
   MICROENVIRONMENT
AB Autophagy is an intracellular pathway for the degradation of long-lived proteins and damaged organelles. It is, in essence, a recycling process allowing cells to survive oxygen and nutrient depletion. The expression of two autophagy-related proteins, beclin 1 and light chain 3A (LC3A) was investigated in 79 nodular cutaneous melanomas. The results were correlated with histopathological factors, vascular density, and hypoxia-related proteins [hypoxia-inducible factors (HIF1 alpha and HIF2 alpha) and lactate dehydrogenase 5]. The reactivity of both autophagy-related proteins was uniformly cytoplasmically diffused. High beclin 1 and LC3A reactivity was related to tumor hypoxia, as this was inferred from the intense expression of HIF1a and lactate dehydrogenase 5, whereas low beclin 1 and LC3A expression was linked with an increased vascular density. In addition, beclin 1 was related to disease-specific survival which, however, exposed a biphasic pattern. A strong beclin 1 expression extending over a tumor area of more than 50% (high) was associated with an increased rate of early deaths, whereas a similarly strong, but less-extensive cytoplasmic reactivity (< 10% tumor area; low) defined a sharp fall in the survival 5 years after surgery. Furthermore, the low beclin 1 expression was associated with high Breslow's depth, high Clark's level, and ulceration. Low LC3A expression was also related to ulceration, but not to other histopathological features nor prognosis. In multivariate analysis, beclin 1 was an independent prognostic variable. It is concluded that extensive autophagic activity is generated by tumor hypoxia and anaerobic glycolysis, whereas angiogenesis maintains low autophagic activity. Atg6/beclin 1 was proved to be capable of deciphering the prognosis in cutaneous malignant melanoma, but the matter requires further investigation. Melanoma Res 21:188-195 (C) 2011 Wolters Kluwer Health vertical bar Lippincott Williams & Wilkins.
C1 [Sivridis, Efthimios; Fiska, Aliki; Giatromanolaki, Alexandra] Democritus Univ Thrace, Sch Med, Dept Pathol, Alexandroupolis 68100, Greece.
   [Koukourakis, Michael I.] Democritus Univ Thrace, Sch Med, Dept Radiotherapy Oncol, Alexandroupolis 68100, Greece.
   [Karpouzis, Antonios; Kouskoukis, Constantinos] Democritus Univ Thrace, Sch Med, Dept Dermatol, Alexandroupolis 68100, Greece.
   Univ Gen Hosp Alexandroupolis, Alexandroupolis 68100, Greece.
   [Mendrinos, Savvas E.] NYU, Sch Med, Langone Med Ctr, Dept Pathol, New York, NY USA.
RP Giatromanolaki, A (corresponding author), Democritus Univ Thrace, Sch Med, Dept Pathol, POB 12, Alexandroupolis 68100, Greece.
EM agiatrom@med.duth.gr
RI Fiska, Aliki/ABE-7231-2020
OI Fiska, Aliki/0000-0003-1787-6116
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NR 74
TC 60
Z9 64
U1 0
U2 9
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA TWO COMMERCE SQ, 2001 MARKET ST, PHILADELPHIA, PA 19103 USA
SN 0960-8931
EI 1473-5636
J9 MELANOMA RES
JI Melanoma Res.
PD JUN
PY 2011
VL 21
IS 3
BP 188
EP 195
DI 10.1097/CMR.0b013e328346612c
PG 8
WC Oncology; Dermatology; Medicine, Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Dermatology; Research & Experimental Medicine
GA 758EO
UT WOS:000290144400004
PM 21537144
DA 2022-04-25
ER

PT J
AU Zhao, Y
   Guo, QL
   Zhao, K
   Zhou, YX
   Li, WJ
   Pan, CY
   Qiang, L
   Li, ZY
   Lu, N
AF Zhao, Yue
   Guo, Qinglong
   Zhao, Kai
   Zhou, Yuxin
   Li, Wenjun
   Pan, Chuyue
   Qiang, Lei
   Li, Zhiyu
   Lu, Na
TI Small molecule GL-V9 protects against colitis-associated colorectal
   cancer by limiting NLRP3 inflammasome through autophagy
SO ONCOIMMUNOLOGY
LA English
DT Article
DE autophagy; colitis-associated colorectal cancer; colitis; GL-V9; NLRP3
   inflammasome
ID ULCERATIVE-COLITIS; INTESTINAL INFLAMMATION; CROHNS-DISEASE;
   BOWEL-DISEASE; RISK-FACTOR; INNATE; MECHANISMS; EXPRESSION;
   PHOSPHORYLATION; CARCINOGENESIS
AB Emerging evidence suggests that NLRP3 inflammasome provides a link between colitis-associated colorectal cancer and inflammatory bowel diseases. Autophagy is induced in macrophages by AMPK activation and regulates NLRP3 inflammasome to maintain intracellular homeostasis. Here we report that a small-molecule AMPK activator (GL-V9) exerts potent anti-inflammatory effects on macrophages invitro and in vivo, which trigger autophagy to degraded NLRP3 inflammasome. Treatment with GL-V9 protected against colitis and tumorigenesis in colitis-associated colorectal cancer. This suggests that GL-V9 may be an interesting candidate for clinical evaluation in the treatment of colitis-associated colorectal cancer.
C1 [Zhao, Yue; Guo, Qinglong; Zhao, Kai; Zhou, Yuxin; Li, Wenjun; Pan, Chuyue; Lu, Na] China Pharmaceut Univ, Jiangsu Key Lab Drug Design & Optimizat, Jiangsu Key Lab Carcinogenesis & Intervent, State Key Lab Nat Med, 24 Tongjiaxiang, Nanjing, Jiangsu, Peoples R China.
   [Li, Zhiyu] China Pharmaceut Univ, Sch Pharm, 24 Tongjiaxiang, Nanjing, Jiangsu, Peoples R China.
   [Qiang, Lei] Univ Chicago, Dept Med, Sect Dermatol, 5841 S Maryland Ave, Chicago, IL 60637 USA.
RP Lu, N (corresponding author), China Pharmaceut Univ, State Key Lab Nat Med, 24 Tongjiaxiang, Nanjing 210009, Jiangsu, Peoples R China.
EM luna555@163.com
RI Qiang, Lei/B-2763-2012
OI Qiang, Lei/0000-0002-7164-3164
FU National Science & Technology Major Project [2012ZX09304-001,
   2013ZX09103-001-007]; Program for Changjiang Scholars and Innovative
   Research Team in UniversityProgram for Changjiang Scholars & Innovative
   Research Team in University (PCSIRT) [IRT1193]; National Natural Science
   Foundation of ChinaNational Natural Science Foundation of China (NSFC)
   [91029744, 81373448, 81373449]; Project Program of State Key Laboratory
   of Natural Medicines, China Pharmaceutical University [SKLNMZZCX201606]
FX This work was supported by the National Science & Technology Major
   Project (No. 2012ZX09304-001, No. 2013ZX09103-001-007), Program for
   Changjiang Scholars and Innovative Research Team in University
   (IRT1193), the National Natural Science Foundation of China (No.
   91029744, No. 81373448 and No. 81373449), the Project Program of State
   Key Laboratory of Natural Medicines, China Pharmaceutical University
   (NO. SKLNMZZCX201606).
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NR 50
TC 25
Z9 29
U1 6
U2 43
PU TAYLOR & FRANCIS INC
PI PHILADELPHIA
PA 530 WALNUT STREET, STE 850, PHILADELPHIA, PA 19106 USA
SN 2162-402X
J9 ONCOIMMUNOLOGY
JI OncoImmunology
PY 2018
VL 7
IS 1
AR e1375640
DI 10.1080/2162402X.2017.1375640
PG 14
WC Oncology; Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Immunology
GA FU8CP
UT WOS:000424080200017
PM 29296531
OA Green Published, gold
DA 2022-04-25
ER

PT J
AU Zhao, HD
   Chen, DL
   Cao, R
   Wang, SQ
   Yu, DD
   Liu, YK
   Jiang, Y
   Xu, M
   Luo, J
   Wang, SY
AF Zhao, Haodong
   Chen, Danlei
   Cao, Rui
   Wang, Shiqing
   Yu, Dandan
   Liu, Yakun
   Jiang, Yu
   Xu, Mei
   Luo, Jia
   Wang, Siying
TI Alcohol consumption promotes colorectal carcinoma metastasis via a
   CCL5-induced and AMPK-pathway-mediated activation of autophagy
SO SCIENTIFIC REPORTS
LA English
DT Article
ID BREAST-CANCER CELLS; PROTEIN-KINASE; CHEMOKINE CCL5; ENERGY SENSOR;
   INVASION; MIGRATION; INHIBITION; STATISTICS; MICROGLIA; BEVERAGES
AB There is a definite relationship between alcohol consumption and colorectal cancer (CRC) development. We investigated effect of alcohol consumption on CRC patients' progression and prognosis by utilizing epidemiological data and found patients with alcohol consumption increased risks of tumor-node-metastasis (TNM), organ metastasis and poorer prognosis. Because their tumor tissues displayed increased expression of C-C chemokine ligand 5 (CCL5), we hypothesized CCL5 might participate in cancer progression in such patients. Ethanol increased the secretion of CCL5 in two CRC cell lines, HT29 and DLD-1. Treatment with CCL5 directly increased migratory ability of these cells, whereas neutralization or knockdown of CCL5 can partially block alcohol-stimulated migration. We further investigated underlying mechanism of CCL5-induced migration. Our results indicated that effects of CCL5 on migration are mediated by the ability of CCL5 to induce autophagy, a cellular process known to be critical for migration. Using high-throughput sequencing and western blotting, we found induction of autophagy by CCL5 takes place via AMPK pathway. Aforementioned ethanol increases CCL5 secretion, CCL5 activates autophagy through AMPK pathway, and autophagy increases migration was confirmed by experiments with autophagy or AMPK inhibitors. To sum up, our study demonstrates that chronic alcohol consumption may promote metastasis of CRC through CCL5-induced autophagy.
C1 [Zhao, Haodong; Chen, Danlei; Cao, Rui; Wang, Shiqing; Yu, Dandan; Liu, Yakun; Jiang, Yu; Wang, Siying] Anhui Med Univ, Sch Basic Med, Dept Pathophysiol, Hefei 230032, Anhui, Peoples R China.
   [Xu, Mei; Luo, Jia] Univ Kentucky, Coll Med, Dept Pharmacol & Nutr Sci, Lexington, KY 40536 USA.
RP Wang, SY (corresponding author), Anhui Med Univ, Sch Basic Med, Dept Pathophysiol, Hefei 230032, Anhui, Peoples R China.; Luo, J (corresponding author), Univ Kentucky, Coll Med, Dept Pharmacol & Nutr Sci, Lexington, KY 40536 USA.
EM jialuo888@uky.edu; sywang@ahmu.edu.cn
OI Luo, Jia/0000-0002-6968-3618
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NR 51
TC 9
Z9 10
U1 0
U2 4
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 2045-2322
J9 SCI REP-UK
JI Sci Rep
PD JUN 5
PY 2018
VL 8
AR 8640
DI 10.1038/s41598-018-26856-w
PG 11
WC Multidisciplinary Sciences
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Science & Technology - Other Topics
GA GI1HZ
UT WOS:000434122600065
PM 29872080
OA Green Published, gold
DA 2022-04-25
ER

PT J
AU Zhao, PM
   Aguilar, AE
   Lee, JY
   Paul, LA
   Suh, JH
   Puri, L
   Zhang, M
   Beckstead, J
   Witkowski, A
   Ryan, RO
   Saba, JD
AF Zhao, Piming
   Aguilar, Ana E.
   Lee, Joanna Y.
   Paul, Lucy A.
   Suh, Jung H.
   Puri, Latika
   Zhang, Meng
   Beckstead, Jennifer
   Witkowski, Andrzej
   Ryan, Robert O.
   Saba, Julie D.
TI Sphingadienes show therapeutic efficacy in neuroblastoma in vitro and in
   vivo by targeting the AKT signaling pathway
SO INVESTIGATIONAL NEW DRUGS
LA English
DT Article
DE Sphingadienes; Sphingolipids; Neuroblastoma; PI3K; AKT; Nanoparticle
ID BONE-MARROW-TRANSPLANTATION; CHEMOPREVENTIVE SPHINGADIENES;
   AMPHOTERICIN-B; COLON-CANCER; CELL-DEATH; SPHINGOLIPIDS; CERAMIDE;
   SPHINGOSINE-1-PHOSPHATE; EXPRESSION; APOPTOSIS
AB Neuroblastoma is a childhood malignancy that accounts for approximately 15% of childhood cancer deaths. Only 20-35% of children with metastatic neuroblastoma survive with standard therapy. Identification of more effective therapies is essential to improving the outcome of children with high-stage disease. Sphingadienes (SD) are growth-inhibitory sphingolipids found in natural sources including soy. They exhibit chemopreventive activity in mouse models of colon cancer, where they mediate cytotoxicity by inhibiting key pro-carcinogenic signaling pathways. In this study, the effect of SD on neuroblastoma was analyzed. Low micromolar concentrations of SD were cytotoxic to transformed and primary neuroblastoma cells independently of N-Myc amplification status. SD induced both caspase-dependent apoptosis and autophagy in neuroblastoma cells. However, only inhibition of caspase-dependent apoptosis protected neuroblastoma cells from SD-mediated cytotoxicity. SD also inhibited AKT activation in neuroblastoma cells as shown by reduced phosphorylated AKT levels. Pre-treatment with insulin attenuated SD-mediated cytotoxicity in vitro. SD-loaded nanoparticles (NP) administered parenterally to immunodeficient mice carrying neuroblastoma xenografts resulted in cytotoxic levels of SD in the circulation and significantly reduced tumor growth compared to vehicle-treated controls. Analysis of tumor extracts demonstrated reduced AKT activation in tumors of mice treated with SD-NP compared to controls treated with empty NP. Our findings indicate SD are novel potential chemotherapeutic agents that promote neuroblastoma cell death and reduce tumorigenicity in vivo.
C1 [Zhao, Piming; Aguilar, Ana E.; Lee, Joanna Y.; Paul, Lucy A.; Suh, Jung H.; Puri, Latika; Zhang, Meng; Beckstead, Jennifer; Witkowski, Andrzej; Ryan, Robert O.; Saba, Julie D.] Childrens Hosp, Oakland Res Inst, UCSF Benioff Childrens Hosp Oakland, 5700 Martin Luther King Jr Way, Oakland, CA 94609 USA.
   [Aguilar, Ana E.] Arnold Palmer Hosp Children, 92 W Miller St MP 318 2nd floor, Orlando, FL 32806 USA.
   [Puri, Latika] St Jude Childrens Res Hosp, 262 Danny Thomas Pl, Memphis, TN 38105 USA.
RP Saba, JD (corresponding author), Childrens Hosp, Oakland Res Inst, UCSF Benioff Childrens Hosp Oakland, 5700 Martin Luther King Jr Way, Oakland, CA 94609 USA.
EM jsaba@chori.org
RI Puri, Latika/N-8120-2018
OI Witkowski, Andrzej/0000-0002-0442-4586
FU St. Baldricks Fellowship [245216]; National Institutes of HealthUnited
   States Department of Health & Human ServicesNational Institutes of
   Health (NIH) - USA [R37 HL-64159, R01CA129438, S10OD018070]; Swim Across
   America Foundation; NATIONAL CANCER INSTITUTEUnited States Department of
   Health & Human ServicesNational Institutes of Health (NIH) - USANIH
   National Cancer Institute (NCI) [R01CA129438] Funding Source: NIH
   RePORTER; NATIONAL HEART, LUNG, AND BLOOD INSTITUTEUnited States
   Department of Health & Human ServicesNational Institutes of Health (NIH)
   - USANIH National Heart Lung & Blood Institute (NHLBI) [R37HL064159]
   Funding Source: NIH RePORTER; OFFICE OF THE DIRECTOR, NATIONAL
   INSTITUTES OF HEALTHUnited States Department of Health & Human
   ServicesNational Institutes of Health (NIH) - USA [S10OD018070] Funding
   Source: NIH RePORTER
FX This study was supported by St. Baldricks Fellowship Grant 245216 (AEA),
   National Institutes of Health grants R01CA129438, S10OD018070 and Swim
   Across America Foundation (JDS) and National Institutes of Health grant
   R37 HL-64159 (ROR).
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NR 54
TC 11
Z9 11
U1 0
U2 5
PU SPRINGER
PI DORDRECHT
PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS
SN 0167-6997
EI 1573-0646
J9 INVEST NEW DRUG
JI Invest. New Drugs
PD OCT
PY 2018
VL 36
IS 5
BP 743
EP 754
DI 10.1007/s10637-017-0558-5
PG 12
WC Oncology; Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Pharmacology & Pharmacy
GA GT4LI
UT WOS:000444475200001
PM 29335887
OA Green Accepted
DA 2022-04-25
ER

PT J
AU Lee, S
   Hallis, SP
   Jung, KA
   Ryu, D
   Kwak, MK
AF Lee, Sujin
   Hallis, Steffanus Pranoto
   Jung, Kyeong-Ah
   Ryu, Dayoung
   Kwak, Mi-Kyoung
TI Impairment of HIF-1 alpha-mediated metabolic adaption by NRF2-silencing
   in breast cancer cells
SO REDOX BIOLOGY
LA English
DT Article
DE Hypoxia; Metabolism; Autophagy; HIF-1 alpha; NFE2L2/NRF2; Metabolome
ID HYPOXIA-INDUCIBLE FACTORS; AUTOPHAGY; INDUCTION; KINASE; BNIP3;
   MITOCHONDRIA; EXPRESSION; RESPONSES; OXYGEN; HIF-1
AB Hypoxia, a common element in the tumor environment, leads to Hypoxia-Inducible Factor-1 alpha (HIF-1 alpha) stabilization to modulate cellular metabolism as an adaptive response. In a previous study, we showed that inhibition of the nuclear factor erythroid 2-like-2 (NFE2L2; NRF2), a master regulator of many genes coping with electrophilic and oxidative stress, elevated the level of miR-181c and induced mitochondrial dysfunction in colon cancer cells. In this study, we demonstrate that NRF2-silencing hindered HIF-1 alpha accumulation in hypoxic breast cancer cells and subsequently suppressed hypoxia-inducible expression of glycolysis-associated glucose transporter-1, hexokinase-2, pyruvate dehydrogenase kinase-1, and lactate dehydrogenase A. HIF-1 alpha dysregulation in NRF2-silenced cancer cells was associated with miR-181c elevation. Overexpression of miR-181c in breast cancer cells blocked HIF-1 alpha accumulation and diminished hypoxia-inducible levels of glycolysis enzymes, whereas the inhibition of miR-181c in NRF2-silenced cells restored HIF-1 alpha accumulation. In a subsequent metabolomic analysis, hypoxic incubation increased the levels of metabolites involved in glycolysis and activated the pentose phosphate pathway (PPP) in control cells. However, these elevations were less pronounced in NRF2-silenced cells. In particular, hypoxic incubation increased the levels of amino acids, which implies a shift to catabolic metabolism, and the increased levels were higher in control cells than in NRF2-silenced cells. Concurrently, hypoxia activated BCL2 interacting protein 3 (BNIP3)-mediated autophagy in the control cells and tniR-181c was found to be involved in this autophagy activation. Taken together, these results show that hypoxia-induced metabolic changes to glycolysis, the PPP, and autophagy are inhibited by NRF2-silencing through miR-181c-mediated HIF-1 alpha dysregulation. Therefore, targeting NRF2/miR-181c could be an effective strategy to counteract HIF-1 alpha-orchestrated metabolic adaptation of hypoxic cancer cells.
C1 [Lee, Sujin; Hallis, Steffanus Pranoto; Ryu, Dayoung; Kwak, Mi-Kyoung] Catholic Univ Korea, Dept Pharm, Grad Sch, 43 Jibong Ro, Bucheon 14562, Gyeonggi Do, South Korea.
   [Lee, Sujin; Hallis, Steffanus Pranoto; Ryu, Dayoung; Kwak, Mi-Kyoung] Catholic Univ Korea, BK21PLUS Team Creat Leader Program Pharmac Based, Grad Sch, 43 Jibong Ro, Bucheon 14562, Gyeonggi Do, South Korea.
   [Hallis, Steffanus Pranoto] Atma Jaya Catholic Univ Indonesia, Fac Biotechnol, Jakarta 12930, Indonesia.
   [Jung, Kyeong-Ah; Kwak, Mi-Kyoung] Catholic Univ Korea, Integrated Res Inst Pharmaceut Sci, Bucheon, Gyeonggi Do, South Korea.
   [Kwak, Mi-Kyoung] Catholic Univ Korea, Coll Pharm, 43 Jibong Ro, Bucheon 14662, Gyeonggi Do, South Korea.
RP Kwak, MK (corresponding author), Catholic Univ Korea, Coll Pharm, 43 Jibong Ro, Bucheon 14662, Gyeonggi Do, South Korea.
EM mkwak@catholic.ac.kr
OI Hallis, Steffanus Pranoto/0000-0002-8841-4835
FU National Research Foundation of Korea (NRF) - Korea government (MSIP)
   [2018R1A2A1A05078894, 2015R1A2A1A10054384, 2018R1A6A1A03025108];
   BK21Plus grant of NRF - Korean government [22A20130012250]
FX This study was financially supported by a grant from the National
   Research Foundation of Korea (NRF) funded by the Korea government (MSIP)
   (2018R1A2A1A05078894, 2015R1A2A1A10054384, and 2018R1A6A1A03025108).
   This study was also supported by the BK21Plus grant of NRF funded by
   Korean government (22A20130012250).
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NR 53
TC 34
Z9 36
U1 0
U2 5
PU ELSEVIER
PI AMSTERDAM
PA RADARWEG 29, 1043 NX AMSTERDAM, NETHERLANDS
SN 2213-2317
J9 REDOX BIOL
JI Redox Biol.
PD JUN
PY 2019
VL 24
AR 101210
DI 10.1016/j.redox.2019.101210
PG 14
WC Biochemistry & Molecular Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology
GA IC8TS
UT WOS:000471255400040
PM 31078780
OA Green Published, gold
DA 2022-04-25
ER

PT J
AU Peixoto, P
   Castronovo, V
   Matheus, N
   Polese, C
   Peulen, O
   Gonzalez, A
   Boxus, M
   Verdin, E
   Thiry, M
   Dequiedt, F
   Mottet, D
AF Peixoto, P.
   Castronovo, V.
   Matheus, N.
   Polese, C.
   Peulen, O.
   Gonzalez, A.
   Boxus, M.
   Verdin, E.
   Thiry, M.
   Dequiedt, F.
   Mottet, D.
TI HDAC5 is required for maintenance of pericentric heterochromatin, and
   controls cell-cycle progression and survival of human cancer cells
SO CELL DEATH AND DIFFERENTIATION
LA English
DT Article
DE histone deacetylases; cancer cells; siRNA; autophagy; cell
   proliferation; chemotherapy
ID II HISTONE DEACETYLASES; S-PHASE PROGRESSION; DNA-REPLICATION;
   MAMMALIAN-CELLS; COLON-CANCER; CHECKPOINT; EXPRESSION; PROTEINS;
   COMPLEX; GROWTH
AB Histone deacetylases (HDACs) form a family of enzymes, which have fundamental roles in the epigenetic regulation of gene expression and contribute to the growth, differentiation, and apoptosis of cancer cells. In this study, we further investigated the biological function of HDAC5 in cancer cells. We found HDAC5 is associated with actively replicating pericentric heterochromatin during late S phase. We demonstrated that specific depletion of HDAC5 by RNA interference resulted in profound changes in the heterochromatin structure and slowed down ongoing replication forks. This defect in heterochromatin maintenance and assembly are sensed by DNA damage checkpoint pathways, which triggered cancer cells to autophagy and apoptosis, and arrested their growth both in vitro and in vivo. Finally, we also demonstrated that HDAC5 depletion led to enhanced sensitivity of DNA to DNA-damaging agents, suggesting that heterochromatin de-condensation induced by histone HDAC5 silencing may enhance the efficacy of cytotoxic agents that act by targeting DNA in vitro. Together, these results highlighted for the first time an unrecognized link between HDAC5 and the maintenance/assembly of heterochromatin structure, and demonstrated that its specific inhibition might contribute to increase the efficacy of DNA alteration-based cancer therapies in clinic. Cell Death and Differentiation (2012) 19, 1239-1252; doi: 10.1038/cdd.2012.3; published online 3 February 2012
C1 [Mottet, D.] Univ Liege, Metastasis Res Lab, GIGA Canc, B-4000 Liege, Belgium.
   [Boxus, M.] Gembloux Agro Biotech GxABT, Cellular & Mol Biol Unit, B-5030 Gembloux, Belgium.
   [Verdin, E.] Univ Calif San Francisco, Gladstone Inst Virol & Immunol, San Francisco, CA 94143 USA.
   [Thiry, M.] Univ Liege, Fac Sci, Dept Life Sci, Cell Biol Lab, B-4000 Liege, Belgium.
   [Dequiedt, F.] Univ Liege, Lab Signalisat & Interact Prote PSI, B-4000 Liege, Belgium.
   [Peixoto, P.; Castronovo, V.; Matheus, N.; Polese, C.; Peulen, O.; Gonzalez, A.; Thiry, M.; Dequiedt, F.; Mottet, D.] Univ Liege, Interdisciplinary Cluster Appl Genoprote GIGA, B-4000 Liege, Belgium.
RP Mottet, D (corresponding author), Univ Liege, Metastasis Res Lab, GIGA Canc, Pathol Bldg,B23,4, B-4000 Liege, Belgium.
EM dmottet@ulg.ac.be
RI Verdin, Eric/AAB-7999-2019; Peulen, Olivier/C-1250-2018
OI Peulen, Olivier/0000-0002-6933-0134; Peixoto, Paul/0000-0001-6302-7823;
   Verdin, Eric/0000-0003-3703-3183; Dequiedt, Franck/0000-0003-1234-7477
FU National Fund for Scientific Research (FNRS) (Belgium)Fonds de la
   Recherche Scientifique - FNRS; Centre Anti-Cancereux pres de
   l'Universite de Liege; Fonds Leon Fredericq; TELEVIE; NATIONAL INSTITUTE
   OF ALLERGY AND INFECTIOUS DISEASESUnited States Department of Health &
   Human ServicesNational Institutes of Health (NIH) - USANIH National
   Institute of Allergy & Infectious Diseases (NIAID) [P30AI027763] Funding
   Source: NIH RePORTER
FX This work was supported by grants from the National Fund for Scientific
   Research (FNRS) (Belgium), the Centre Anti-Cancereux pres de
   l'Universite de Liege, the Fonds Leon Fredericq, and TELEVIE. D Mottet
   and F Dequiedt are Research Associates at the National Fund for
   Scientific Research (FNRS). M Boxus is Postdoctoral Researcher at the
   FNRS. N Matheus is an FRIA Fellow. A Gonzalez is TELEVIE Fellow. We
   thank Dr D DiPaola for expert advice on the nascent-strand DNA abundance
   assay.
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NR 40
TC 47
Z9 48
U1 0
U2 10
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 1350-9047
J9 CELL DEATH DIFFER
JI Cell Death Differ.
PD JUL
PY 2012
VL 19
IS 7
BP 1239
EP 1252
DI 10.1038/cdd.2012.3
PG 14
WC Biochemistry & Molecular Biology; Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Cell Biology
GA 959EJ
UT WOS:000305295300015
PM 22301920
OA Green Published, Bronze
DA 2022-04-25
ER

PT J
AU Alves-Fernandes, DK
   Jasiulionis, MG
AF Alves-Fernandes, Debora Kristina
   Jasiulionis, Miriam Galvonas
TI The Role of SIRT1 on DNA Damage Response and Epigenetic Alterations in
   Cancer
SO INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
LA English
DT Review
DE SIRT1; DNA damage; repair; epigenetics; cancer development
ID OXIDATIVE STRESS; WERNER-SYNDROME; HISTONE H2AX; GENOMIC STABILITY;
   TUMOR-SUPPRESSOR; REACTIVE OXYGEN; REPAIR PROTEINS; EXCISION-REPAIR;
   DEACETYLATION; GENE
AB Sirtuin-1 (SIRT1) is a class-III histone deacetylase (HDAC), an NAD+-dependent enzyme deeply involved in gene regulation, genome stability maintenance, apoptosis, autophagy, senescence, proliferation, aging, and tumorigenesis. It also has a key role in the epigenetic regulation of tissue homeostasis and many diseases by deacetylating both histone and non-histone targets. Different studies have shown ambiguous implications of SIRT1 as both a tumor suppressor and tumor promoter. However, this contradictory role seems to be determined by the cell type and SIRT1 localization. SIRT1 upregulation has already been demonstrated in some cancer cells, such as acute myeloid leukemia (AML) and primary colon, prostate, melanoma, and non-melanoma skin cancers, while SIRT1 downregulation was described in breast cancer and hepatic cell carcinomas. Even though new functions of SIRT1 have been characterized, the underlying mechanisms that define its precise role on DNA damage and repair and their contribution to cancer development remains underexplored. Here, we discuss the recent findings on the interplay among SIRT1, oxidative stress, and DNA repair machinery and its impact on normal and cancer cells.
C1 [Alves-Fernandes, Debora Kristina; Jasiulionis, Miriam Galvonas] Univ Fed Sao Paulo, Escola Paulista Med, Dept Pharmacol, BR-04039032 Sao Paulo, Brazil.
RP Jasiulionis, MG (corresponding author), Univ Fed Sao Paulo, Escola Paulista Med, Dept Pharmacol, BR-04039032 Sao Paulo, Brazil.
EM mjasiulionis@gmail.com
RI Jasiulionis, Miriam/G-2207-2012; Alves-Fernandes, Debora
   Kristina/AAC-5983-2019; Alves-Fernandes, Débora Kristina/AAQ-3385-2020
OI Jasiulionis, Miriam/0000-0002-4135-0440; Alves-Fernandes, Débora
   Kristina/0000-0002-0917-9292
FU FAPESPFundacao de Amparo a Pesquisa do Estado de Sao Paulo (FAPESP);
   CNPqConselho Nacional de Desenvolvimento Cientifico e Tecnologico (CNPQ)
   [400036/2016-9]; CAPESCoordenacao de Aperfeicoamento de Pessoal de Nivel
   Superior (CAPES); Coordenacao de Aperfeicoamento de Pessoal de Nivel
   Superior-Brasil (Capes)Coordenacao de Aperfeicoamento de Pessoal de
   Nivel Superior (CAPES) [001]
FX This research was funded by FAPESP, CNPq (grant number 400036/2016-9)
   and CAPES (Post-Doctoral Fellow)". This study was financed in part by
   the Coordenacao de Aperfeicoamento de Pessoal de Nivel Superior-Brasil
   (Capes)-Finance Code 001.
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NR 110
TC 81
Z9 85
U1 6
U2 12
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
SN 1422-0067
J9 INT J MOL SCI
JI Int. J. Mol. Sci.
PD JUL 1
PY 2019
VL 20
IS 13
AR 3153
DI 10.3390/ijms20133153
PG 13
WC Biochemistry & Molecular Biology; Chemistry, Multidisciplinary
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Chemistry
GA IL1EG
UT WOS:000477041100041
PM 31261609
OA Green Submitted, Green Published, gold
DA 2022-04-25
ER

PT J
AU Dai, XY
   Zhou, BF
   Xie, YY
   Lou, J
   Li, KQ
AF Dai, Xiao-Yu
   Zhou, Bao-Feng
   Xie, Yang-Yang
   Lou, Jie
   Li, Ke-Qiang
TI Bufalin and 5-fluorouracil synergistically induce apoptosis in
   colorectal cancer cells
SO ONCOLOGY LETTERS
LA English
DT Article
DE colorectal cancer; 5-fluorouracil; bufalin; apoptosis; B-cell
   lymphoma-2-associated X protein
ID HEPATOCELLULAR-CARCINOMA; OSTEOSARCOMA CELLS; CYCLE ARREST; LUNG-CANCER;
   STEM-CELLS; CHEMOTHERAPY; ACTIVATION; MECHANISMS; AUTOPHAGY; PATHWAYS
AB 5-fluorouracil (5-FU) has been used in the treatment of colorectal cancer for >50 years. However, drug resistance remains an obstacle in the application of 5-FU-based chemotherapy. Bufalin, a type of steroid with anti-tumor activity, may be purified from the skin and parotid venom glands of toads. In order to improve the anti-tumor effect of 5-FU, the present study examined the combined effects of bufalin with 5-FU on human colorectal cancer HCT116 cells. Following treatment, cell proliferation was quantified using MIT assay and apoptotic cell percentage was assessed by flow cytometry. The apoptosis-associated protein expression was evaluated by western blotting. It was observed that bufalin enhanced the cytotoxicity of 5-FU in HCT116 cells via the induction of the mitochondria' apoptotic pathway. Additionally, bufalin combined with 5-FU reduced the expression levels of anti-apoptotic proteins, such as Mcl-1, XIAP and Bcl-2 and upregulated the levels of the pro-apoptotic proteins, Bax and Bad. To verify the role of Bax, RNA interference was used to knock-down Bax. It was determined that the synergistic effect between 5-FU and bufalin was diminished following the silencing of Bax. In summary, bufalin in combination with 5-FU may induce a higher level of apoptosis compared with monotherapy, and the combination mat be a potential therapeutic strategy for the treatment of colorectal cancer.
C1 [Dai, Xiao-Yu; Zhou, Bao-Feng; Xie, Yang-Yang] Ningbo 2 Hosp, Clin Res Ctr, Dept Anorectal Surg, 41 Xibei Rd, Ningbo 315010, Zhejiang, Peoples R China.
   [Lou, Jie] Ningbo 2 Hosp, Clin Res Ctr, Dept Digest, Ningbo 315010, Zhejiang, Peoples R China.
   [Li, Ke-Qiang] Ningbo 2 Hosp, Clin Res Ctr, Key Lab Mol Biol Canc, 41 Xibei Rd, Ningbo 315010, Zhejiang, Peoples R China.
RP Dai, XY (corresponding author), Ningbo 2 Hosp, Clin Res Ctr, Dept Anorectal Surg, 41 Xibei Rd, Ningbo 315010, Zhejiang, Peoples R China.; Li, KQ (corresponding author), Ningbo 2 Hosp, Clin Res Ctr, Key Lab Mol Biol Canc, 41 Xibei Rd, Ningbo 315010, Zhejiang, Peoples R China.
EM daixiaoyu0106@126.com; likeqiang1264@163.com
FU Natural Science Foundation of Ningbo [2014A610225]; Medical Foundation
   of Ningbo [211B10]; Social Development and Scientific and Technological
   Projects Foundation of Ningbo [2014C50068]; Huamei Foundation of Ningbo;
   Huamei Foundation of Ningbo No. 2 Hospital [2015HMKY07, 2015HMKY08,
   2015HMKY36]
FX The present study was supported by grants from the Natural Science
   Foundation of Ningbo (grant no. 2014A610225), Medical Foundation of
   Ningbo (grant no. 211B10), Social Development and Scientific and
   Technological Projects Foundation of Ningbo (grant no. 2014C50068),
   Huamei Foundation of Ningbo No. 2 Hospital (grant nos. 2015HMKY07,
   2015HMKY08 and 2015HMKY36).
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NR 31
TC 10
Z9 11
U1 1
U2 7
PU SPANDIDOS PUBL LTD
PI ATHENS
PA POB 18179, ATHENS, 116 10, GREECE
SN 1792-1074
EI 1792-1082
J9 ONCOL LETT
JI Oncol. Lett.
PD MAY
PY 2018
VL 15
IS 5
BP 8019
EP 8026
DI 10.3892/ol.2018.8332
PG 8
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA GF3DN
UT WOS:000431825900253
PM 29849804
OA gold, Green Published
DA 2022-04-25
ER

PT J
AU Kim, YS
   Shin, JH
   Bae, MK
   Lee, CY
   Kim, DJ
   Chung, KY
   Lee, JG
AF Kim, Young Sam
   Shin, Ju Hye
   Bae, Mi Kyung
   Lee, Chang Young
   Kim, Dae Joon
   Chung, Kyung Young
   Lee, Jin Gu
TI Autophagy Activity in Pulmonary Metastatic Tumor Tissues from Colorectal
   Cancer: A Pilot Study
SO YONSEI MEDICAL JOURNAL
LA English
DT Article
DE Colorectal cancer; metastasis; treatment failure; autophagy
ID DOUBLE-EDGED-SWORD; CELL-SURVIVAL; APOPTOSIS
AB Purpose: Autophagy has been reported to be involved in treatment failure in tumor. We aimed to evaluate autophagy activity in tumor tissue and compare them between the recurrence and non-recurrence groups. Materials and Methods: We analyzed expressions of autophagy-related proteins in tumor tissues which were obtained from pulmonary metastases of colorectal cancer patients by Western blot. We also analyzed autophagosomes by transmission electron microscopy. Results: Tumor tissues from recurrence group showed increased levels of LC3B-II, decreased levels of p62/SQSTM1, and also a marked accumulation of autophagosomes compared with tissues from non-recurrence group. Conclusion: The present study suggests that autophagy may be associated with treatment failure of metastatic colorectal cancer.
C1 [Kim, Young Sam; Shin, Ju Hye] Yonsei Univ, Coll Med, Dept Internal Med, Seoul 120752, South Korea.
   [Bae, Mi Kyung; Lee, Chang Young; Kim, Dae Joon; Chung, Kyung Young; Lee, Jin Gu] Yonsei Univ, Coll Med, Dept Thorac & Cardiovasc Surg, Seoul 120752, South Korea.
RP Lee, JG (corresponding author), Yonsei Univ, Coll Med, Dept Thorac & Cardiovasc Surg, 50-1 Yonsei Ro, Seoul 120752, South Korea.
EM csjglee@yuhs.ac
OI Kim, Young Sam/0000-0001-9656-8482
FU Bumsuk Academic Research Fund
FX This paper was supported by Bumsuk Academic Research Fund in 2012.
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NR 17
TC 6
Z9 6
U1 0
U2 4
PU YONSEI UNIV COLL MEDICINE
PI SEOUL
PA 50-1 YONSEI-RO, SEODAEMUN-GU, SEOUL 120-752, SOUTH KOREA
SN 0513-5796
EI 1976-2437
J9 YONSEI MED J
JI Yonsei Med. J.
PD NOV 1
PY 2014
VL 55
IS 6
BP 1484
EP 1488
DI 10.3349/ymj.2014.55.6.1484
PG 5
WC Medicine, General & Internal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC General & Internal Medicine
GA AR7UL
UT WOS:000343785100004
PM 25323883
OA Green Published, Green Submitted, gold
DA 2022-04-25
ER

PT J
AU He, K
   Wu, L
   Ding, QS
   Haider, F
   Yu, HG
   Wang, HH
   Xiang, GA
AF He, Ke
   Wu, Lu
   Ding, Qianshan
   Haider, Farhan
   Yu, Honggang
   Wang, Haihe
   Xiang, Guoan
TI Apatinib Promotes Apoptosis of Pancreatic Cancer Cells through
   Downregulation of Hypoxia-Inducible Factor-1 alpha and Increased Levels
   of Reactive Oxygen Species
SO OXIDATIVE MEDICINE AND CELLULAR LONGEVITY
LA English
DT Article
ID TYROSINE KINASE; COLON-CANCER; AUTOPHAGY; INHIBITOR; GROWTH
AB At present, apatinib is considered a new generation agent for the treatment of patients with gastric cancer. However, the effects of apatinib on pancreatic cancer have not been clarified. This study investigated the impact of apatinib on the biological function of pancreatic cancer cells and the potential mechanism involved in this process. Using the Cell Counting Kit-8 method, we confirmed that apatinib treatment inhibited cell proliferation in vitro. Moreover, the migration rate of pancreatic cells was inhibited. The effects of apatinib on apoptosis and cell cycle distribution of pancreatic carcinoma cells were detected by flow cytometry. The number of apoptotic cells was significantly increased, and the cell cycle was altered. Furthermore, we demonstrated that apatinib inhibited the expression of hypoxia-inducible factor-1 alpha (HIF-1 alpha), vascular endothelial growth factor, and markers of the phosphoinositide 3-kinase (PI3K)/Akt/mTOR signaling pathway, which increased the levels of reactive oxygen species in vitro. Apatinib significantly inhibited the biological function of pancreatic cancer cells. It promoted apoptosis, downregulated the expression of HIF-1 alpha, and increased the levels of reactive oxygen species.
C1 [He, Ke; Haider, Farhan; Wang, Haihe] Sun Yat Sen Univ, Dept Biochem, Zhongshan Sch Med, Guangzhou 510080, Guangdong, Peoples R China.
   [He, Ke; Haider, Farhan; Wang, Haihe] Sun Yat Sen Univ, Ctr Stern Cell Biol & Tissue Engn, Key Lab Minist Educ, Guangzhou 510080, Guangdong, Peoples R China.
   [He, Ke; Xiang, Guoan] Guangdong Second Prov Gen Hosp, Dept Gen Surg, Guangzhou 510317, Guangdong, Peoples R China.
   [Wu, Lu] Wuhan Univ, Zhongnan Hosp, Dept Radiat & Med Oncol, Wuhan 430071, Hubei, Peoples R China.
   [Wu, Lu; Ding, Qianshan; Yu, Honggang] Wuhan Univ, Dept Gastroenterol, Renmin Hosp, Wuhan 430060, Hubei, Peoples R China.
   [Wu, Lu] Wuhan Univ, Dept Radiat & Med Oncol, Hubei Key Lab Tumor Biol Behav, Hubei Clin Canc Study Ctr,Zhongnan Hosp, Wuhan 430071, Hubei, Peoples R China.
RP Wang, HH (corresponding author), Sun Yat Sen Univ, Dept Biochem, Zhongshan Sch Med, Guangzhou 510080, Guangdong, Peoples R China.; Wang, HH (corresponding author), Sun Yat Sen Univ, Ctr Stern Cell Biol & Tissue Engn, Key Lab Minist Educ, Guangzhou 510080, Guangdong, Peoples R China.; Xiang, GA (corresponding author), Guangdong Second Prov Gen Hosp, Dept Gen Surg, Guangzhou 510317, Guangdong, Peoples R China.
EM wanghaih@mail.sysu.edu.cn; guoan_66@163.com
RI Haihe, Wang/AAD-4036-2021
OI , Haihe/0000-0002-9302-2334; He, Ke/0000-0002-9194-8408
FU National Natural Science Foundation of ChinaNational Natural Science
   Foundation of China (NSFC) [81071990, 81641110]; Natural Science
   Foundation of Guangdong Province, ChinaNational Natural Science
   Foundation of Guangdong Province [2015A030313725]; Science and
   Technology Program of Guangdong Province, China [201707010305]; Medical
   Research Foundation of Guangdong Province, China [A2017427]; Youth
   Science Foundation of Guangdong Second Provincial General Hospital
   [YQ2016-001]
FX The authors would like to thank Dr. Liu Fei and Mr. Xia Hong for their
   excellent technical assistance in this work. This work was supported by
   grants from the National Natural Science Foundation of China (nos.
   81071990 and 81641110), the Natural Science Foundation of Guangdong
   Province, China (no. 2015A030313725), the Science and Technology Program
   of Guangdong Province, China (no. 201707010305), the Medical Research
   Foundation of Guangdong Province, China (no. A2017427), and the Youth
   Science Foundation of Guangdong Second Provincial General Hospital (no.
   YQ2016-001).
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NR 34
TC 11
Z9 13
U1 1
U2 10
PU HINDAWI LTD
PI LONDON
PA ADAM HOUSE, 3RD FLR, 1 FITZROY SQ, LONDON, W1T 5HF, ENGLAND
SN 1942-0900
EI 1942-0994
J9 OXID MED CELL LONGEV
JI Oxidative Med. Cell. Longev.
PY 2019
VL 2019
AR 5152072
DI 10.1155/2019/5152072
PG 9
WC Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Cell Biology
GA HM1XY
UT WOS:000459250500001
PM 30863481
OA Green Published, Green Submitted, gold
DA 2022-04-25
ER

PT J
AU Wang, LJ
   Yu, ZX
   Wei, C
   Zhang, L
   Song, H
   Chen, B
   Yang, QF
AF Wang, Lijuan
   Yu, Zhongxia
   Wei, Chao
   Zhang, Li
   Song, Hui
   Chen, Bing
   Yang, Qifeng
TI Huaier aqueous extract protects against dextran sulfate sodium-induced
   experimental colitis in mice by inhibiting NLRP3 inflammasome activation
SO ONCOTARGET
LA English
DT Article
DE Huaier; colitis; NLRP3; inflammasome; IL-1 beta
ID INTESTINAL INFLAMMATION; ULCERATIVE-COLITIS; BOWEL-DISEASE;
   BREAST-CANCER; CELLS; POLYSACCHARIDE; PROLIFERATION; APOPTOSIS; PATHWAY
AB The use of Trametes robiniophila Murr. (Huaier) as a complementary therapy for cancer has recently become increasingly common in China. However, whether Huaier can regulate host immune responses, especially innate immunity, remains largely unknown. The NLRP3 inflammasome is a multimeric complex consisting of NLRP3, ASC and caspase-1. NLRP3 inflammasomes respond to a variety of endogenous (damage-associated molecular patterns) and exogenous (pathogen-associated molecular patterns) stimuli, and play crucial roles in host defense against pathogens and multiple diseases such as ulcerative colitis (UC). In this study, we investigated the anti-inflammatory effect of Huaier in dextran sulfate sodium (DSS)-induced murine colitis and revealed the underlying mechanisms by targeting NLRP3 inflammasomes. In C57BL/6 mice, oral administration of Huaier attenuated DSS-induced colon shortening and colonic pathological damage. Furthermore, we analyzed the effect of Huaier on NLRP3 inflammasome activation in macrophages. Huaier inhibited NLRP3 inflammasome activation-induced IL-1 beta secretion and caspase-1 cleavage. Moreover, Huaier decreased NLRP3 protein expression via promoting NLRP3 degradation through the autophagy lysosome pathway. Therefore, our findings demonstrate a novel function for Huaier in the regulation of NLRP3 inflammasome activation and suggest a potential role for Huaier in NLRP3 inflammasome-associated diseases.
C1 [Wang, Lijuan; Zhang, Li; Chen, Bing; Yang, Qifeng] Shandong Univ, Qilu Hosp, Pathol Tissue Bank, Jinan 250012, Shandong, Peoples R China.
   [Yu, Zhongxia; Song, Hui] Shandong Univ, Dept Immunol, Sch Med, Jinan 250012, Shandong, Peoples R China.
   [Yu, Zhongxia; Song, Hui] Shandong Univ, Key Lab Infect & Immun Shandong Prov, Sch Med, Jinan 250012, Shandong, Peoples R China.
   [Wei, Chao] Shandong Univ, Hosp 2, Dept Ophthalmol, Jinan 250033, Shandong, Peoples R China.
   [Zhang, Li; Yang, Qifeng] Shandong Univ, Qilu Hosp, Dept Breast Surg, Jinan 250012, Shandong, Peoples R China.
RP Yang, QF (corresponding author), Shandong Univ, Qilu Hosp, Pathol Tissue Bank, Jinan 250012, Shandong, Peoples R China.; Yang, QF (corresponding author), Shandong Univ, Qilu Hosp, Dept Breast Surg, Jinan 250012, Shandong, Peoples R China.
EM qifengy_sdu@163.com
OI Yang, Qifeng/0000-0003-0576-8513
FU National Natural Science Foundation of ChinaNational Natural Science
   Foundation of China (NSFC) [31500699]; Foundation for Excellent Young
   Scientist of Shandong Province [BS2015WS002, BS2015SW005]; Science
   Foundation of Qilu Hospital of Shandong University [2015QLQN24];
   Fundamental Research Funds of Shandong University [2016JC023]
FX This work was supported by grants from the National Natural Science
   Foundation of China (31500699), the Foundation for Excellent Young
   Scientist of Shandong Province (BS2015WS002), the Foundation for
   Excellent Young Scientist of Shandong Province (BS2015SW005), the
   Science Foundation of Qilu Hospital of Shandong University(2015QLQN24),
   and the Fundamental Research Funds of Shandong University (2016JC023).
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NR 36
TC 15
Z9 16
U1 3
U2 43
PU IMPACT JOURNALS LLC
PI ORCHARD PARK
PA 6666 E QUAKER ST, STE 1, ORCHARD PARK, NY 14127 USA
EI 1949-2553
J9 ONCOTARGET
JI Oncotarget
PD MAY 16
PY 2017
VL 8
IS 20
BP 32937
EP 32945
DI 10.18632/oncotarget.16513
PG 9
WC Oncology; Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Cell Biology
GA EV4XS
UT WOS:000401767700046
PM 28380426
OA Green Published, gold, Green Submitted
DA 2022-04-25
ER

PT J
AU Zhang, DD
   Gao, CX
   Li, RY
   Zhang, L
   Tian, JK
AF Zhang, Dandan
   Gao, Cuixia
   Li, Ruyi
   Zhang, Lin
   Tian, Jingkui
TI TEOA, a triterpenoid from Actinidia eriantha, induces autophagy in SW620
   cells via endoplasmic reticulum stress and ROS-dependent mitophagy
SO ARCHIVES OF PHARMACAL RESEARCH
LA English
DT Article
DE Actinidia eriantha root; TEOA; SW620; Autophagy; ER stress; Mitophagy
ID UNFOLDED PROTEIN RESPONSE; OXIDATIVE STRESS; PARKIN; PERK; NIX;
   SURVIVAL; DISEASE; GLUCOSE; PINK1; PHOSPHORYLATION
AB 2 alpha,3 alpha,24-Thrihydroxyurs-12-en-28-oicacid (TEOA), a pentacyclic triterpenoid, isolated from the roots of Actinidia eriantha, exhibits significant cytotoxicity against SW620, BGC-823, HepG-2, A549 and PC-3 cancer cells. In this study, we investigated the underlying molecular mechanism of the anticancer activity of TEOA in SW620 cells. We demonstrated that TEOA induced apoptosis through cleavage of caspase-9 and PARP in SW620 cells. In addition, evidence of TEOA-mediated autophagy included the induction of autophagolysosomes and activation of autophagic markers LC-3B and p62. Further analysis illustrated that TEOA promoted the phosphorylation of PERK and elF2 alpha, followed by up-regulation of the downstream protein CHOP, suggesting the involvement of PERK/eIF2 alpha/CHOP pathway and ER stress in TEOA-induced autophagy in SW620 cells. Meanwhile, TEOA-mediated PINK1, Parkin, ubiquitin and p62 activation revealed that TEOA induced specific autophagy-mitophagy in SW620 cells. Additionally, an antioxidant NAC attenuated the TEOA-induced mitophagy, indicating that TEOA triggers mitophagy via a ROS-dependent pathway. Collectively, our findings revealed a novel cellular mechanism of TEOA in the colon cancer cell line SW620, thus providing a molecular basis for developing TEOA into an anti-tumor candidate.
C1 [Zhang, Dandan; Gao, Cuixia; Li, Ruyi; Zhang, Lin; Tian, Jingkui] Zhejiang Univ, Inst Biomed Engn, Coll Biomed Engn & Instrument Sci, Hangzhou, Zhejiang, Peoples R China.
   [Tian, Jingkui] Zhejiang Univ, Zhejiang Malaysia Joint Res Ctr Tradit Med, Hangzhou, Zhejiang, Peoples R China.
RP Tian, JK (corresponding author), Zhejiang Univ, Inst Biomed Engn, Coll Biomed Engn & Instrument Sci, Hangzhou, Zhejiang, Peoples R China.; Tian, JK (corresponding author), Zhejiang Univ, Zhejiang Malaysia Joint Res Ctr Tradit Med, Hangzhou, Zhejiang, Peoples R China.
EM tjk@zju.edu.cn
FU National Science Foundation of ChinaNational Natural Science Foundation
   of China (NSFC) [81473182]; Jiangsu Provincial Natural Science
   Foundation of ChinaNatural Science Foundation of Jiangsu Province
   [BK20161269]; Jiangsu Technology Support Program [BE2014654]
FX This work was supported by the National Science Foundation of China
   (Grant No. 81473182), the Jiangsu Provincial Natural Science Foundation
   of China (Grant No. BK20161269) and the Jiangsu Technology Support
   Program (Grant No. BE2014654).
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U1 1
U2 16
PU PHARMACEUTICAL SOC KOREA
PI SEOUL
PA 1489-3 SUHCHO-DONG, SUHCHO-KU, SEOUL 137-071, SOUTH KOREA
SN 0253-6269
EI 1976-3786
J9 ARCH PHARM RES
JI Arch. Pharm. Res.
PD MAY
PY 2017
VL 40
IS 5
BP 579
EP 591
DI 10.1007/s12272-017-0899-9
PG 13
WC Chemistry, Medicinal; Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA EV4IH
UT WOS:000401721700005
PM 28211011
DA 2022-04-25
ER

PT J
AU Choi, SW
   Song, JK
   Yim, YS
   Yun, HG
   Chun, KH
AF Choi, Seung-Won
   Song, Jun-Kyu
   Yim, Ye-Seal
   Yun, Ho-Geun
   Chun, Kyung-Hee
TI Glucose Deprivation Triggers Protein Kinase C-dependent beta-Catenin
   Proteasomal Degradation
SO JOURNAL OF BIOLOGICAL CHEMISTRY
LA English
DT Article
ID GASTRIC-CANCER; COLON-CARCINOMA; MELANOMA-CELLS; BREAST-CANCER; PATHWAY;
   AUTOPHAGY; WNT; INACTIVATION; SENESCENCE; EXPRESSION
AB Autophagy is a conserved process that contributes to cell homeostasis. It is well known that induction mainly occurs in response to nutrient starvation, such as starvation of amino acids and insulin, and its mechanisms have been extensively characterized. However, the mechanisms behind cellular glucose deprivation-induced autophagy are as of now poorly understood. In the present study, we determined a mechanism by which glucose deprivation induced the PKC-dependent proteasomal degradation of beta-catenin, leading to autophagy. Glucose deprivation was shown to cause a sub-G(1) transition and enhancement of the LC3-II protein levels, whereas beta-catenin protein underwent degradation in a proteasome-dependent manner. Moreover, the inhibition of GSK3 beta was unable to abolish the glucose deprivation-mediated beta-catenin degradation or up-regulation of LC3-II protein levels, which suggested GSK3 beta-independent protein degradation. Intriguingly, the inhibition of PKC beta using a pharmacological inhibitor and transfection of siRNA for PKC alpha was observed to effectively block glucose deprivation- induced beta-catenin degradation as well as the increase in LC3-II levels and the accumulation of a sub-G(1) population. Together, our results demonstrated a molecular mechanism by which glucose deprivation can induce the GSK3 beta-independent protein degradation of beta-catenin, leading to autophagy.
C1 [Choi, Seung-Won; Song, Jun-Kyu; Yim, Ye-Seal; Yun, Ho-Geun; Chun, Kyung-Hee] Yonsei Univ, Coll Med, Dept Biochem & Mol Biol, 50 Yonsei Ro, Seoul 120752, South Korea.
   [Song, Jun-Kyu; Yim, Ye-Seal; Yun, Ho-Geun; Chun, Kyung-Hee] Yonsei Univ, Brain Korea Plus Project Med Sci 21, Seoul 120752, South Korea.
RP Chun, KH (corresponding author), Yonsei Univ, Coll Med, Dept Biochem & Mol Biol, 50 Yonsei Ro, Seoul 120752, South Korea.
EM khchun@yuhs.ac
FU National Research Foundation of Korea (NRF) - Korean government
   (Ministry of Science, ICT and Future Planning) [NRF-2014R1A2A1A11050600,
   NRF-2011-0030086]; Korea Health Technology RAMP;D Project, Ministry of
   Health and Welfare [A121982]
FX This work was supported by National Research Foundation of Korea (NRF)
   grants funded by the Korean government (Ministry of Science, ICT and
   Future Planning) (Grants NRF-2014R1A2A1A11050600 and NRF-2011-0030086)
   and by the Korea Health Technology R&D Project, Ministry of Health and
   Welfare, Grant A121982.
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NR 50
TC 16
Z9 18
U1 0
U2 7
PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3996 USA
EI 1083-351X
J9 J BIOL CHEM
JI J. Biol. Chem.
PD APR 10
PY 2015
VL 290
IS 15
BP 9863
EP 9873
DI 10.1074/jbc.M114.606756
PG 11
WC Biochemistry & Molecular Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology
GA CF7IJ
UT WOS:000352729400045
PM 25691573
OA Green Published, hybrid
DA 2022-04-25
ER

PT J
AU Zhao, XG
   Sun, RJ
   Yang, XY
   Liu, DY
   Lei, DP
   Jin, T
   Pan, XL
AF Zhao, Xing-guo
   Sun, Rui-jie
   Yang, Xiao-yan
   Liu, Da-yu
   Lei, Da-peng
   Jin, Tong
   Pan, Xin-liang
TI Chloroquine-Enhanced Efficacy of Cisplatin in the Treatment of
   Hypopharyngeal Carcinoma in Xenograft Mice
SO PLOS ONE
LA English
DT Article
ID CELL LUNG-CANCER; CONCURRENT CHEMORADIOTHERAPY;
   HEPATOCELLULAR-CARCINOMA; BREAST-CANCER; AUTOPHAGY; RESISTANCE;
   INHIBITION; APOPTOSIS; TUMORIGENESIS; COMBINATION
AB Hypopharyngeal squamous cell carcinoma (HSCC) has the worst prognosis among head and neck cancers. Cisplatin (DDP)-based chemotherapy is an important part of multimodal treatments. However, resistance to DDP severely impairs the effectiveness of chemotherapy for HSCC. Chloroquine (CQ) has been reported to enhance the effectiveness of chemotherapy and radiotherapy in liver, pancreas, breast, prostate and colon tumors, but it is unclear whether CQ could increase the efficacy of DDP for treating HSCC. We inoculated BALB/c nude mice with a subcutaneous injection of human hypopharyngeal FaDu cells to generate our animal model. Mice were randomly divided into 4 groups and treated with vehicle control, CQ (60 mg/kg/day), DDP (5 mg/kg/6 days), or a combination of DDP and CQ. Tumor growth and survival of the mice were monitored. We found that CQ inhibited autophagy and increased DDP-induced apoptosis in the xenograft mouse model. CQ enhanced the efficacy of DDP, resulting in decreased tumor growth and prolonged survival of the mice. To test whether blocking autophagy enhanced the efficacy of DDP, FaDu cells were infected with lentiviral shRNA to Beclin-1 and inoculated into the flanks of nude mice. Inhibition of autophagy markedly enhanced the DDP-induced antitumor effect. Our study suggests that the addition of CQ to DDP-based chemotherapy could be a potential therapeutic strategy for treating HSCC, and the inhibition of autophagy may contribute to chemotherapy sensitization in HSCC.
C1 [Zhao, Xing-guo; Sun, Rui-jie; Liu, Da-yu; Lei, Da-peng; Jin, Tong; Pan, Xin-liang] Shandong Univ, Qilu Hosp, Dept Otolaryngol, Jinan 250100, Shandong, Peoples R China.
   [Yang, Xiao-yan] Shandong Univ, Qilu Hosp, Key Lab Cardiovasc Remodeling & Funct Res, Jinan 250100, Shandong, Peoples R China.
RP Pan, XL (corresponding author), Shandong Univ, Qilu Hosp, Dept Otolaryngol, Jinan 250100, Shandong, Peoples R China.
EM pan_xinl@163.com
FU Independent Innovation Foundation of Shandong University (IIFSDU)
   [2012TS156]; Shandong Provincial Natural Science Foundation,
   ChinaNatural Science Foundation of Shandong Province [ZR2013HM107]
FX This work was supported by Independent Innovation Foundation of Shandong
   University (IIFSDU, #2012TS156 for DYL) and Shandong Provincial Natural
   Science Foundation, China (#ZR2013HM107 for XLP). XLP had a role in the
   study design. DYL had a role in data analysis.
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PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 1160 BATTERY STREET, STE 100, SAN FRANCISCO, CA 94111 USA
SN 1932-6203
J9 PLOS ONE
JI PLoS One
PD APR 29
PY 2015
VL 10
IS 4
AR e0126147
DI 10.1371/journal.pone.0126147
PG 12
WC Multidisciplinary Sciences
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Science & Technology - Other Topics
GA CH0LO
UT WOS:000353711600172
PM 25923669
OA Green Published, Green Submitted, gold
DA 2022-04-25
ER

PT J
AU Fu, L
   Han, B
   Zhou, Y
   Ren, J
   Cao, WZ
   Patel, G
   Kai, GY
   Zhang, J
AF Fu, Li
   Han, Bing
   Zhou, Yang
   Ren, Jie
   Cao, Wenzhi
   Patel, Gopal
   Kai, Guoyin
   Zhang, Jun
TI The Anticancer Properties of Tanshinones and the Pharmacological Effects
   of Their Active Ingredients
SO FRONTIERS IN PHARMACOLOGY
LA English
DT Review
DE Salvia miltiorrhiza; tanshinones; autophagy; migration; tumor
   immunology; apoptosis
ID COLON-CANCER CELLS; IIA INHIBITS ANGIOGENESIS; MILTIORRHIZA HAIRY ROOTS;
   IN-VITRO; PROTEIN EXPRESSION; DEPENDENT APOPTOSIS; SIGNALING PATHWAY;
   HERBAL MEDICINE; DOWN-REGULATION; CYCLE ARREST
AB Cancer is a common malignant disease worldwide with an increasing mortality in recent years. Salvia miltiorrhiza, a well-known traditional Chinese medicine, has been used for the treatment of cardiovascular and cerebrovascular diseases for thousands of years. The liposoluble tanshinones in S. miltiorrhiza are important bioactive components and mainly include tanshinone IIA, dihydrodanshinone, tanshinone I, and cryptotanshinone. Previous studies showed that these four tanshinones exhibited distinct inhibitory effects on tumor cells through different molecular mechanisms in vitro and in vivo. The mechanisms mainly include the inhibition of tumor cell growth, metastasis, invasion, and angiogenesis, apoptosis induction, cell autophagy, and antitumor immunity, and so on. In this review, we describe the latest progress on the antitumor functions and mechanisms of these four tanshinones to provide a deeper understanding of the efficacy. In addition, the important role of tumor immunology is also reviewed.
C1 [Fu, Li; Zhou, Yang; Ren, Jie; Cao, Wenzhi; Kai, Guoyin; Zhang, Jun] Shanghai Normal Univ, Sch Life Sci, Inst Plant Biotechnol, Shanghai, Peoples R China.
   [Han, Bing; Patel, Gopal; Kai, Guoyin] Zhejiang Chinese Med Univ, Coll Pharmaceut Sci, Lab Med Plant Biotechnol, Hangzhou, Peoples R China.
RP Kai, GY; Zhang, J (corresponding author), Shanghai Normal Univ, Sch Life Sci, Inst Plant Biotechnol, Shanghai, Peoples R China.; Kai, GY (corresponding author), Zhejiang Chinese Med Univ, Coll Pharmaceut Sci, Lab Med Plant Biotechnol, Hangzhou, Peoples R China.
EM guoyinkai@yahoo.com; zhj@shnu.edu.cn
RI Patel, Gopal/AAH-4185-2020
OI Patel, Gopal/0000-0001-6193-6847
FU National Natural Science Fund of ChinaNational Natural Science
   Foundation of China (NSFC) [81522049, 81670151, 31571735, 31270007];
   "Dawn" Program of Shanghai Education Commission [16SG38]; Open project
   of Shanghai Key Laboratory Atmospheric Particle Pollution Prevention
   [C-6105-17-029]; Shanghai Science and Technology Committee
   ProjectShanghai Science & Technology Committee [17JC1404300,
   15430502700]; Zhejiang Provincial Ten Thousands Program for Leading
   Talents of Science and Technology Innovation; Zhejiang Provincial
   Program for the Cultivation of High-level Innovative Health talents;
   Opening project of Zhejiang provincial preponderant and characteristic
   subject of Key University (Traditional Chinese Pharmacology); Zhejiang
   Chinese Medical University [ZYAOXYB2019005, ZYAOX2018019]
FX This work was supported by the National Natural Science Fund of China
   (81522049, 81670151, 31571735, and 31270007), the "Dawn" Program of
   Shanghai Education Commission (16SG38), Open project of Shanghai Key
   Laboratory Atmospheric Particle Pollution Prevention (C-6105-17-029),
   Shanghai Science and Technology Committee Project (17JC1404300 and
   15430502700), Zhejiang Provincial Ten Thousands Program for Leading
   Talents of Science and Technology Innovation, Zhejiang Provincial
   Program for the Cultivation of High-level Innovative Health talents,
   Opening project of Zhejiang provincial preponderant and characteristic
   subject of Key University (Traditional Chinese Pharmacology), and
   Zhejiang Chinese Medical University (ZYAOXYB2019005 and ZYAOX2018019).
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NR 154
TC 25
Z9 26
U1 13
U2 22
PU FRONTIERS MEDIA SA
PI LAUSANNE
PA AVENUE DU TRIBUNAL FEDERAL 34, LAUSANNE, CH-1015, SWITZERLAND
EI 1663-9812
J9 FRONT PHARMACOL
JI Front. Pharmacol.
PD MAR 19
PY 2020
VL 11
AR 193
DI 10.3389/fphar.2020.00193
PG 18
WC Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA LC8MC
UT WOS:000525586000001
PM 32265690
OA Green Published, gold
DA 2022-04-25
ER

PT J
AU Ohashi, Y
   Tremel, S
   Williams, RL
AF Ohashi, Yohei
   Tremel, Shirley
   Williams, Roger L.
TI VPS34 complexes from a structural perspective
SO JOURNAL OF LIPID RESEARCH
LA English
DT Review
DE vacuolar protein sorting 34; X-ray crystallography; cryo-electron
   microscopy; hydrogen-deuterium exchange mass-spectrometry; lipid
ID PHOSPHATIDYLINOSITOL 3-KINASE COMPLEXES; BECLIN 1; REGULATES AUTOPHAGY;
   PROTEIN-KINASE; SELECTIVE INHIBITOR; NUTRIENT STRESS; COLON-CANCER; HOPS
   COMPLEX; UVRAG; GENE
AB VPS34 phosphorylates phosphatidylinositol to produce PtdIns3P and is the progenitor of the phosphoinositide 3-kinase (PI3K) family. VPS34 has a simpler domain organization than class I PI3Ks, which belies the complexity of its quaternary organization, with the enzyme always functioning within larger assemblies. PtdIns3P recruits specific recognition modules that are common in protein-sorting pathways, such as autophagy and endocytic sorting. It is best characterized in two heterotetramers, complexes I and II. Complex I is composed of VPS34, VPS15, Beclin 1, and autophagy-related gene (ATG)14L, whereas complex II replaces ATG14L with UVRAG. Because VPS34 can form a component of several distinct complexes, it enables independent regulation of various pathways that are controlled by PtdIns3P. Complexes I and II are critical for early events in autophagy and endocytic sorting, respectively. Autophagy has a complex association with cancer. In early stages, it inhibits tumorigenesis, but in later stages, it acts as a survival factor for tumors. Recently, various disease-associated somatic mutations were found in genes encoding complex I and II subunits. Lipid kinase activities of the complexes are also influenced by posttranslational modifications (PTMs). Mapping PTMs and somatic mutations on three-dimensional models of the complexes suggests mechanisms for how these affect VPS34 activity.
C1 [Ohashi, Yohei; Tremel, Shirley; Williams, Roger L.] MRC Lab Mol Biol, Cambridge CB2 0QH, England.
RP Williams, RL (corresponding author), MRC Lab Mol Biol, Cambridge CB2 0QH, England.
EM rlw@mrc-lmb.cam.ac.uk
RI Ohashi, Yohei/AAT-4006-2021
OI Ohashi, Yohei/0000-0002-2288-130X; Tremel, Shirley/0000-0002-4077-0021;
   Williams, Roger/0000-0001-7754-4207
FU Medical Research CouncilUK Research & Innovation (UKRI)Medical Research
   Council UK (MRC)European Commission [MC_U105184308]; MRCUK Research &
   Innovation (UKRI)Medical Research Council UK (MRC) [MC_U105184308]
   Funding Source: UKRI
FX This work was supported by Medical Research Council Grant MC_U105184308.
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NR 121
TC 37
Z9 37
U1 0
U2 9
PU ELSEVIER
PI AMSTERDAM
PA RADARWEG 29, 1043 NX AMSTERDAM, NETHERLANDS
SN 0022-2275
EI 1539-7262
J9 J LIPID RES
JI J. Lipid Res.
PD FEB
PY 2019
VL 60
IS 2
BP 229
EP 241
DI 10.1194/jlr.R089490
PG 13
WC Biochemistry & Molecular Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology
GA HK8AX
UT WOS:000458212900003
PM 30397185
OA Green Published, hybrid
DA 2022-04-25
ER

PT J
AU Yang, LF
   Wan, JF
   Xiao, S
   Barkhouse, D
   Zhu, J
   Li, GC
   Lu, B
   Zhang, Z
AF Yang, Lifeng
   Wan, Juefeng
   Xiao, Sheng
   Barkhouse, Darryll
   Zhu, Ji
   Li, Guichao
   Lu, Bo
   Zhang, Zhen
TI BH3 mimetic ABT-737 sensitizes colorectal cancer cells to ixazomib
   through MCL-1 downregulation and autophagy inhibition
SO AMERICAN JOURNAL OF CANCER RESEARCH
LA English
DT Article
DE Colorectal cancer; MLN9708; ABT-737; autophagy; MCL-1
ID RELAPSED/REFRACTORY MULTIPLE-MYELOMA; ORAL PROTEASOME INHIBITOR;
   PHASE-II TRIAL; INDUCED APOPTOSIS; ENDOPLASMIC-RETICULUM; TARGETING
   MCL-1; PROSTATE-CANCER; BCL-2 FAMILY; TUMOR-CELLS; DNA-DAMAGE
AB The proteasome inhibitor MLN9708 is an orally administered drug that is hydrolyzed into its active form, MLN2238 (ixazomib). Compared with Bortezomib, MLN2238 has a shorter proteasome dissociation half-life and a lower incidence and severity of peripheral neuropathy, which makes it an attractive candidate for colorectal cancer treatment. In the present study, we observed that MLN2238 induced autophagy, as evidenced by conversion of the autophagosomal marker LC3 from LC3I to LC3II, in colorectal cancer cell lines. Mcl-1, an anti-apoptotic Bcl-2 family protein, was markedly elevated after treating a colorectal cancer cell line with MLN2238. We proved that inhibiting Mcl-1 expression enhances MLN2238 induced apoptosis and negatively regulates autophagy. Co-administration of BH3 mimetic ABT-737 with MLN2238 synergistically kills colorectal cancer cells through MCL-1 neutralization and autophagy inhibition. Furthermore, the synergistic killing effect of the combination therapy is correlated with P53 status in colorectal cancer. These data highlight that the combination of ABT-737 with MLN9708 is a promising therapeutic strategy for human colorectal cancer.
C1 [Yang, Lifeng; Wan, Juefeng; Zhu, Ji; Li, Guichao; Zhang, Zhen] Fudan Univ, Shanghai Canc Ctr, Dept Radiat Oncol, Shanghai 200032, Peoples R China.
   [Yang, Lifeng; Wan, Juefeng; Zhu, Ji; Li, Guichao; Zhang, Zhen] Fudan Univ, Shanghai Med Coll, Dept Oncol, Shanghai 200032, Peoples R China.
   [Xiao, Sheng] Fudan Univ, Shanghai Med Coll, Inst Brain Sci, Dept Integrat Med & Neurobiol,Inst Acupuncture Re, Shanghai 200032, Peoples R China.
   [Barkhouse, Darryll; Lu, Bo] Thomas Jefferson Univ, Dept Radiat Oncol, Kimmel Canc Ctr, Philadelphia, PA 19107 USA.
RP Lu, B (corresponding author), G 301 Bodine Canc Ctr, 111 S 11th St, Philadelphia, PA 19107 USA.; Zhang, Z (corresponding author), Floor 16,Bldg 3,270 Dongan Rd, Shanghai 200032, Peoples R China.
EM Bo.Lu@jefferson.edu; zhenzhang6@hot-mail.com
OI wan, juefeng/0000-0001-5361-1663; Zhu, Ji/0000-0001-7134-9419
FU Natural Science Foundation of ChinaNational Natural Science Foundation
   of China (NSFC) [81372432]
FX The authors would like to thank Dr. Eric Wickstrom and Dr. Scott Waldman
   for the cell lines. This work was supported by the grants from Natural
   Science Foundation of China (81372432). LY, JW participated in
   manuscript drafting, table creation, and manuscript revision. SX, GL and
   DB participated the study design and revised the manuscript. JZ revised
   the manuscript and performed statistical analyses of data. BL and ZZ
   participated in the study design and were responsible for final approval
   of the manuscript. All authors have read and approved the final
   manuscript. The authors declare that they have no conflicts of
   interests.
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NR 50
TC 9
Z9 9
U1 0
U2 1
PU E-CENTURY PUBLISHING CORP
PI MADISON
PA 40 WHITE OAKS LN, MADISON, WI 53711 USA
SN 2156-6976
J9 AM J CANCER RES
JI Am. J. Cancer Res.
PY 2016
VL 6
IS 6
BP 1345
EP +
PG 15
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA DQ8GX
UT WOS:000379448200011
PM 27429848
DA 2022-04-25
ER

PT J
AU Zhang, ZL
   Guo, M
   Zhao, SF
   Xu, WX
   Shao, JJ
   Zhang, F
   Wu, L
   Lu, Y
   Zheng, SZ
AF Zhang, Zili
   Guo, Mei
   Zhao, Shifeng
   Xu, Wenxuan
   Shao, Jiangjuan
   Zhang, Feng
   Wu, Li
   Lu, Yin
   Zheng, Shizhong
TI The update on transcriptional regulation of autophagy in normal and
   pathologic cells: A novel therapeutic target
SO BIOMEDICINE & PHARMACOTHERAPY
LA English
DT Review
DE Autophagy; Transcriptional regulation; Transcription factors;
   Therapeutic target
ID NF-KAPPA-B; FARNESOID X RECEPTOR; PPAR-GAMMA ACTIVATION; COLON-CANCER
   CELLS; POLYCYSTIC-OVARY-SYNDROME; TFEB-MEDIATED AUTOPHAGY; ACUTE LUNG
   INJURY; UP-REGULATION; IN-VITRO; ENERGY-METABOLISM
AB Autophagy is a genetically programmed, evolutionarily conserved catabolic process that occurs in response to stress. While short-lived proteins are degraded via the ubiquitin/proteasome pathway in higher eukaryotes, autophagy refers to intracellular pathway for development, differentiation, survival, and homeostasis through the lysosomal-dependent machinery, which regulates the synthesis, degradation, and recycling of long-lived proteins and even whole cytoplasmic organelles. The newly discovery shows that autophagy plays an important role in recycling nutrients upon starvation and maintaining cellular energy homeostasis. Recent basic and clinical investigations further demonstrate that autophagic abnormalities have been considered underlying reasons for lots of human diseases, including liver disease, cardiovascular and cerebrovascular diseases, neurodegenerative diseases, neoplastic diseases, and cancers. Pharmacological modulation of autophagy might point to possible therapeutic strategies for combating a broad range of diseases. Regrettably, although the mechanisms underlying the regulation of autophagy have long been attracted extensive concern of numerous scholars and its acute regulation by nutrient-sensing signaling pathways is well described, the overview on longer-term transcriptional regulation of autophagy is still filled with confusion. This review summarizes current knowledge on transcriptional regulation of autophagy and expands our horizons on the autophagy repertoire. On the other hand, it also offers a glimpse into different strategies that have been used in experimental models to counteract excessive pathological autophagy via transcriptional regulation mechanism in the prevention and treatment of disease. (C) 2015 Elsevier Masson SAS. All rights reserved.
C1 [Zhang, Zili; Zhao, Shifeng; Xu, Wenxuan; Zhang, Feng; Wu, Li; Lu, Yin; Zheng, Shizhong] Nanjing Univ Chinese Med, Dept Pharmacol, Coll Pharm, 138 Xianlin Ave, Nanjing 210023, Jiangsu, Peoples R China.
   [Guo, Mei] Southeast Univ, Sch Med, Dept Pathogen Biol & Immunol, Nanjing 210009, Peoples R China.
   [Shao, Jiangjuan] Nanjing Univ Chinese Med, Dept Pharm, Coll Pharm, Nanjing 210023, Jiangsu, Peoples R China.
   [Zhang, Feng; Wu, Li; Lu, Yin; Zheng, Shizhong] Nanjing Univ Chinese Med, Jiangsu Key Lab Pharmacol & Safety Evaluat Chines, Nanjing 210023, Jiangsu, Peoples R China.
RP Zheng, SZ (corresponding author), Nanjing Univ Chinese Med, Dept Pharmacol, Coll Pharm, 138 Xianlin Ave, Nanjing 210023, Jiangsu, Peoples R China.
EM nytws@163.com
FU National Natural Science Foundation of ChinaNational Natural Science
   Foundation of China (NSFC) [81270514, 31401210]; Program for Excellent
   Scientific and Technological Innovation Team of Jiangsu Higher
   Education; Priority Academic Program Development of Jiangsu Higher
   Education Institutions [ysxk-2010]; Youth Natural Science Foundation of
   Jiangsu Province [BK20140955]; Natural Science Research General Program
   of Jiangsu Higher Education Institutions [14KJB310011]
FX The nancial support was from the National Natural Science Foundation of
   China (81270514, 31401210), 2013 Program for Excellent Scientific and
   Technological Innovation Team of Jiangsu Higher Education, the Project
   Funded by the Priority Academic Program Development of Jiangsu Higher
   Education Institutions (ysxk-2010), the Youth Natural Science Foundation
   of Jiangsu Province (BK20140955), and the Natural Science Research
   General Program of Jiangsu Higher Education Institutions (14KJB310011).
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NR 186
TC 14
Z9 17
U1 0
U2 28
PU ELSEVIER FRANCE-EDITIONS SCIENTIFIQUES MEDICALES ELSEVIER
PI ISSY-LES-MOULINEAUX
PA 65 RUE CAMILLE DESMOULINS, CS50083, 92442 ISSY-LES-MOULINEAUX, FRANCE
SN 0753-3322
EI 1950-6007
J9 BIOMED PHARMACOTHER
JI Biomed. Pharmacother.
PD AUG
PY 2015
VL 74
BP 17
EP 29
DI 10.1016/j.biopha.2015.06.003
PG 13
WC Medicine, Research & Experimental; Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Research & Experimental Medicine; Pharmacology & Pharmacy
GA CR2TD
UT WOS:000361182600003
PM 26349958
DA 2022-04-25
ER

PT J
AU Zhang, Y
   Tian, ZM
   Wan, HY
   Liu, W
   Kong, FP
   Ma, GP
AF Zhang, Yi
   Tian, Zhiming
   Wan, Hongyan
   Liu, Wen
   Kong, Fanping
   Ma, Guoping
TI Deltonin Ameliorates Cerebral Ischemia/Reperfusion Injury in Correlation
   with Modulation of Autophagy and Inflammation
SO NEUROPSYCHIATRIC DISEASE AND TREATMENT
LA English
DT Article
DE deltonin; cerebral I/R; MCAO/R; autophagy; inflammation
ID APOPTOSIS; PROTECTS; RATS
AB Introduction: Deltonin, an active component extracted from Dioscorea zingiberensis C.H. WRIGHT, was widely utilized in traditional Chinese medicines. It has been shown to have anticancer functions such as colon cancer, breast cancer, and head and neck squamous carcinoma. Herein, we will investigate the role of deltonin in cerebral ischemia/reperfusion injuries.
   Methods: Ly294002 and anisomycin were used as inhibitors to monitor the effects of deltonin. Middle cerebral artery occlusion UR model was constructed. Infarct volumes, neurological deficits and brain water contents were evaluated under different conditions. Rotarod test, ELISA, and Western blotting were carried to investigate the effects in vitro.
   Results: We found that deltonin in ischemia/reperfusion (UR) rats greatly enhanced brain damages as well as neurological functions through up-regulating p-Akt and p-mTOR as well as inhibiting the expressions of LC3-IULC3-I, Beclin-1, IL-1, TLR4, and p-p38. Deltonin exerted neuroprotection effect through relieving autophagy activity by regulating PI3K/Akt/ mTOR signaling. Deltonin suppressed inflammation reactions through modulation TLR4/ p38/MAPK signaling as well.
   Conclusion: Overall, our data suggested that deltonin could suppress ischemic brain injury by regulating autophagy and inflammation during I/R. Deltonin can be a potential therapeutic method for patient with I/R.
C1 [Zhang, Yi; Tian, Zhiming; Wan, Hongyan; Liu, Wen] Southeast Univ, Zhongda Hosp, Cerebral Vasc Ctr, Nanjing 210044, Jiangsu, Peoples R China.
   [Kong, Fanping] Fu Ning Peoples Hosp, Dept Neurol, 111 Bucheng St, Yancheng City 224400, Jiangsu, Peoples R China.
   [Ma, Guoping] Tian Shui First Peoples Hosp, Dept Neurol, 105 Jianshe Rd, Tianshui City 741000, Gansu, Peoples R China.
RP Kong, FP (corresponding author), Fu Ning Peoples Hosp, Dept Neurol, 111 Bucheng St, Yancheng City 224400, Jiangsu, Peoples R China.; Ma, GP (corresponding author), Tian Shui First Peoples Hosp, Dept Neurol, 105 Jianshe Rd, Tianshui City 741000, Gansu, Peoples R China.
EM kongfanping_07@163.com; ahygmcynbiis9@163.com
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NR 19
TC 3
Z9 6
U1 2
U2 9
PU DOVE MEDICAL PRESS LTD
PI ALBANY
PA PO BOX 300-008, ALBANY, AUCKLAND 0752, NEW ZEALAND
EI 1178-2021
J9 NEUROPSYCH DIS TREAT
JI Neuropsychiatr. Dis. Treat.
PY 2020
VL 16
BP 871
EP 879
DI 10.2147/NDT.S227988
PG 9
WC Clinical Neurology; Psychiatry
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Neurosciences & Neurology; Psychiatry
GA KY3LV
UT WOS:000522473700001
PM 32280228
OA Green Published, gold
DA 2022-04-25
ER

PT J
AU Grosch, S
   Schiffmann, S
   Geisslinger, G
AF Groesch, Sabine
   Schiffmann, Susanne
   Geisslinger, Gerd
TI Chain length-specific properties of ceramides
SO PROGRESS IN LIPID RESEARCH
LA English
DT Review
DE Ceramide; Ceramide synthase; Chain length-specific; Apoptosis; Cancer
ID PROTEIN PHOSPHATASE 2A; LONGEVITY ASSURANCE GENE-1; RADIATION-INDUCED
   APOPTOSIS; TANDEM MASS-SPECTROMETRY; SQUAMOUS-CELL CARCINOMAS;
   COLON-CANCER CELLS; KINASE C-ZETA; CYSTIC-FIBROSIS; LONG-CHAIN;
   SPHINGOLIPID SYNTHESIS
AB Ceramides are a class of sphingolipids that are abundant in cell membranes. They are important structural components of the membrane but can also act as second messengers in various signaling pathways. Until recently, ceramides and dihydroceramides were considered as a single functional class of lipids and no distinction was made between molecules with different chain lengths. However, based on the development of high-throughput, structure-specific and quantitative analytical methods to measure ceramides, it has now become clear that in cellular systems the amounts of ceramides differ with respect to their chain length. Further studies have indicated that some functions of ceramides are chain-length dependent. In this review, we discuss the chain length-specific differences of ceramides including their pathological impact on Alzheimer's disease, inflammation, autophagy, apoptosis and cancer. (c) 2011 Elsevier Ltd. All rights reserved.
C1 [Groesch, Sabine; Schiffmann, Susanne; Geisslinger, Gerd] Klinikum Johann Wolfgang Goethe Univ Frankfurt, Inst Klin Pharmakol, Pharmazentrum Frankfurt ZAFES, D-60590 Frankfurt, Germany.
RP Grosch, S (corresponding author), Klinikum Johann Wolfgang Goethe Univ Frankfurt, Inst Klin Pharmakol, Pharmazentrum Frankfurt ZAFES, Theodor Stern Kai 7, D-60590 Frankfurt, Germany.
EM groesch@em.uni-frankfurt.de
RI Groesch, Sabine/H-4251-2018
OI Groesch, Sabine/0000-0002-7262-6307; Schiffmann,
   Susanne/0000-0001-5035-2504
FU Deutsche Forschungsgemeinschaft (DFG) Forschergruppe FOG 784/TP5German
   Research Foundation (DFG) [GR2011/2-1]; DFGGerman Research Foundation
   (DFG)European Commission [GR2011/3-1]; LOEWE Lipid Signaling
   Forschungszentrum Frankfurt (LiFF)
FX This work was supported by the Deutsche Forschungsgemeinschaft (DFG)
   Forschergruppe FOG 784/TP5 (GR2011/2-1) and DFG project GR2011/3-1 and
   the LOEWE Lipid Signaling Forschungszentrum Frankfurt (LiFF).
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NR 152
TC 305
Z9 307
U1 11
U2 93
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0163-7827
EI 1873-2194
J9 PROG LIPID RES
JI Prog. Lipid Res.
PD JAN
PY 2012
VL 51
IS 1
BP 50
EP 62
DI 10.1016/j.plipres.2011.11.001
PG 13
WC Biochemistry & Molecular Biology; Nutrition & Dietetics
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Nutrition & Dietetics
GA 909JY
UT WOS:000301562000005
PM 22133871
HC Y
HP N
DA 2022-04-25
ER

PT J
AU Aredia, F
   Giansanti, V
   Mazzini, G
   Savio, M
   Ortiz, LMG
   Jaadane, I
   Zaffaroni, N
   Forlino, A
   Torriglia, A
   Scovassi, AI
AF Aredia, Francesca
   Giansanti, Vincenzo
   Mazzini, Giuliano
   Savio, Monica
   Guaman Ortiz, Luis Miguel
   Jaadane, Imene
   Zaffaroni, Nadia
   Forlino, Antonella
   Torriglia, Alicia
   Scovassi, Anna Ivana
TI Multiple effects of the Na+/H+ antiporter inhibitor HMA on cancer cells
SO APOPTOSIS
LA English
DT Article
DE Amiloride; Apoptosis; Autophagy; LEI/L-DNase II; MDR; Parthanatos
ID MYC AMPLIFICATION LEVEL; DNASE-II; APOPTOSIS; AMILORIDE; THERAPY;
   PATHWAY; FIBROBLASTS; RESISTANCE; PHENOTYPE; ETOPOSIDE
AB Amiloride derivatives are a class of new promising chemotherapeutic agents. A representative member of this family is the sodium-hydrogen antiporter inhibitor HMA (5-(N,N-hexamethylene amiloride), which has been demonstrated to induce cellular intracytosolic acidification and cell death through the apoptotic pathway(s). This work aims at characterizing drug response of human cancer cell lines to HMA. After a first screening revealing that HMA interferes with cancer cell survival, we focused our attention on SW613-B3 colon carcinoma cells, which are intrinsically resistant to a panel of drugs. Searching for the activation of canonical apoptosis, we found that this process was abortive, given that the final steps of this process, i.e. PARP-1 cleavage and DNA ladder, were not detectable. Thus, we addressed caspase-independent paradigms of cell death and we observed that HMA promotes the induction of the LEI/L-DNase II pathway as well as of parthanatos. Finally, we explored the possible impact of autophagy of cell response to HMA, providing the evidence that autophagy is activated in our experimental system. On the whole, our results defined the biochemical reactions triggered by HMA, and elucidated its multiple effects, thus adding further complexity to the intricate network leading to drug resistance.
C1 [Aredia, Francesca; Giansanti, Vincenzo; Mazzini, Giuliano; Guaman Ortiz, Luis Miguel; Scovassi, Anna Ivana] CNR, Ist Genet Mol, I-27100 Pavia, Italy.
   [Savio, Monica] Univ Pavia, Dipartimento Med Mol, Sez Patol Gen, I-27100 Pavia, Italy.
   [Guaman Ortiz, Luis Miguel] UTPL, Dept Ciencias Salud, Loja 1101608, Ecuador.
   [Jaadane, Imene; Torriglia, Alicia] INSERM, Ctr Rech Cordeliers, U872, F-75006 Paris, France.
   [Jaadane, Imene; Torriglia, Alicia] Univ Paris 06, F-75006 Paris, France.
   [Jaadane, Imene; Torriglia, Alicia] Univ Paris 05, F-75006 Paris, France.
   [Zaffaroni, Nadia] Fdn IRCCS, Ist Nazl Tumori, I-20133 Milan, Italy.
   [Forlino, Antonella] Univ Pavia, Dipartimento Biochim, I-27100 Pavia, Italy.
RP Scovassi, AI (corresponding author), CNR, Ist Genet Mol, I-27100 Pavia, Italy.
EM scovassi@igm.cnr.it
RI Torriglia, Alicia/L-6957-2017; Torriglia, Alicia/Q-3509-2019; Ortiz,
   Luis Miguel Guaman/X-9496-2019; Zaffaroni, Nadia/J-8178-2016; Forlino,
   Antonella/H-5385-2015
OI Torriglia, Alicia/0000-0003-1181-6710; Ortiz, Luis Miguel
   Guaman/0000-0003-2919-4905; Zaffaroni, Nadia/0000-0002-4669-0890;
   Forlino, Antonella/0000-0002-6385-1182; Imene,
   Jaadane/0000-0003-1887-1659; Scovassi, Anna Ivana/0000-0003-3484-9881
FU Italian Regione Lombardia; CariploFondazione Cariplo [2011-0270];
   SENESCYT (Quito, Ecuador); UTPL (Loja, Ecuador); ADEME
FX We are indebted to Maria Grazia Bottone for cytoskeleton
   immunofluorescence, Roberta Gioia for qPCR analysis and Marzia Pennati
   for survivin experiments. Research was partially granted by Italian
   Regione Lombardia (Project Plant Cell to A. I. S) and Cariplo (Project
   2011-0270 to A. F.). F. A. is a PhD student (Dottorato in Genetica,
   Biologia Cellulare e Molecolare, University of Pavia, Italy). L.M.G.O.
   is a PhD student (Dottorato in Genetica, Biologia Cellulare e
   Molecolare, University of Pavia, Italy) supported by SENESCYT (Quito,
   Ecuador) and UTPL (Loja, Ecuador). I.J. is supported by an ADEME grant
   to A.T.
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NR 35
TC 13
Z9 13
U1 0
U2 17
PU SPRINGER
PI DORDRECHT
PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS
SN 1360-8185
EI 1573-675X
J9 APOPTOSIS
JI Apoptosis
PD DEC
PY 2013
VL 18
IS 12
BP 1586
EP 1598
DI 10.1007/s10495-013-0898-3
PG 13
WC Biochemistry & Molecular Biology; Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Cell Biology
GA 251JY
UT WOS:000326925900012
PM 23996609
DA 2022-04-25
ER

PT J
AU Xiong, B
   Chen, S
   Zhu, P
   Huang, ML
   Gao, WJ
   Zhu, R
   Qian, JQ
   Peng, YF
   Zhang, YN
   Dai, H
   Ling, Y
AF Xiong, Biao
   Chen, Shi
   Zhu, Peng
   Huang, Meiling
   Gao, Weijie
   Zhu, Rui
   Qian, Jianqiang
   Peng, Yanfu
   Zhang, Yanan
   Dai, Hong
   Ling, Yong
TI Design, Synthesis, and Biological Evaluation of Novel Thiazolyl Stibst
   tilted Bis-pyrazole Oxime Derivatives with Potent Antitumor Activities
   by Selectively Inducing Apoptosis and ROS in Cancer Cells
SO MEDICINAL CHEMISTRY
LA English
DT Article
DE Antitumor activities; His-pyrazole oxime derivatives; antiproliferative
   activity; selectivity; apoptosis; Reactive Oxygen Species (ROS)
ID ANTICANCER; INDUCTION; AUTOPHAGY
AB Background: A large number of pyrazole derivatives have different biological activities such as anticancer, antimicrobial, anti-inflammatory, analgesic and antiepileptic activity. Among them, pyrazole oximes have attracted much attention due to their potential phannacological activities, particularly anticancer activities.
   Objective: Our goal is to synthesize novel thiazolyl substituted bis-pyrazole oxime derivatives with potent antitumor activities by selectively inducing apoptosis and Reactive Oxygen Species (ROS) accumulation in cancer cells.
   Methods: Eighteen his-pyrazole oxirnes were synthesized by conjugating thiazolyl substituted pyrazoles with pyrazoxime. The target compounds were characterized by (HNMR)-H-1, C-13 NMR, and HRMS, and screened for their antiproliferative activity against four cancer cells in MTT assay. The most potent compound was examined for its inhibitory effect and ROS accumulation in both cancer cells HCT116 and normal intestinal epithelial cells CCD841. Finally, the most potent compound was further evaluated for its apoptotic induction by flow cytometry analysis and immunoblot analysis of apoptosis-related proteins and DNA damage proteins.
   Results: Most compounds displayed potent antiproliferative activity against four cancer cell lines in vitro, displaying potencies superior to 5-FU. In particular, the most potent compound 131 selectively inhibited proliferation of colorectal cancer HCT116 cells but not normal colon CCD841 cells. Furthermore, compound 131 also selectively promoted intracellular ROS accumulation in HCT I 16 which was involved in 131 inhibition of cancer cell proliferation and induction of cell alxmptosis. Finally, compound 131 also dose-dependently induced cancer cell apoptosis by regulating apoptotic and DNA damage related proteins expressions,
   Conclusion: Our synthetic his-pyrazole oxime derivatives possess potent antitumor activities by selectively inducing apoptosis and ROS accumulation in cancer cells, Which may hold great promise as therapeutic agents for the treatment of human cancers.
C1 [Xiong, Biao; Chen, Shi; Zhu, Peng; Huang, Meiling; Gao, Weijie; Zhu, Rui; Qian, Jianqiang; Peng, Yanfu; Zhang, Yanan; Dai, Hong; Ling, Yong] Nantong Univ, Sch Pharm, Nantong 226001, Peoples R China.
   [Xiong, Biao; Chen, Shi; Zhu, Peng; Huang, Meiling; Gao, Weijie; Zhu, Rui; Qian, Jianqiang; Peng, Yanfu; Zhang, Yanan; Dai, Hong; Ling, Yong] Nantong Univ, Jiangsu Prov Key Lab Inflammat & Mol Drug Target, Nantong 226001, Peoples R China.
   [Huang, Meiling; Dai, Hong; Ling, Yong] Nantong Univ, Coll Chem & Chem Engn, Nantong 226001, Peoples R China.
   [Ling, Yong] China Pharmaceut Univ, State Key Lab Nat Med, Nanjing 210009, Jiangsu, Peoples R China.
RP Dai, H; Ling, Y (corresponding author), Nantong Univ, Sch Pharm, Nantong 226001, Peoples R China.; Dai, H; Ling, Y (corresponding author), Nantong Univ, Jiangsu Prov Key Lab Inflammat & Mol Drug Target, Nantong 226001, Peoples R China.; Dai, H; Ling, Y (corresponding author), Nantong Univ, Coll Chem & Chem Engn, Nantong 226001, Peoples R China.; Ling, Y (corresponding author), China Pharmaceut Univ, State Key Lab Nat Med, Nanjing 210009, Jiangsu, Peoples R China.
EM dh123@ntu.edu.cn; lyyy111@sina.com
OI zhu, peng/0000-0002-4148-9135
FU Natural Science Foundation of ChinaNational Natural Science Foundation
   of China (NSFC) [81302628, 21372135]; Project of "Jiangsu Six Peaks of
   Talent", China [2013-SWYY-013, 2014-SWYY-044, 2016-SWYYCXTD-008];
   Jiangsu Province Postdoctoral Science Foundation [2018T110533,
   2016M590488, 1601136B]; Applied Research Projects of Nantong City
   [MS12018079, JC2018125]; Priority Academic Programs Development of
   Jiangsu Higher Education Institutions (PAPD); Project of "Jiangsu 333
   high-level talents"
FX We gratefully acknowledge the financial support by the Natural Science
   Foundation of China (Grant Nos. 81302628 and 21372135), the Project of
   "Jiangsu Six Peaks of Talent" (2013-SWYY-013, 2014-SWYY-044, and
   2016-SWYYCXTD-008), China and Jiangsu Province Postdoctoral Science
   Foundation (2018T110533, 2016M590488, and 1601136B), the Project of
   "Jiangsu 333 high-level talents", Applied Research Projects of Nantong
   City (MS12018079 and JC2018125), and also thank a project funded by the
   Priority Academic Programs Development of Jiangsu Higher Education
   Institutions (PAPD).
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NR 38
TC 4
Z9 4
U1 3
U2 20
PU BENTHAM SCIENCE PUBL LTD
PI SHARJAH
PA EXECUTIVE STE Y-2, PO BOX 7917, SAIF ZONE, 1200 BR SHARJAH, U ARAB
   EMIRATES
SN 1573-4064
EI 1875-6638
J9 MED CHEM
JI Med. Chem.
PY 2019
VL 15
IS 7
BP 743
EP 754
DI 10.2174/1573406414666180827112724
PG 12
WC Chemistry, Medicinal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA JD4QE
UT WOS:000489963500004
PM 30147012
DA 2022-04-25
ER

PT J
AU Ahmed, S
   Khan, H
   Aschner, M
   Mirzae, H
   Akkol, EK
   Capasso, R
AF Ahmed, Salman
   Khan, Haroon
   Aschner, Michael
   Mirzae, Hamed
   Akkol, Esra Kupeli
   Capasso, Raffaele
TI Anticancer Potential of Furanocoumarins: Mechanistic and Therapeutic
   Aspects
SO INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
LA English
DT Review
DE furanocoumarin; apoptosis; autophagy; metastasis; cell cycle arrest
ID NF-KAPPA-B; MEDIATED MULTIDRUG-RESISTANCE; CELL-CYCLE ARREST; IN-VITRO;
   ANGELICA-DAHURICA; CANCER-CELLS; MATRIX METALLOPROTEINASES; DIETARY
   FUROCOUMARINS; SIGNALING PATHWAY; PSORALEN REVERSES
AB Cancer is one of the most extreme medical conditions in both developing and developed countries around the world, causing millions of deaths each year. Chemotherapy and/or radiotherapy are key for treatment approaches, but both have numerous adverse health effects. Furthermore, the resistance of cancerous cells to anticancer medication leads to treatment failure. The rising burden of cancer overall requires novel efficacious treatment modalities. Natural medications offer feasible alternative options against malignancy in contrast to western medication. Furanocoumarins' defensive and restorative impacts have been observed in leukemia, glioma, breast, lung, renal, liver, colon, cervical, ovarian, and prostate malignancies. Experimental findings have shown that furanocoumarins activate multiple signaling pathways, leading to apoptosis, autophagy, antioxidant, antimetastatic, and cell cycle arrest in malignant cells. Additionally, furanocoumarins have been shown to have chemo preventive and chemotherapeutic synergistic potential when used in combination with other anticancer drugs. Here, we address different pathways which are activated by furanocoumarins and their therapeutic efficacy in various tumors. Ideally, this review will trigger interest in furanocoumarins and their potential efficacy and safety as a cancer lessening agents.
C1 [Ahmed, Salman] Univ Karachi, Fac Pharm & Pharmaceut Sci, Dept Pharmacognosy, Karachi 75270, Pakistan.
   [Khan, Haroon] Abdul Wali Khan Univ, Dept Pharm, Mardan 23200, Pakistan.
   [Aschner, Michael] Albert Einstein Coll Med, Dept Mol Pharmacol, Bronx, NY 10463 USA.
   [Mirzae, Hamed] Kashan Univ Med Sci, Res Ctr Biochem & Nutr Metab Dis, Inst Basic Sci, Kashan 8715973474, Iran.
   [Akkol, Esra Kupeli] Gazi Univ, Fac Pharm, Dept Pharmacognosy, TR-06330 Ankara, Turkey.
   [Capasso, Raffaele] Univ Naples Federico II, Dept Agr Sci, Via Univ 100, I-80055 Portici, Italy.
RP Capasso, R (corresponding author), Univ Naples Federico II, Dept Agr Sci, Via Univ 100, I-80055 Portici, Italy.
EM salmanahmed@uok.edu.pk; haroonkhan@awkum.edu.pk;
   michael.aschner@einsteinmed.org; mirzaeih911h@mums.ac.ir;
   esrak@gazi.edu.tr; rafcapas@unina.it
RI Akkol, Esra/ABI-4678-2020; Ahmed, Salman/B-8789-2015; Khan,
   Haroon/AAY-1785-2020
OI Ahmed, Salman/0000-0003-2033-0181; Khan, Haroon/0000-0002-1736-4404;
   Capasso, Raffaele/0000-0002-3335-1822; Kupeli Akkol,
   Esra/0000-0002-5829-7869
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NR 139
TC 36
Z9 36
U1 7
U2 12
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 1422-0067
J9 INT J MOL SCI
JI Int. J. Mol. Sci.
PD AUG
PY 2020
VL 21
IS 16
AR 5622
DI 10.3390/ijms21165622
PG 20
WC Biochemistry & Molecular Biology; Chemistry, Multidisciplinary
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Chemistry
GA NI1OD
UT WOS:000565126300001
PM 32781533
OA Green Published, gold
DA 2022-04-25
ER

PT J
AU Emama, AA
   Abo-Elkhair, SM
   Sobh, M
   El-Sokkary, AMA
AF Emama, Ahmed A.
   Abo-Elkhair, Salwa M.
   Sobh, Mohamed
   El-Sokkary, Ahmed M. A.
TI Role of exopolysaccharides (EPSs) as anti-Mir-155 in cancer cells
SO HELIYON
LA English
DT Article
DE Exopolysaccharides; miR-155; Cancer cell lines; HCC; Breast cancer;
   Colon cancer
ID TUMOR-SUPPRESSOR; BREAST-CANCER; HEPATOCELLULAR-CARCINOMA; BETA-CATENIN;
   EXPRESSION; MICRORNA-155; APOPTOSIS; AUTOPHAGY; ONCOMIR
AB Micro-RNAs (MiRNAs) are a class of small non-coding RNAs that regulate cellular gene expression. MiR-155 overexpression has been implicated in many types of cancer. Besides, miR-155 appears to help tumor invasion and migration and works as a moderator of epithelial-to-mesenchymal transition (EMT). Exopolysaccharides (EPSs) are a large group of natural heterogeneous polymers of sugars with a biologically antitumor effect. Herein, we test a hypothesis that EPS might promote its anti-tumorigenic effect via regulating miR-155 expression and its target pathways. Expression of miR-155 and a panel of targeted genes were investigated by real-time PCR. In our study, we have succeeded in the extraction, purification of exopolysaccharide with great cytotoxicity to different cancer cell lines, HepG II, Caco-2, and MCF-7. We reported that EPSs have a suppression effect on the oncogenic miR-155. In conclusion, this work clarifies a new possible mechanism for the anti-tumorigenic effect of EPSs in cancer cells and provides insights into the biological pathways through which EPSs act. Moreover, it paves the way for new prospective cancer therapeutics as anti-miRNA.
C1 [Emama, Ahmed A.; Sobh, Mohamed] Mansoura Univ, Fac Med, Med Expt Res Ctr MERC, Mansoura, Egypt.
   [Abo-Elkhair, Salwa M.] Mansoura Univ, Fac Med, Med Biochem & Mol Biol Dept, Mansoura, Egypt.
   [Sobh, Mohamed] Mansoura Univ, Urol & Nephrol Ctr, Fac Med, Mansoura, Egypt.
   [El-Sokkary, Ahmed M. A.] Mansoura Univ, Fac Sci, Chem Dept, Biochem Div, Mansoura, Egypt.
RP El-Sokkary, AMA (corresponding author), Mansoura Univ, Fac Sci, Chem Dept, Biochem Div, Mansoura, Egypt.
EM aelsokkary@mans.edu.eg
OI Emam, Ahmed Abdou/0000-0002-4391-9725
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   Zadeh MM, 2016, J BREAST CANCER, V19, P45, DOI 10.4048/jbc.2016.19.1.45
NR 39
TC 0
Z9 0
U1 0
U2 2
PU ELSEVIER SCI LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND
EI 2405-8440
J9 HELIYON
JI Heliyon
PD APR
PY 2021
VL 7
IS 4
AR e06698
DI 10.1016/j.heliyon.2021.e06698
EA APR 2021
PG 9
WC Multidisciplinary Sciences
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Science & Technology - Other Topics
GA UW4KX
UT WOS:000700128000018
PM 33869874
OA gold, Green Published
DA 2022-04-25
ER

PT J
AU Chen, MB
   Liu, YY
   Xing, ZY
   Zhang, ZQ
   Jiang, Q
   Lu, PH
   Cao, C
AF Chen, Min-Bin
   Liu, Yuan-Yuan
   Xing, Zhao-Yu
   Zhang, Zhi-Qing
   Jiang, Qin
   Lu, Pei-Hua
   Cao, Cong
TI Itraconazole-Induced Inhibition on Human Esophageal Cancer Cell Growth
   Requires AMPK Activation
SO MOLECULAR CANCER THERAPEUTICS
LA English
DT Article
ID PROTEIN-KINASE; COLORECTAL-CANCER; LIVER-CELLS; PATHWAY;
   PHOSPHORYLATION; METABOLISM; APOPTOSIS; MTOR; AUTOPHAGY; ULK1
AB We here evaluated the antiesophageal cancer cell activity by the antifungal drug itraconazole. Our results show that mg/mL concentrations of itraconazole potently inhibited survival and proliferation of established (TE-1 and Eca-109) and primary human esophageal cancer cells. Itraconazole activated AMPK signaling, which was required for subsequent esophageal cancer cell death. Pharmacologic AMPK inhibition, AMPKa1 shRNA, or dominant negative mutation (T172A) almost completely abolished itraconazole-induced cytotoxicity against esophageal cancer cells. Significantly, itraconazole induced AMPK-dependent autophagic cell death (but not apoptosis) in esophageal cancer cells. Furthermore, AMPK activation by itraconazole induced multiple receptor tyrosine kinases (RTKs: EGFR, PDGFRa, and PDGFRb), lysosomal translocation, and degradation to inhibit downstream Akt activation. In vivo, itraconazole oral gavage potently inhibited Eca-109 tumor growth in SCID mice. It was yet ineffective against AMPKa1 shRNA-expressing Eca-109 tumors. The in vivo growth of the primary human esophageal cancer cells was also significantly inhibited by itraconazole administration. AMPK activation, RTK degradation, and Akt inhibition were observed in itraconazole-treated tumors. Together, itraconazole inhibits esophageal cancer cell growth via activating AMPK signaling. (C) 2018 AACR.
C1 [Chen, Min-Bin] Jiangsu Univ, Kunshan Peoples Hosp 1, Dept Radiotherapy & Oncol, Kunshan, Peoples R China.
   [Liu, Yuan-Yuan] Jiangsu Univ, Kunshan Peoples Hosp 1, Clin Res & Lab Ctr, Kunshan, Peoples R China.
   [Xing, Zhao-Yu] Soochow Univ, Affiliated Hosp 3, Dept Urol, Changzhou, Peoples R China.
   [Zhang, Zhi-Qing; Cao, Cong] Soochow Univ, Inst Neurosci, Suzhou, Peoples R China.
   [Jiang, Qin; Cao, Cong] Nanjing Med Univ, Affiliated Eye Hosp, Nanjing, Jiangsu, Peoples R China.
   [Lu, Pei-Hua] Nanjing Med Univ, Wuxi Peoples Hosp, Dept Med Oncol, 299 Qingyang Rd, Wuxi 214023, Peoples R China.
   [Cao, Cong] Municipal Hosp Suzhou, Suzhou, Peoples R China.
RP Lu, PH (corresponding author), Nanjing Med Univ, Wuxi Peoples Hosp, Dept Med Oncol, 299 Qingyang Rd, Wuxi 214023, Peoples R China.; Jiang, Q (corresponding author), Nanjing Med Univ, Affiliated Eye Hosp, 138 Han Zhong Rd, Nanjing 210029, Jiangsu, Peoples R China.; Cao, C (corresponding author), Soochow Univ, SIP, 199 Renai Rd, Suzhou 215123, Jiangsu, Peoples R China.
EM Jqin710@vip.sina.com; lphty1_1@163.com; caocong@suda.edu.cn
OI Lu, Peihua/0000-0002-4622-3061; , Min-Bin/0000-0003-1453-8664
FU National Natural Science FoundationNational Natural Science Foundation
   of China (NSFC) [81771457/81302195/31371139/81571282, 81472786/81773192,
   81502162, 81472305]; Six Talents Peak Project of Jiangsu Province
   [2014-WSN-012, 2014-WSN-061]; Kunshan Science and Technology Program
   [KS1418]; Natural Science Foundation of Jiangsu ProvinceNatural Science
   Foundation of Jiangsu Province [BK20130301/BK20170060, BK20171248]
FX This work is supported by the National Natural Science Foundation
   (81771457/81302195/31371139/81571282 to C. Cao, 81472786/81773192 to M.
   B. Chen, 81472305 to P. H. Lu, and 81502162 to Z. Q. Zhang), the Six
   Talents Peak Project of Jiangsu Province (2014-WSN-012 to M. B. Chen and
   2014-WSN-061 to P. H. Lu), Kunshan Science and Technology Program
   (KS1418 to M. B. Chen), and by grants from Natural Science Foundation of
   Jiangsu Province (BK20130301/BK20170060 to C. Cao and BK20171248 to M.
   B. Chen).
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NR 39
TC 21
Z9 22
U1 1
U2 8
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 1535-7163
EI 1538-8514
J9 MOL CANCER THER
JI Mol. Cancer Ther.
PD JUN
PY 2018
VL 17
IS 6
BP 1229
EP 1239
DI 10.1158/1535-7163.MCT-17-1094
PG 11
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA GH8QG
UT WOS:000433932800009
PM 29592879
OA Bronze
DA 2022-04-25
ER

PT J
AU Panganiban, RAM
   Snow, AL
   Day, RM
AF Panganiban, Ronald-Allan M.
   Snow, Andrew L.
   Day, Regina M.
TI Mechanisms of Radiation Toxicity in Transformed and Non-Transformed
   Cells
SO INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
LA English
DT Review
DE ionizing radiation; apoptosis; necrosis; senescence; autophagy; cancer;
   primary cell
ID ENDOPLASMIC-RETICULUM STRESS; RAT LUNG IRRADIATION; DOUBLE-STRAND
   BREAKS; CASPASE RECRUITMENT DOMAIN; COLON-CANCER CELLS; FACTOR-KAPPA-B;
   WILD-TYPE P53; IONIZING-RADIATION; INDUCED APOPTOSIS; CELLULAR
   SENESCENCE
AB Radiation damage to biological systems is determined by the type of radiation, the total dosage of exposure, the dose rate, and the region of the body exposed. Three modes of cell deathnecrosis, apoptosis, and autophagyas well as accelerated senescence have been demonstrated to occur in vitro and in vivo in response to radiation in cancer cells as well as in normal cells. The basis for cellular selection for each mode depends on various factors including the specific cell type involved, the dose of radiation absorbed by the cell, and whether it is proliferating and/or transformed. Here we review the signaling mechanisms activated by radiation for the induction of toxicity in transformed and normal cells. Understanding the molecular mechanisms of radiation toxicity is critical for the development of radiation countermeasures as well as for the improvement of clinical radiation in cancer treatment.
C1 [Panganiban, Ronald-Allan M.; Snow, Andrew L.; Day, Regina M.] Uniformed Serv Univ Hlth Sci, Dept Pharmacol, Bethesda, MD 20814 USA.
RP Day, RM (corresponding author), Uniformed Serv Univ Hlth Sci, Dept Pharmacol, 4301 Jones Bridge Rd, Bethesda, MD 20814 USA.
EM ronald-allan.panganiban@usuhs.edu; andrew.snow@usuhs.edu;
   regina.day@usuhs.edu
RI Panganiban, Ronald Allan/AAH-3859-2020
OI Panganiban, Ronald Allan/0000-0003-0894-1318; Snow,
   Andrew/0000-0002-8728-6691
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NR 208
TC 60
Z9 62
U1 0
U2 17
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
SN 1422-0067
J9 INT J MOL SCI
JI Int. J. Mol. Sci.
PD AUG
PY 2013
VL 14
IS 8
BP 15931
EP 15958
DI 10.3390/ijms140815931
PG 28
WC Biochemistry & Molecular Biology; Chemistry, Multidisciplinary
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Chemistry
GA 272ZE
UT WOS:000328501300039
PM 23912235
OA gold, Green Submitted, Green Published
DA 2022-04-25
ER

PT J
AU Kandouz, M
AF Kandouz, Mustapha
TI Dying to communicate: apoptotic functions of Eph/Ephrin proteins
SO APOPTOSIS
LA English
DT Review
DE Eph receptor; Ephrin; Cell-cell communication; Intercellular
   communication; Apoptosis
ID RECEPTOR TYROSINE KINASE; AUTOPHAGIC CELL-DEATH; SPINAL-CORD-INJURY;
   COLORECTAL-CANCER PROGRESSION; TRAUMATIC BRAIN-INJURY; RETINAL
   GANGLION-CELLS; MAMMARY-GLAND DEVELOPMENT; LIPID-BINDING PROTEIN; EPH
   RECEPTORS; TUMOR-GROWTH
AB The Erythropoietin-producing human hepatocellular carcinoma (Eph) receptors constitute the largest family of receptor tyrosine kinases and interact with a group of ligands called Ephrins. An essential feature of the Eph receptors and Ephrin ligands is that both are membrane-bound and, upon cell-cell interaction, initiate a bidirectional signaling involving both the receptor (forward signaling) and the ligand (reverse signaling). They regulate a large set of pleiotropic functions in virtually every tissue and physiological system. In vitro as well as in vivo data support a role for Eph and Ephrin molecules in cellular processes such as proliferation, cell-cell attraction and repulsion, motility and sorting. An increasing amount of evidence supports a role for these molecules in apoptosis and, although this function in cell death has been barely examined, the available information warrants a global consideration, to identify unmet needs and potential research avenues. Here we propose a comprehensive analysis of the data available regarding the importance of Ephs and Ephrins in cell death mechanisms throughout a large array of physiological systems.
C1 [Kandouz, Mustapha] Wayne State Univ, Sch Med, Dept Pathol, Scott Hall Bldg Room 9207,540 East Canfield, Detroit, MI 48201 USA.
   [Kandouz, Mustapha] Wayne State Univ, Karmanos Canc Inst, Detroit, MI USA.
RP Kandouz, M (corresponding author), Wayne State Univ, Sch Med, Dept Pathol, Scott Hall Bldg Room 9207,540 East Canfield, Detroit, MI 48201 USA.; Kandouz, M (corresponding author), Wayne State Univ, Karmanos Canc Inst, Detroit, MI USA.
EM ag1764@wayne.edu
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NR 245
TC 4
Z9 4
U1 0
U2 10
PU SPRINGER
PI DORDRECHT
PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS
SN 1360-8185
EI 1573-675X
J9 APOPTOSIS
JI Apoptosis
PD JUN
PY 2018
VL 23
IS 5-6
BP 265
EP 289
DI 10.1007/s10495-018-1458-7
PG 25
WC Biochemistry & Molecular Biology; Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Cell Biology
GA GJ2SP
UT WOS:000435123200003
PM 29767378
DA 2022-04-25
ER

PT J
AU Yang, PM
   Lin, YT
   Shun, CT
   Lin, SH
   Wei, TT
   Chuang, SH
   Wu, MS
   Chen, CC
AF Yang, Pei-Ming
   Lin, Yi-Ting
   Shun, Chia-Tung
   Lin, Shan-Hu
   Wei, Tzu-Tang
   Chuang, Shu-Hui
   Wu, Ming-Shiang
   Chen, Ching-Chow
TI Zebularine inhibits tumorigenesis and stemness of colorectal cancer via
   p53-dependent endoplasmic reticulum stress
SO SCIENTIFIC REPORTS
LA English
DT Article
ID UNFOLDED PROTEIN RESPONSE; ACUTE MYELOID-LEUKEMIA; CYTIDINE DEAMINASE;
   CELL-DEATH; CARCINOMA-CELLS; DNA METHYLATION; AUTOPHAGY; P53;
   5-AZACYTIDINE; GENE
AB Aberrant DNA hypermethylation is frequently found in tumor cells and inhibition of DNA methylation is an effective anticancer strategy. In this study, the therapeutic effect of DNA methyltransferase (DNMT) inhibitor zebularine (Zeb) on colorectal cancer (CRC) was investigated. Zeb exhibited anticancer activity in cell cultures, tumor xenografts and mouse colitis-associated CRC model. It stabilizes p53 through ribosomal protein S7 (RPS7)/MDM2 pathways and DNA damage. Zeb-induced cell death was dependent on p53. Microarray analysis revealed that genes related to endoplasmic reticulum (ER) stress and unfolded protein response (UPR) were affected by Zeb. Zeb induced p53-dependent ER stress and autophagy. Pro-survival markers of ER stress/UPR (GRP78) and autophagy (p62) were increased in tumor tissues of CRC patients, AOM/DSS-induced CRC mice and HCT116-derived colonospheres. Zeb downregulates GRP78 and p62, and upregulates a pro-apoptotic CHOP. Our results reveal a novel mechanism for the anticancer activity of Zeb.
C1 [Yang, Pei-Ming; Lin, Yi-Ting; Lin, Shan-Hu; Wei, Tzu-Tang; Chuang, Shu-Hui; Chen, Ching-Chow] Natl Taiwan Univ, Coll Med, Dept Pharmacol, Taipei 10764, Taiwan.
   [Yang, Pei-Ming] Taipei Med Univ, Coll Med Sci & Technol, PhD Program Canc Biol & Drug Discovery, Taipei, Taiwan.
   [Shun, Chia-Tung] Natl Taiwan Univ Hosp, Dept Forens Med & Pathol, Taipei, Taiwan.
   [Wu, Ming-Shiang] Natl Taiwan Univ Hosp, Dept Internal Med, Div Gastroenterol, Taipei 100, Taiwan.
RP Chen, CC (corresponding author), Natl Taiwan Univ, Coll Med, Dept Pharmacol, Taipei 10764, Taiwan.
EM chingchowchen@ntu.edu.tw
RI Shun, Chia-Tung/M-1400-2019; Yang, Pei-Ming/G-3763-2014; WEI,
   TZU-TANG/AAT-8447-2020; CHUANG, SHU-HUI/F-8625-2017
OI Yang, Pei-Ming/0000-0002-4004-2518; Wu, Ming-Shiang/0000-0002-1940-6428;
   CHEN, CHING-CHOW/0000-0002-7810-0939; SHUN,
   CHIA-TUNG/0000-0002-0468-4468; CHUANG, SHU-HUI/0000-0002-6123-3874
FU National Science Council of TaiwanMinistry of Science and Technology,
   Taiwan
FX This work was supported by a research grant from the National Science
   Council of Taiwan.
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NR 52
TC 48
Z9 49
U1 1
U2 26
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 2045-2322
J9 SCI REP-UK
JI Sci Rep
PD NOV 14
PY 2013
VL 3
AR 3219
DI 10.1038/srep03219
PG 11
WC Multidisciplinary Sciences
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Science & Technology - Other Topics
GA 252PV
UT WOS:000327020700009
PM 24225777
OA Green Published, gold, Green Submitted
DA 2022-04-25
ER

PT J
AU Hu, JL
   He, GY
   Lan, XL
   Zeng, ZC
   Guan, J
   Ding, Y
   Qian, XL
   Liao, WT
   Ding, YQ
   Liang, L
AF Hu, J. L.
   He, G. Y.
   Lan, X. L.
   Zeng, Z. C.
   Guan, J.
   Ding, Y.
   Qian, X. L.
   Liao, W. T.
   Ding, Y. Q.
   Liang, L.
TI Inhibition of ATG12-mediated autophagy by miR-214 enhances
   radiosensitivity in colorectal cancer
SO ONCOGENESIS
LA English
DT Article
ID HYPOXIA-INDUCED AUTOPHAGY; DOWN-REGULATION; BREAST-CANCER;
   HEPATOCELLULAR-CARCINOMA; NASOPHARYNGEAL CARCINOMA; LUNG-CANCER; CELLS;
   RADIATION; APOPTOSIS; RADIORESISTANCE
AB Radioresistance hampers success in the treatment of patients with advanced colorectal cancer (CRC). Improving our understanding of the underlying mechanisms of radioresistance could increase patients' response to irradiation (IR). MicroRNAs are a class of small RNAs involved in tumor therapy response to radiation. Here we found that miR-214 was markedly decreased in CRC cell lines and blood of CRC patients after IR exposure. Meanwhile, autophagy was enhanced in irradiated CRC cells. Mechanically, ATG12 was predicted and identified as a direct target of miR-214 by dual luciferase assay, qPCR, and Western blot. In vitro and in vivo experiments showed that miR-214 promoted radiosensitivity by inhibiting IR-induced autophagy. Restoration of ATG12 attenuated miR-214-mediated inhibition of cell growth and survival in response to IR. Importantly, miR-214 was highly expressed in radiosensitive CRC specimens and negatively correlated with plasma level of CEA. Moreover, ATG12 and LC3 expressions were increased in radioresistant CRC specimens. Our study elucidates that miR-214 promotes radiosensitivity by inhibition of ATG12-mediated autophagy in CRC. Importantly, miR-214 is a determinant of CRC irradiation response and may serve as a potential therapeutic target in CRC treatment.
C1 [Hu, J. L.; He, G. Y.; Lan, X. L.; Zeng, Z. C.; Liao, W. T.; Ding, Y. Q.; Liang, L.] Southern Med Univ, Nanfang Hosp, Dept Pathol, Guangzhou 510515, Guangdong, Peoples R China.
   [Hu, J. L.; He, G. Y.; Lan, X. L.; Zeng, Z. C.; Liao, W. T.; Ding, Y. Q.; Liang, L.] Southern Med Univ, Dept Pathol, Guangzhou 510515, Guangdong, Peoples R China.
   [Hu, J. L.; Zeng, Z. C.; Liao, W. T.; Ding, Y. Q.; Liang, L.] Guangdong Prov Key Lab Mol Tumor Pathol, Guangzhou 510515, Guangdong, Peoples R China.
   [He, G. Y.; Qian, X. L.] Xinxiang Med Univ, Dept Pathol, Xinxiang 453003, Henan, Peoples R China.
   [Lan, X. L.] Southern Med Univ, Nanfang Hosp, Dept Gen Surg, Guangzhou 510515, Guangdong, Peoples R China.
   [Guan, J.; Ding, Y.] Southern Med Univ, Nanfang Hosp, Dept Radiotherapy, Guangzhou 510515, Guangdong, Peoples R China.
RP Liang, L (corresponding author), Southern Med Univ, Nanfang Hosp, Dept Pathol, Guangzhou 510515, Guangdong, Peoples R China.; Liang, L (corresponding author), Southern Med Univ, Dept Pathol, Guangzhou 510515, Guangdong, Peoples R China.
EM redsnow007@hotmail.com
RI liang, li/AAB-9126-2022
FU National Key R&D program of China [2017YFC1309002]; National Basic
   Research Program of China (973 Program)National Basic Research Program
   of China [2015CB554002]; National Natural Science Foundation of
   ChinaNational Natural Science Foundation of China (NSFC) [81672821,
   81272759, 81472313, 81401927, 81773101]
FX This work was supported by the National Key R&D program of China
   (2017YFC1309002), National Basic Research Program of China (973 Program,
   2015CB554002), and National Natural Science Foundation of China
   (81672821, 81272759, 81472313, 81401927, 81773101).
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NR 38
TC 66
Z9 73
U1 2
U2 11
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 2157-9024
J9 ONCOGENESIS
JI Oncogenesis
PD FEB
PY 2018
VL 7
AR 16
DI 10.1038/s41389-018-0028-8
PG 12
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA GC0LT
UT WOS:000429469500004
PM 29459645
OA Green Published, gold
DA 2022-04-25
ER

PT J
AU Ranjbar, K
   Ballaro, R
   Bover, Q
   Pin, F
   Beltra, M
   Penna, F
   Costelli, P
AF Ranjbar, Kia
   Ballaro, Riccardo
   Bover, Quim
   Pin, Fabrizio
   Beltra, Marc
   Penna, Fabio
   Costelli, Paola
TI Combined Exercise Training Positively Affects Muscle Wasting in
   Tumor-Bearing Mice
SO MEDICINE AND SCIENCE IN SPORTS AND EXERCISE
LA English
DT Article
DE CANCER CACHEXIA; AEROBIC TRAINING; RESISTANCE TRAINING; AUTOPHAGY; PGC-1
   alpha
ID RESISTANCE EXERCISE; CANCER CACHEXIA; ADIPOSE-TISSUE; MECHANISMS;
   PGC-1-ALPHA; PROGRESSION; ADAPTATION; PREVENTION; AUTOPHAGY; ATROPHY
AB Introduction Cancer cachexia is characterized by loss of muscle mass and function. Increased protein catabolism, inflammation, impaired anabolism, and mitochondrial function markedly contribute to the pathogenesis of this syndrome. Physical activity has been suggested as a useful tool to prevent or at least delay the onset and progression of cancer-induced muscle wasting. Two main types of exercise can be adopted, namely, resistance and endurance training. The present study is aimed to investigate the effectiveness of a combined (resistance + endurance) exercise protocol in preventing/reverting cancer-induced muscle wasting. Methods Mice bearing the C26 colon carcinoma have been used as a model of cancer cachexia. They have been exposed to combined exercise training during 6 wk (4 before tumor implantation, 2 during tumor growth). Climbing a 1-m ladder inclined at 85 degrees has been used for resistance training, while aerobic (endurance) exercise has been carried out on the same day using a motorized wheel. Results In C26-bearing mice, both muscle mass and strength are improved by combined training, while just the latter increased in exercised healthy animals. Such a pattern is associated with modulations of two markers of autophagy, namely, LC3B-I/II ratio, increased in sedentary tumor hosts and reduced in exercised C26-bearing mice, and p62, steadily increased in both sedentary and trained tumor-bearing animals. Finally, combined training is not able to modify PGC-1 alpha protein levels, but it improves succinate dehydrogenase activity, both reduced in the muscle of the C26 hosts. Conclusion The data reported in the present study show that combined training improves muscle mass and function in the C26 hosts, likely modulating autophagy and improving mitochondrial function; these observations suggest that combined exercise might become part of a multimodal approach to treat cancer cachexia.
C1 [Ranjbar, Kia; Ballaro, Riccardo; Bover, Quim; Pin, Fabrizio; Beltra, Marc; Penna, Fabio; Costelli, Paola] Univ Turin, Dept Clin & Biol Sci, Corso Raffaello 30, I-10125 Turin, Italy.
   [Ranjbar, Kia] Tarbiat Modares Univ, Phys Educ & Sport Sci Dept, Tehran, Iran.
   [Ballaro, Riccardo; Beltra, Marc; Penna, Fabio; Costelli, Paola] Interuniv Inst Myol, Urbino, Italy.
   [Pin, Fabrizio] Indiana Univ Sch Med, Dept Anat & Cell Biol, Indianapolis, IN 46202 USA.
RP Costelli, P (corresponding author), Univ Turin, Dept Clin & Biol Sci, Corso Raffaello 30, I-10125 Turin, Italy.
EM paola.costelli@unito.it
RI Ballarò, Riccardo/ABC-1988-2020
OI Ballarò, Riccardo/0000-0001-5505-9024; Beltra Bach,
   Marc/0000-0001-6070-9861
FU University of Turin; Ministry of Science, Research and Technology,
   Islamic Republic of Iran
FX This work was supported by the University of Turin. K. Ranjbar was
   recipient of a scholarship funded by the Ministry of Science, Research
   and Technology, Islamic Republic of Iran. The authors are grateful to
   Dr. Conrad P. Earnest, Department of Health and Kinesiology, Texas A&M
   University, College Station, TX, for his critical discussion of results.
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NR 39
TC 22
Z9 22
U1 2
U2 12
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA TWO COMMERCE SQ, 2001 MARKET ST, PHILADELPHIA, PA 19103 USA
SN 0195-9131
EI 1530-0315
J9 MED SCI SPORT EXER
JI Med. Sci. Sports Exerc.
PD JUL
PY 2019
VL 51
IS 7
BP 1387
EP 1395
DI 10.1249/MSS.0000000000001916
PG 9
WC Sport Sciences
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Sport Sciences
GA ID4WK
UT WOS:000471676800005
PM 30724848
OA Bronze
DA 2022-04-25
ER

PT J
AU Carew, JS
   Giles, FJ
   Nawrocki, ST
AF Carew, Jennifer S.
   Giles, Francis J.
   Nawrocki, Steffan T.
TI Histone deacetylase inhibitors: Mechanisms of cell death and promise in
   combination cancer therapy
SO CANCER LETTERS
LA English
DT Review
DE historic deacetylase inhibitor; apoptosis; autophagy; bortezomib; TRAIL
ID SUBEROYLANILIDE HYDROXAMIC ACID; HUMAN LEUKEMIA-CELLS; PROAPOPTOTIC
   PROTEIN BIM; HUMAN COLON-CANCER; INDUCED APOPTOSIS; HDAC INHIBITORS;
   PANCREATIC-CANCER; SODIUM-BUTYRATE; DOWN-REGULATION; SYNERGISTIC
   INDUCTION
AB Histone deacetylases (HDACs) play an important role in the epigenetic regulation of gene expression by catalyzing the removal of acetyl groups, stimulating chromatin condensation and promoting transcriptional repression. Since aberrant epigenetic changes are a hallmark of cancer, HDACs are a promising target for pharmacological inhibition. HDAC inhibitors can induce cell-cycle arrest, promote differentiation, and stimulate tumor cell death. These properties have prompted numerous preclinical and clinical investigations evaluating the potential efficacy of HDAC inhibitors for a variety of malignancies. The preferential toxicity of HDAC inhibitors in transformed cells and their ability to synergistically enhance the anticancer activity of many chemotherapeutic agents has further generated interest in this novel class of drugs. Here we summarize the different mechanisms of HDAC inhibitor-induced apoptosis and discuss their use in combination with other anticancer agents. (C) 2008 Elsevier Ireland Ltd. All rights reserved.
C1 [Carew, Jennifer S.; Giles, Francis J.; Nawrocki, Steffan T.] Univ Texas Hlth Sci Ctr San Antonio, Inst Drug Dev, Canc Therapy & Res Ctr, San Antonio, TX 78245 USA.
RP Nawrocki, ST (corresponding author), Univ Texas Hlth Sci Ctr San Antonio, Inst Drug Dev, Canc Therapy & Res Ctr, 14960 Omicron Dr, San Antonio, TX 78245 USA.
EM nawrocki@uthscsa.edu
RI qiao, zhixin/I-3408-2012
FU Institute for Drug Development, Cancer Therapy and Research Center at
   The Umversity of Texas Health Science Center at San Antonio
FX This work was supported by funding from The Institute for Drug
   Development, Cancer Therapy and Research Center at The Umversity of
   Texas Health Science Center at San Antonio.
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   [No title captured]
NR 73
TC 346
Z9 371
U1 2
U2 81
PU ELSEVIER IRELAND LTD
PI CLARE
PA ELSEVIER HOUSE, BROOKVALE PLAZA, EAST PARK SHANNON, CO, CLARE, 00000,
   IRELAND
SN 0304-3835
EI 1872-7980
J9 CANCER LETT
JI Cancer Lett.
PD SEP 28
PY 2008
VL 269
IS 1
BP 7
EP 17
DI 10.1016/j.canlet.2008.03.037
PG 11
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA 357LK
UT WOS:000259847100002
PM 18462867
DA 2022-04-25
ER

PT J
AU Zhang, YS
   Wang, F
   Cui, SX
   Qu, XJ
AF Zhang, Yu-Sheng
   Wang, Feng
   Cui, Shu-Xiang
   Qu, Xian-Jun
TI Natural dietary compound naringin prevents azoxymethane/dextran sodium
   sulfate-induced chronic colorectal inflammation and carcinogenesis in
   mice
SO CANCER BIOLOGY & THERAPY
LA English
DT Article
DE Colitis; colorectal carcinogenesis; Endoplasmic reticulum (ER) stress;
   autophagy; MDSCs; Naringin; Aspirin
ID SUPPRESSOR-CELLS; CANCER; DISEASE; DYSFUNCTION; AUTOPHAGY; COLITIS;
   RISK; ACTIVATION; APOPTOSIS; ASPIRIN
AB Naringin, a natural occurring flavonoid compound, enriches in citrus fruits. We aimed to evaluate the inhibitory effect of naringin on colitis and chronic inflammation-driven carcinogenesis. Male C57BL/6 mice were exposed to AOM/DSS to induce colorectal inflammation and carcinogenesis. Naringin by oral administration prevented AOM/DSS-induced ulcerative colitis and carcinogenesis without significant side effects. Naringin attenuated the severity of colitis and colorectal adenomas through inhibiting myeloid-derived suppressor cells (MDSCs), pro-inflammatory mediators GM-CSF/M-CSF, IL-6 and TNF-alpha and the NF-kappa B/IL-6/STAT3 cascades in colorectal tissues. Naringin-treated mice exhibited normalized structures of colorectal tissues. Electron microscopy analysis showed the suppression of robust endoplasmic reticulum (ER) stress-induced autophagy. Naringin inhibited the secretion of the ER-spanning transmembrane proteins, such as GRP78 ATF6, IRE1 alpha and activated PERK phosphorylated eIF-2 alpha and complex of autophagosomes ATG3, ATG5, ATG7, ATG12, ATG16 and ATG16L1 in the colorectal mucosal cells. Conclusion: Naringin prevented colitis and colorectal carcinogenesis through suppressing robust ER stress-induced autophagy in colorectal mucosal cells. Naringin could develop a promising therapeutic agent for the prevention of ulcerative colitis and colorectal tumor.
C1 [Zhang, Yu-Sheng; Qu, Xian-Jun] Shandong Univ, Sch Pharmaceut Sci, Jinan, Shandong, Peoples R China.
   [Wang, Feng; Cui, Shu-Xiang] Capital Med Univ, Beijing Key Lab Environm Toxicol, Sch Publ Hlth, Dept Toxicol & Sanit Chem, Beijing, Peoples R China.
RP Cui, SX; Qu, XJ (corresponding author), 10 You An Men Wai, Beijing 100069, Peoples R China.
EM sxccui@ccmu.edu.cn; qxj@sdu.edu.cn
FU Shandong Natural Science FoundationNatural Science Foundation of
   Shandong Province [ZR2009CQ019]; Natural Science Foundation of
   ChinaNational Natural Science Foundation of China (NSFC) [91629303]
FX This project was supported by the Shandong Natural Science Foundation
   (ZR2009CQ019). This project was supported by the Natural Science
   Foundation of China (91629303).
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NR 36
TC 20
Z9 21
U1 10
U2 15
PU TAYLOR & FRANCIS INC
PI PHILADELPHIA
PA 530 WALNUT STREET, STE 850, PHILADELPHIA, PA 19106 USA
SN 1538-4047
EI 1555-8576
J9 CANCER BIOL THER
JI Cancer Biol. Ther.
PY 2018
VL 19
IS 8
BP 735
EP 744
DI 10.1080/15384047.2018.1453971
PG 10
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA GN9ZO
UT WOS:000439574300012
PM 29580144
OA Green Published, Bronze
DA 2022-04-25
ER

PT J
AU Sun, JW
   Yang, JY
   Chen, X
   Li, L
   Hao, J
   Niu, H
   Lai, MH
   Qiu, S
AF Sun, Jian-Wei
   Yang, Jing-Yu
   Chen, Xin
   Li, Li
   Hao, Jie
   Niu, Heng
   Lai, Ming-Hua
   Qiu, Shuang
TI Silencing of VMP1 makes breast cancer cells more aggressive and
   resistant to 5-Fu
SO INTERNATIONAL JOURNAL OF CLINICAL AND EXPERIMENTAL MEDICINE
LA English
DT Article
DE VMP1; breast cancer; lentivirus; chemotherapy; 5-Fu
ID BECLIN 1; AUTOPHAGY; EXPRESSION; COLON; METASTASIS; PATTERNS
AB Background: Vacuole membrane protein 1 (VMP1) was recently characterized to be involved in the process of cancer metastasis, and is also considered to play a vital role in balancing apoptosis and autophagy. Methods and results: Here, we evaluated the expression of VMP1 in 98 breast cancer and 54 matched adjacent noncancerous tissues with immunohistochemistry (IHC). The results showed a lower expression of VMP1 in advanced stages of breast cancer. Moreover, the patients with low expression of VMP1 were related to poor prognosis than those with high expression. Furthermore, to investigate whether the downregulation of VMP1 could confer malignant potential to breast cancer cells, we constructed and verified a lentivirus-based knockdown system to silence the expression of VMP1 in Michigan Cancer Foundation-7 cells (MCF7). After infection with lentivirus, the shVMP1 cells, which had VMP1 stably suppressed, gained significant aggressive properties of invasion and proliferation, and these mechanisms may relate to the activation of phosphatidylinositol 3-hydroxy kinase (PI3K)/protein kinase B(Akt)/zonulaoccludens-1 (ZO-1)/E-Cadherin pathway. On the other hand, we also found that shVMP1 cells were more sensitive to 5-Fluorouracil (5-Fu), but not cisplatin and oxaliplatin. Conclusions: In all, the above data suggest that patients with lower expression of VMP1 may have a poor prognosis, which may be ascribed to the more aggressive potential after down-regulation of VMP1 in breast cancer cells. In addition, these patients who have low expression of VMP1 may benefit from chemotherapy regimens containing 5-Fu.
C1 [Sun, Jian-Wei; Yang, Jing-Yu; Chen, Xin; Li, Li; Hao, Jie; Niu, Heng; Lai, Ming-Hua; Qiu, Shuang] Kunming Univ Technol, Affiliated Hosp, Peoples Hosp Yunnan Prov 1, Dept Breast & Thyroid Surg, Kunming 650221, Yunnan, Peoples R China.
RP Sun, JW (corresponding author), Kunming Univ Technol, Affiliated Hosp, Peoples Hosp Yunnan Prov 1, Dept Breast & Thyroid Surg, Kunming 650221, Yunnan, Peoples R China.
EM drsunjianwei@163.com
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NR 24
TC 0
Z9 0
U1 0
U2 2
PU E-CENTURY PUBLISHING CORP
PI MADISON
PA 40 WHITE OAKS LN, MADISON, WI 53711 USA
SN 1940-5901
J9 INT J CLIN EXP MED
JI Int. J. Clin. Exp. Med.
PY 2019
VL 12
IS 11
BP 13096
EP 13107
PG 12
WC Medicine, Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Research & Experimental Medicine
GA JS4TZ
UT WOS:000500300700062
DA 2022-04-25
ER

PT J
AU Mun, JG
   Han, YH
   Jeon, HD
   Yoon, DH
   Lee, YG
   Hong, SH
   Kee, JY
AF Mun, Jeong-Geon
   Han, Yo-Han
   Jeon, Hee-Dong
   Yoon, Dae Hwan
   Lee, Yeong Gyeong
   Hong, Seung-Heon
   Kee, Ji-Ye
TI Inhibitory Effect of Gallotannin on Lung Metastasis of Metastatic
   Colorectal Cancer Cells by Inducing Apoptosis, Cell Cycle Arrest and
   Autophagy
SO AMERICAN JOURNAL OF CHINESE MEDICINE
LA English
DT Article
DE GT; Metastatic Colorectal Cancer; Apoptosis; Cell Cycle Arrest;
   Autophagy
ID SENESCENCE; EXPRESSION; PATHWAY; AMPK; P53
AB Colorectal cancer (CRC) is the second most common cause of cancer death in the world, and metastatic CRC is a major cause of cancer death. Gallotannin (GT), a polyphenolic compound, has shown various biological effects such as anti-oxidant, anti-inflammatory, antimicrobial, and antitumor effects. However, the effects of GT on metastatic CRC cells are not completely understood. This study aimed to investigate the anti-metastatic effect of GT and the underlying mechanisms on metastatic CRC cells. Oral administration of GT suppressed the lung metastasis of metastatic CRC cells in the experimental mouse model. GT decreased the viability of metastatic CRC cell lines, including CT26, HCT116, and SW620, by inducing apoptosis through the activation of extrinsic and intrinsic pathways, cell cycle arrest through inactivation of CDK2/cyclin A complex, and autophagic cell death through up-regulation of LC3B and p62 levels. GT regulated PI3K/AKT/mTOR and AMPK signaling pathways, which are critical for the development and maintenance of cancer. Additionally, non-cytotoxic concentrations of GT can suppress migration and invasion of CRC cells by inhibiting the expression and activity of matrix metalloproteinase (MMP)-2 and MMP-9 and epithelial-mesenchymal transition by downregulating the expression of mesenchymal markers including snail, twist, and vimentin. In conclusion, GT prevented colorectal lung metastasis by reducing survival and inhibiting the metastatic phenotypes of CRC cells.
C1 [Mun, Jeong-Geon; Han, Yo-Han; Jeon, Hee-Dong; Yoon, Dae Hwan; Lee, Yeong Gyeong; Hong, Seung-Heon; Kee, Ji-Ye] Wonkwang Univ, Coll Pharm, Wonkwang Oriental Med Res Inst, Dept Oriental Pharm, 460 Iksandae Ro, Iksan 54538, Jeonbuk, South Korea.
RP Hong, SH; Kee, JY (corresponding author), Wonkwang Univ, Coll Pharm, Wonkwang Oriental Med Res Inst, Dept Oriental Pharm, 460 Iksandae Ro, Iksan 54538, Jeonbuk, South Korea.
EM jooklim@wku.ac.kr; keejy@wku.ac.kr
FU Wonkwang University
FX This study was supported by Wonkwang University in 2019.
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NR 50
TC 2
Z9 2
U1 2
U2 2
PU WORLD SCIENTIFIC PUBL CO PTE LTD
PI SINGAPORE
PA 5 TOH TUCK LINK, SINGAPORE 596224, SINGAPORE
SN 0192-415X
EI 1793-6853
J9 AM J CHINESE MED
JI Am. J. Chin. Med.
PY 2021
VL 49
IS 06
BP 1535
EP 1555
DI 10.1142/S0192415X21500725
PG 21
WC Integrative & Complementary Medicine; Medicine, General & Internal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Integrative & Complementary Medicine; General & Internal Medicine
GA TP9ZS
UT WOS:000677950800012
PM 34247563
DA 2022-04-25
ER

PT J
AU Lee, YH
   Chen, HY
   Su, LJ
   Chueh, PJ
AF Lee, Yi-Hui
   Chen, Huei-Yu
   Su, Lilly J.
   Chueh, Pin Ju
TI Sirtuin 1 (SIRT1) Deacetylase Activity and NAD(+)/VNADH Ratio Are
   Imperative for Capsaicin-Mediated Programmed Cell Death
SO JOURNAL OF AGRICULTURAL AND FOOD CHEMISTRY
LA English
DT Article
DE apoptosis; autophagy; capsaicin; silent mating type information
   regulation 1 (sirtuin 1, SIRT1); tumor-associated NADH oxidase (tNOX,
   ENOX2)
ID ENDOPLASMIC-RETICULUM STRESS; PANCREATIC TUMOR-GROWTH; COLON-CANCER
   CELLS; IN-VITRO; SELECTIVE INDUCTION; TRANSFORMED-CELLS; SIGNALING
   PATHWAY; GENE-EXPRESSION; UP-REGULATION; APOPTOSIS
AB Capsaicin is considered a chemopreventive agent by virtue of its selective antigrowth activity, commonly associated with apoptosis, against cancer cells. However, noncancerous cells possess relatively higher tolerance to capsaicin, although the underlying mechanism for this difference remains unclear. Hence, this study aimed to elucidate the differential effects of capsaicin on cell lines from lung tissues by addressing the signal pathway leading to two types of cell death. In MRC-5 human fetal lung cells, capsaicin augmented silent mating type information regulation 1 (SIRT1) deacetylase activity and the intracellular NAD(+)/VNADH ratio, decreasing acetylation of p53 and inducing autophagy. In contrast, capsaicin decreased the intracellular NAD(+)/NADH ratio, possibly through inhibition of tumor-associated NADH oxidase (tNOX), and diminished SIRT1 expression leading to enhanced p53 acetylation and apoptosis. Moreover, SIRT1 depletion by RNA interference attenuated capsaicin-induced apoptosis in A549 cancer cells and autophagy in MRC-5 cells, suggesting a vital role for SIRT1 in capsaicin-mediated cell death. Collectively, these data not only explain the differential cytotoxicity of capsaicin but shed light on the distinct cellular responses to capsaicin in cancerous and noncancerous cell lines.
C1 [Lee, Yi-Hui; Chen, Huei-Yu; Su, Lilly J.; Chueh, Pin Ju] Natl Chung Hsing Univ, Inst Biomed Sci, Taichung 40227, Taiwan.
   [Chueh, Pin Ju] China Med Univ, Grad Inst Basic Med, Taichung 40402, Taiwan.
   [Chueh, Pin Ju] China Med Univ Hosp, Dept Med Res, Taichung 40402, Taiwan.
   [Chueh, Pin Ju] Asia Univ, Dept Biotechnol, Taichung 41354, Taiwan.
RP Chueh, PJ (corresponding author), Natl Chung Hsing Univ, Inst Biomed Sci, Taichung 40227, Taiwan.
EM pjchueh@dragon.nchu.edu.tw
OI Lee, YiHui/0000-0002-3690-6547; Chueh, Pin Ju/0000-0002-3200-7552
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NR 63
TC 34
Z9 35
U1 2
U2 12
PU AMER CHEMICAL SOC
PI WASHINGTON
PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA
SN 0021-8561
EI 1520-5118
J9 J AGR FOOD CHEM
JI J. Agric. Food Chem.
PD AUG 26
PY 2015
VL 63
IS 33
BP 7361
EP 7370
DI 10.1021/acs.jafc.5b02876
PG 10
WC Agriculture, Multidisciplinary; Chemistry, Applied; Food Science &
   Technology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Agriculture; Chemistry; Food Science & Technology
GA CQ0XO
UT WOS:000360322100007
PM 26255724
DA 2022-04-25
ER

PT J
AU Zhou, N
   Wei, ZX
   Qi, ZX
AF Zhou, Nan
   Wei, Zi Xuan
   Qi, Zeng Xin
TI Inhibition of autophagy triggers melatonin-induced apoptosis in
   glioblastoma cells
SO BMC NEUROSCIENCE
LA English
DT Article
DE Melatonin; Agomelatine; Autophagy; Apoptosis; Glioma
ID GROWTH IN-VIVO; SIGNALING PATHWAYS; INDUCED CYTOTOXICITY; PINEAL
   HORMONE; PHASE-II; BECLIN 1; CANCER; EXPRESSION; RECEPTOR; PROTEIN
AB Background Autophagy is considered to be another restorative focus for the treatment of brain tumors. Although several research have demonstrated that melatonin induces autophagy in colon cancer and hepatoma cells, there has not been any direct evidence of whether melatonin is capable of inducing autophagy in human glioma cells. Results In the present research, we report that melatonin or its agonist, agomelatine, induced autophagy in A172 and U87-MG glioblastoma cells for a concentration-and time-dependent way, which was significantly attenuated by treatment with luzindole, a melatonin receptor antagonist. Furthermore, by suppressing autophagy at the late-stage with bafilomycin A1 and early stage with 3-MA, we found that the melatonin-induced autophagy was activated early, and the autophagic flux was complete. Melatonin treatment alone did not induce any apoptotic changes in the glioblastoma cells, as measured by flow cytometry. Western blot studies confirmed that melatonin alone prominently upregulated the levels of Beclin 1 and LC3 II, which was accompanied by an increase in the expression of Bcl-2, whereas it had no effect on the expression of Bax in the glioblastoma cells. Remarkably, co-treatment with 3-MA and melatonin significantly enhanced the apoptotic cell population in the glioblastoma cells, along with a prominent decrease in the expression of bcl-2 and increase in the Bax expression levels, which collectively indicated that the disruption of autophagy triggers the melatonin-induced apoptosis in glioblastoma cells. Conclusions These results provide information indicating that melatonin may act as a common upstream signal between autophagy and apoptosis, which may lead to the development of new therapeutic strategies for glioma.
C1 [Zhou, Nan; Wei, Zi Xuan; Qi, Zeng Xin] Fudan Univ, Huashan Hosp, Dept Neurosurg, Middle Urumqi Rd 12, Shanghai 200040, Peoples R China.
RP Qi, ZX (corresponding author), Fudan Univ, Huashan Hosp, Dept Neurosurg, Middle Urumqi Rd 12, Shanghai 200040, Peoples R China.
EM 462644725@qq.com
OI Qi, Zengxin/0000-0001-5206-9948
FU Natural Science FoundationNational Natural Science Foundation of China
   (NSFC) [81702461, 81702175]; Shanghai Sailing Programe [17YF1426500]
FX This study was supported by the Natural Science Foundation Grants
   (81702461, 81702175). Shanghai Sailing Programe (17YF1426500). The
   funder had no role in study design, data collection and analysis,
   decision to publish, or preparation request.
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U1 3
U2 5
PU BMC
PI LONDON
PA CAMPUS, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 1471-2202
J9 BMC NEUROSCI
JI BMC Neurosci.
PD DEC 23
PY 2019
VL 20
IS 1
AR 63
DI 10.1186/s12868-019-0545-1
PG 12
WC Neurosciences
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Neurosciences & Neurology
GA KJ3XV
UT WOS:000511993300001
PM 31870319
OA gold, Green Submitted, Green Published
DA 2022-04-25
ER

PT J
AU Kim, YS
   Lee, HJ
   Park, JM
   Han, YM
   Kangwan, N
   Oh, JY
   Lee, DY
   Hahm, KB
AF Kim, Yong Seok
   Lee, Ho Jae
   Park, Jong-Min
   Han, Young-Min
   Kangwan, Napapan
   Oh, Ji Young
   Lee, Dong Yoon
   Hahm, Ki Baik
TI Targeted molecular ablation of cancer stem cells for curing
   gastrointestinal cancers
SO EXPERT REVIEW OF GASTROENTEROLOGY & HEPATOLOGY
LA English
DT Review
DE Cancer stem cells; GI cancers; proton pump inhibitors; sonic hedgehog
   inhibitor; chloroquine; kimchi
ID EPITHELIAL-MESENCHYMAL TRANSITION; HELICOBACTER-PYLORI; SONIC-HEDGEHOG;
   GASTRIC-CANCER; SELF-RENEWAL; BARRETTS-ESOPHAGUS; POLARIZING ACTIVITY;
   INHIBITION; PREVENTION; GROWTH
AB Introduction: Abundance of the ATPase-binding cassette (ABC) transporters and deranged self-renewal pathways characterize the presence of cancer stem cells (CSCs) in gastrointestinal cancers (GI cancers), which play crucial roles in tumorigenesis, chemotherapy resistance, tumor recurrence, and cancer metastasis. Therefore, in order to ensure high cure rates, chemoquiescence, CSCs should be ablated. Recent advances in either understanding CSCs or biomarker identification enable scientists to develop techniques for ablating CSCs and clinicians to provide cancer cure, especially in GI cancers characterized by inflammation-driven carcinogenesis.Areas covered: A novel approach to ablate CSCs in GI cancers, including esophageal, gastric, and colon cancers, is introduced along with explored underlying molecular mechanisms.Expert commentary: Though CSC ablation is still in the empirical stages and not in clinical practice, several strategies for ablating CSCs in GI cancers had been published, proton-pump inhibitors (PPIs) that regulate the membrane-bound ABC transporters, which underlie drug resistance; chloroquine (CQ) that inhibits autophagy, which is responsible for tumor survival; Hedgehog/Wnt/Notch inhibitors that influence the underlying stem-cell growth, and some natural products including Korean red ginseng, cancer-preventive kimchi, Artemisia extract, EGCG from green tea, and walnut extracts.
C1 [Kim, Yong Seok; Hahm, Ki Baik] Hanyang Univ, Dept Biochem & Mol Biol, Coll Med, Seoul, South Korea.
   [Lee, Ho Jae] Gachon Univ, Dept Biochem, Coll Med, Incheon, South Korea.
   [Park, Jong-Min; Han, Young-Min; Hahm, Ki Baik] CHA Univ, CHA Canc Prevent Res Ctr, 59 Yatap Ro, Seongnam 463712, South Korea.
   [Kangwan, Napapan] Univ Phayao, Sch Med Sci, Div Physiol, Phayao, Thailand.
   [Oh, Ji Young; Lee, Dong Yoon] CJ Food, Suwon, South Korea.
   [Hahm, Ki Baik] CHA Univ, Ctr Digest Dis, Bundang Med Ctr, 59 Yatap Ro, Seongnam 463712, South Korea.
RP Hahm, KB (corresponding author), CHA Univ, CHA Canc Prevent Res Ctr, 59 Yatap Ro, Seongnam 463712, South Korea.; Hahm, KB (corresponding author), CHA Univ, Ctr Digest Dis, Bundang Med Ctr, 59 Yatap Ro, Seongnam 463712, South Korea.
EM hahmkb@cha.ac.kr
RI ; Kim, Yong-Seok/P-7501-2015
OI Kangwan, Napapan/0000-0002-9184-7850; Kim, Yong-Seok/0000-0001-5062-7408
FU Korea Institute of Planning and Evaluation for Technology in Food,
   Agriculture, Forestry and Fisheries (IPET) through High Value-added Food
   Technology Development Program - Ministry of Agriculture, Food and Rural
   Affairs (MAFRA) [116015-03-1-CG000]
FX This research was supported by Korea Institute of Planning and
   Evaluation for Technology in Food, Agriculture, Forestry and Fisheries
   (IPET) through High Value-added Food Technology Development Program,
   funded by Ministry of Agriculture, Food and Rural Affairs (MAFRA)
   (116015-03-1-CG000).
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NR 109
TC 9
Z9 10
U1 1
U2 18
PU TAYLOR & FRANCIS LTD
PI ABINGDON
PA 2-4 PARK SQUARE, MILTON PARK, ABINGDON OR14 4RN, OXON, ENGLAND
SN 1747-4124
EI 1747-4132
J9 EXPERT REV GASTROENT
JI Expert Rev. Gastroenterol. Hepatol.
PY 2017
VL 11
IS 11
BP 1059
EP 1070
DI 10.1080/17474124.2017.1356224
PG 12
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA FM3VR
UT WOS:000414938300007
PM 28707966
DA 2022-04-25
ER

PT J
AU Marucci, G
   Santinelli, C
   Buccioni, M
   Navia, AM
   Lambertucci, C
   Zhurina, A
   Yli-Harja, O
   Volpini, R
   Kandhavelu, M
AF Marucci, Gabriella
   Santinelli, Claudia
   Buccioni, Michela
   Navia, Aleix Marti
   Lambertucci, Catia
   Zhurina, Anastasia
   Yli-Harja, Olli
   Volpini, Rosaria
   Kandhavelu, Meenakshisundaram
TI Anticancer activity study of A(3) adenosine receptor agonists
SO LIFE SCIENCES
LA English
DT Article
DE A(3) adenosine receptor; A(3) adenosine receptor ligands; Adenosine
   derivatives; Cancer cells; Signal activation; Apoptosis; Autophagy;
   Migration; Reactive oxygen species
ID CELL-LINE; IB-MECA; PROSTATE-CANCER; AUTOPHAGY; APOPTOSIS; TARGET;
   PROLIFERATION; DERIVATIVES; PHARMACOLOGY; MECHANISMS
AB Aims: A(3) adenosine receptor (A(3)AR) signalling activation seems to mediate anticancer effect, and it has been targeted for drug development. The identification of potent and selective A3AR agonists could be crucial for cancer drug development.
   Materials and methods: In the present study was determined the in vitro activity of known 1-3 and newly 4-6 synthesized compounds with high A(3)AR affinity and selectivity (K-i in the low nanomolar range) in binding studies. Effect of known and novel A(3)AR agonists on human prostate cancer (PC3), hepatocellular carcinoma (Hep G2), and epithelial colorectal carcinoma (Caco-2) cells were analysed by cytotoxicity assay, dose and time dependent inhibitor assay, migration, apoptosis, autophagy and reactive oxygen species (ROS) assays.
   Key findings: Results show that the anticancer effect is not due to A(3)AR activation alone. In fact, the more active and selective agonist versus A3AR, compound 1, results inactive on cancer cells such as compounds 2-4. Moreover, results show that the novel compound 5, at micromolar concentration range (IC50 = 28.0 mu M), inhibits the growth of PC3, Hep G2, and Caco-2 cells and their migration in time-and dose-dependent manner. The mechanism involved in cell death is attributable to apoptosis. At the same time compound 5 promotes autophagy, which induce apoptosis producing autophagic cell death. Further investigation revealed that compound 5 elevates the level of ROS in all cancer cells tested, suggesting the involvement of ROS in cell death.
   Significance: These results show that the new compound 5 exerts inhibitory effect on cancer cells through differential effect and may serve as a potential anticancer agent.
C1 [Marucci, Gabriella; Santinelli, Claudia; Buccioni, Michela; Navia, Aleix Marti; Volpini, Rosaria] Univ Camerino, Sch Pharm, Via S Agostino 1, I-62032 Camerino, MC, Italy.
   [Santinelli, Claudia; Zhurina, Anastasia; Yli-Harja, Olli; Kandhavelu, Meenakshisundaram] Tampere Univ Technol, Fac Biomed Sci & Engn, Computat Syst Biol Res Grp, Mol Signaling Lab, POB 553, FIN-33101 Tampere, Finland.
   [Yli-Harja, Olli] Inst Syst Biol, 1441N 34th St, Seattle, WA 98103 USA.
RP Kandhavelu, M (corresponding author), Tampere Univ Technol, Fac Biomed Sci & Engn, Computat Syst Biol Res Grp, Mol Signaling Lab, POB 553, FIN-33101 Tampere, Finland.
EM meenakshisundaram.kandhavelu@tut.fi
RI Kandhavelu, Meenakshisundaram/AAZ-7503-2021
OI Kandhavelu, Meenakshisundaram/0000-0002-4986-055X
FU Tampere University of Technology [85482, 85486]
FX MK and OYH acknowledge Tampere University of Technology (85482 and
   85486) for Instrumental facility grant support. We also thank Prof.
   Matti Karp for providing the access to Fluorescence Plate reader
   instrumental facility at TUT.
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NR 51
TC 5
Z9 5
U1 0
U2 3
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0024-3205
EI 1879-0631
J9 LIFE SCI
JI Life Sci.
PD JUL 15
PY 2018
VL 205
BP 155
EP 163
DI 10.1016/j.lfs.2018.05.028
PG 9
WC Medicine, Research & Experimental; Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Research & Experimental Medicine; Pharmacology & Pharmacy
GA GI3TK
UT WOS:000434293900018
PM 29763615
DA 2022-04-25
ER

PT J
AU Kim, JH
   Kim, IW
AF Kim, Ju Hee
   Kim, In-Wook
TI p62 manipulation affects chlorin e6-mediated photodynamic therapy
   efficacy in colorectal cancer cell lines
SO ONCOLOGY LETTERS
LA English
DT Article
DE p62; colorectal cancer; therapeutic agents; apoptosis; tumor genesis;
   autophagy
ID INDUCED APOPTOSIS; AUTOPHAGY; INHIBITION; RESISTANCE; P62/SQSTM1;
   PATHWAY; PHOTOSENSITIZER; MECHANISMS; SURVIVAL; PROTEIN
AB p62 is a multifunctional protein that mediates cell signaling pathways, autophagy and tumorigenesis, and participates in important regulation processes at the intersection between autophagy and cancer. Photodynamic therapy (PDT) is a treatment that involves photosensitizing agents and light to kill cancer cells. However, whether the efficacy of PDT depends on the expression level of p62 in colorectal cancer cell lines is not known. The present study aimed to examine the role of p62 expression levels in chlorin e6-based PDT in colorectal cancer cells. To study the effect of p62 on cancer cell death, we used PDT to treat a stable cell line overexpressing p62. Cells overexpressing p62 showed a higher cell death rate than cells not expressing this protein. Overexpression of p62 may contribute to colorectal cancer cell death. These results provide preliminary evidence for use of p62 as a therapy target to treat colorectal cancer.
C1 [Kim, Ju Hee] Seoul Natl Univ Hosp, Biomed Res Inst, Seoul 03080, South Korea.
   [Kim, In-Wook] Hanyang Univ, Coll Engn, Dept Bioengn, 222 Wangsimni Ro, Seoul 04763, South Korea.
RP Kim, IW (corresponding author), Hanyang Univ, Coll Engn, Dept Bioengn, 222 Wangsimni Ro, Seoul 04763, South Korea.
EM iwkim@hanyang.ac.kr
RI Kim, In-Wook/AAN-8123-2020
OI Kim, In-Wook/0000-0002-5501-2928
FU Basic Science Research Program through The National Research Foundation
   of Korea (NRF) - Ministry of Education, Science and Technology
   [NRF-2017R1A2B4011122, NRF-2019R1C1C1006898]
FX The present study was supported by The Basic Science Research Program
   through The National Research Foundation of Korea (NRF) funded by The
   Ministry of Education, Science and Technology (grant nos.
   NRF-2017R1A2B4011122 and NRF-2019R1C1C1006898).
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NR 36
TC 4
Z9 4
U1 1
U2 5
PU SPANDIDOS PUBL LTD
PI ATHENS
PA POB 18179, ATHENS, 116 10, GREECE
SN 1792-1074
EI 1792-1082
J9 ONCOL LETT
JI Oncol. Lett.
PD JUN
PY 2020
VL 19
IS 6
BP 3907
EP 3916
DI 10.3892/ol.2020.11522
PG 10
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA LR6CN
UT WOS:000535780700031
PM 32391099
OA Green Published, gold
DA 2022-04-25
ER

PT J
AU Liang, CY
   Sir, D
   Lee, S
   Ou, JHJ
   Jung, JU
AF Liang, Chengyu
   Sir, Donna
   Lee, Steven
   Ou, Jing-hsiung James
   Jung, Jae U.
TI Beyond autophagy
SO AUTOPHAGY
LA English
DT Article
DE UVRAG; the class C Vps complex; autophagy; autophagosome maturation;
   membrane trafficking
ID C-VPS COMPLEX; MAMMALIAN-CELLS; PROTEIN-TRANSPORT; SELF-DIGESTION;
   COLON-CANCER; UVRAG; MATURATION; VACUOLE; DISEASE; FUSION
AB Autophagy is a lysosome-directed membrane trafficking event for the degradation of cytoplasmic components, including organelles. The past few years have seen a great advance in our understanding of the cellular machinery of autophagosome biogenesis, the hallmark of autophagy. However, our global understanding of autophagosome maturity remains relatively poor and fragmented. The topological similarity of autophagosome and endosome delivery to lysosomes suggests that autophagic and endosomal maturation may have evolved to share associated machinery to promote the lysosomal delivery of their cargoes. We have recently discovered that UVRAG, originally identified as a Beclin 1-binding autophagy protein, appears to be an important factor in autophagic and endosomal trafficking through its interaction with the class C Vps tethering complex. Given the ability of UVRAG to bind Beclin I and the class C Vps complex in a genetically and functionally separable manner, it may serve as an important regulator for the spatial and/or temporal control of diverse cellular trafficking events. As more non-autophagic functions of UVRAG are unveiled, our understanding of seemingly different cellular processes may move a step further.
C1 [Liang, Chengyu; Sir, Donna; Lee, Steven; Ou, Jing-hsiung James; Jung, Jae U.] Univ So Calif, Dept Mol Microbiol & Immunol, Los Angeles, CA 90033 USA.
RP Liang, CY (corresponding author), Univ So Calif, Dept Mol Microbiol & Immunol, Room 5517,MC NRT 9605,1450 Biggy St, Los Angeles, CA 90033 USA.
EM chengyu.liang@usc.edu
OI LIANG, CHENGYU/0000-0001-6082-2143
FU U.S. Public Health ServiceUnited States Department of Health & Human
   ServicesUnited States Public Health Service [CA82057, CA91819, CA31363,
   CA106156, RR00168]; NATIONAL CANCER INSTITUTEUnited States Department of
   Health & Human ServicesNational Institutes of Health (NIH) - USANIH
   National Cancer Institute (NCI) [R01CA082057, R01CA031363, R01CA091819,
   R01CA106156] Funding Source: NIH RePORTER; NATIONAL CENTER FOR RESEARCH
   RESOURCESUnited States Department of Health & Human ServicesNational
   Institutes of Health (NIH) - USANIH National Center for Research
   Resources (NCRR) [P51RR000168, K26RR000168] Funding Source: NIH
   RePORTER; NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASESUnited
   States Department of Health & Human ServicesNational Institutes of
   Health (NIH) - USANIH National Institute of Allergy & Infectious
   Diseases (NIAID) [R01AI073099] Funding Source: NIH RePORTER
FX We would like to thank B. Levine, M.J. Hardwick, S. Virgin, S. Field, T
   Yoshimori and Y. Ohsumi for providing reagents. We also thank Steven Lee
   for proofreading. This work was partly supported by U.S. Public Health
   Service grants CA82057, CA91819, CA31363, CA106156, RR00168 (J.U.J.).
   C.L. is a Leukemia & Lymphoma Society Fellow.
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NR 34
TC 21
Z9 21
U1 0
U2 2
PU LANDES BIOSCIENCE
PI AUSTIN
PA 1002 WEST AVENUE, 2ND FLOOR, AUSTIN, TX 78701 USA
SN 1554-8627
J9 AUTOPHAGY
JI Autophagy
PD AUG 16
PY 2008
VL 4
IS 6
BP 817
EP 820
DI 10.4161/auto.6496
PG 4
WC Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Cell Biology
GA 339TT
UT WOS:000258600900013
PM 18612260
OA Green Accepted, Bronze
DA 2022-04-25
ER

PT J
AU Zhao, Z
   Xia, GG
   Li, N
   Su, RP
   Chen, X
   Zhong, L
AF Zhao, Zhi
   Xia, Guanggai
   Li, Ni
   Su, Ruping
   Chen, Xiao
   Zhong, Li
TI Autophagy Inhibition Promotes Bevacizumab-induced Apoptosis and
   Proliferation Inhibition in Colorectal Cancer Cells
SO JOURNAL OF CANCER
LA English
DT Article
DE Autophagy; Anti-VEGF; Bevacizumab; Colorectal cancer
ID ANTIANGIOGENIC THERAPY; ANGIOGENESIS INHIBITION; OVARIAN-CANCER;
   LUNG-CANCER; METASTASIS; EXPRESSION
AB Aim: Anti-VEGF therapy plays an important role in the treatment of malignant tumors, especially metastatic malignant tumors. However, resistance and an inefficient response to anti-VEGF therapy exist. The current study aimed to investigate whether autophagy plays a part in the anti-tumor effect of bevacizumab in colorectal cancer cells.
   Methods: VEGF-A expression was measured by immunohistochemical methods. Cell viability and cell apoptosis were detected using 3-(4,5-dimethylthiazol-2-yl)-3,5-diphenylformazan (MTT) and flow cytometry. Autophagy was assessed by a western blot, fluorescence microscopy and transmission electron microscopy. HIF-1 alpha was measured using a western blot. A xenograft tumor model of colorectal cancer was constructed to determine the efficacy of the treatment of bevacizumab and chloroquine.
   Results: VEGF-A protein was upregulated in colorectal cancer tissue. Anti-VEGF (bevacizumab) inhibited cell viability and induced apoptosis. Moreover, bevacizumab induced autophagy. The inhibition of autophagy by chloroquine or by small interfering RNA promoted bevacizumab-induced apoptosis and proliferation inhibition. Further study showed that bevacizumab treatment significantly augmented HIF-la. Furthermore, cells pretreated with YC-1, a HIF-1 alpha inhibitor, displayed significantly attenuated bevacizumab-induced autophagy. Finally, a combinatory treatment of bevacizumab and chloroquine synergistically inhibited tumor growth in a xenograft tumor model of colorectal cancer cells.
   Conclusions: Our results showed that the inhibition of autophagy promoted the anti-tumor effect of bevacizumab and may offer a promising therapeutic strategy for colorectal cancer.
C1 [Zhao, Zhi; Su, Ruping; Chen, Xiao; Zhong, Li] Peoples Hosp Guilin, Dept Gastrointestinal & Hernia Surg, Guilin 541002, Peoples R China.
   [Xia, Guanggai] Shanghai Jiao Tong Univ, Affiliated Peoples Hosp 6, Dept Gen Surg, Shanghai 200233, Peoples R China.
   [Li, Ni] Peoples Hosp Guilin, Hlth Management Ctr, Guilin 541002, Peoples R China.
RP Zhong, L (corresponding author), Peoples Hosp Guilin, Dept Gastrointestinal & Hernia Surg, Guilin 541002, Peoples R China.
EM Zhongli0302@163.com
FU Wu Jieping medical fund [320.6750.13390]
FX This study was supported by the Wu Jieping medical fund (No.
   320.6750.13390).
CR Chebib R, 2017, SEMIN ONCOL, V44, P114, DOI 10.1053/j.seminoncol.2017.07.004
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NR 26
TC 18
Z9 21
U1 3
U2 7
PU IVYSPRING INT PUBL
PI LAKE HAVEN
PA PO BOX 4546, LAKE HAVEN, NSW 2263, AUSTRALIA
SN 1837-9664
J9 J CANCER
JI J. Cancer
PY 2018
VL 9
IS 18
BP 3407
EP 3416
DI 10.7150/jca.24201
PG 10
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA GS9DJ
UT WOS:000444015800024
PM 30271503
OA Green Published, Green Submitted, gold
DA 2022-04-25
ER

PT J
AU Kurdi, A
   Cleenewerck, M
   Vangestel, C
   Lyssens, S
   Declercq, W
   Timmermans, JP
   Stroobants, S
   Augustyns, K
   De Meyer, GRY
   Van Der Veken, P
   Martinet, W
AF Kurdi, Ammar
   Cleenewerck, Matthias
   Vangestel, Christel
   Lyssens, Sophie
   Declercq, Wim
   Timmermans, Jean-Pierre
   Stroobants, Sigrid
   Augustyns, Koen
   De Meyer, Guido R. Y.
   Van Der Veken, Pieter
   Martinet, Wim
TI ATG4B inhibitors with a benzotropolone core structure block autophagy
   and augment efficiency of chemotherapy in mice
SO BIOCHEMICAL PHARMACOLOGY
LA English
DT Article
DE ATG4B; Autophagy; Osmotic minipump; Colorectal tumor; Benzotropolone
ID ADVANCED SOLID TUMORS; PHASE-I TRIAL; BREAST-CANCER; THERAPEUTIC TARGET;
   RADIATION-THERAPY; CARCINOMA-CELLS; HYDROXYCHLOROQUINE; MTOR;
   RESISTANCE; MECHANISM
AB Autophagy is a cell survival mechanism hijacked by advanced tumors to endure a rough microenvironment. Late autophagy inhibitors such as (hydroxy)chloroquine have been used clinically to halt tumor progression with modest success. However, given the toxic nature of these compounds and their lack of specificity, novel targets should be considered. We recently identified a benzotropolone derivative that significantly inhibited the essential autophagy protein ATG4B. Therefore, we synthesized and tested additional benzotropolone compounds to identify a promising ATG4B inhibitor that impairs autophagy both in vitro and in vivo. A compound library containing 27 molecules with a benzotropolone backbone was synthesized and screened for inhibition of recombinant ATG4B. Depending on the benzotropolone compound, inhibition of recombinant ATG4B ranged from 3 to 82%. Active compounds were evaluated in cellular assays to confirm inhibition of ATG4B and suppression of autophagy. Seven compounds inhibited processing of the autophagy protein LC3 and autophagosome formation. Compound UAMC-2526 was selected for further in vivo use because of its fair plasma stability. This compound abolished autophagy both in nutrient-deprived GFP-LC3 mice and in CD1(-/-) Foxn1nu mice bearing HT29 colorectal tumor xenografts. Moreover, addition of UAMC-2526 to the chemotherapy drug oxaliplatin significantly improved inhibition of tumor growth. Our data indicate that suppression of autophagy via ATG4B inhibition is a feasible strategy to augment existing chemotherapy efficacy and to halt tumor progression. (C) 2017 Elsevier Inc. All rights reserved.
C1 [Kurdi, Ammar; De Meyer, Guido R. Y.; Martinet, Wim] Univ Antwerp, Dept Pharmaceut Sci, Lab Physiopharmacol, Antwerp, Belgium.
   [Cleenewerck, Matthias; Lyssens, Sophie; Augustyns, Koen; Van Der Veken, Pieter] Univ Antwerp, Dept Pharmaceut Sci, Lab Med Chem UAMC, Antwerp, Belgium.
   [Vangestel, Christel; Stroobants, Sigrid] Univ Antwerp, MICA, Antwerp, Belgium.
   [Declercq, Wim] VIB Inflammat Res Ctr, Ghent, Belgium.
   [Declercq, Wim] Univ Ghent, Dept Biomed Mol Biol, Ghent, Belgium.
   [Timmermans, Jean-Pierre] Univ Antwerp, Dept Vet Sci, Lab Cell Biol & Histol, Antwerp, Belgium.
RP Martinet, W (corresponding author), Univ Antwerp, Lab Physiopharmacol, Univ Pl 1, B-2610 Antwerp, Belgium.
EM wim.martinet@uantwerpen.be
RI Augustyns, Koen/ABG-2306-2020; De Meyer, Guido/R-8129-2016; Martinet,
   Wim/I-7375-2015; Augustyns, Koen/C-1102-2008; Van der Veken,
   Pieter/P-5819-2016
OI Augustyns, Koen/0000-0002-5203-4339; De Meyer,
   Guido/0000-0003-3848-8702; Martinet, Wim/0000-0003-1967-9343; Augustyns,
   Koen/0000-0002-5203-4339; Van der Veken, Pieter/0000-0003-1208-3571;
   Stroobants, Sigrid/0000-0002-6450-9944
FU Fund for Scientific Research (FWO)-FlandersFWO [G.0431.11, G.0412.16N];
   University of Antwerp (BOF); Stichting tegen Kanker [2016/868]
FX This work was supported by the Fund for Scientific Research
   (FWO)-Flanders (projects G.0431.11 and G.0412.16N), the University of
   Antwerp (BOF) and Stichting tegen Kanker (2016/868 to W.D.). The FEI
   Tecnai transmission electron microscope was purchased with support of
   the Hercules Foundation. The authors thank Dr. Noboru Mizushima (Tokyo
   Medical and Dental University, Japan) for GFP-LC3 mice, Dr. Robin
   Ketteler (MRC Laboratory for Molecular Cell Biology, UK) for pEAK12
   plasmid DNA encoding beta-actine-LC3-dNGLUC and Dr. Nobuo N. Noda
   (Hokkaido University, Japan) for LC3B-GST and ATG4B plasmids. We also
   acknowledge Rita Van Den Bossche, Hermine Fret, Anne-Elise Van Hoydonck,
   Ria Roelandt, Carine Moers and Francis Terloo for excellent technical
   support. We dedicate this paper to our colleague, Prof Sandra Apers, who
   passed away much too early on February 5th, 2017.
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NR 56
TC 37
Z9 38
U1 0
U2 21
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0006-2952
EI 1873-2968
J9 BIOCHEM PHARMACOL
JI Biochem. Pharmacol.
PD AUG 15
PY 2017
VL 138
BP 150
EP 162
DI 10.1016/j.bcp.2017.06.119
PG 13
WC Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA FB4BO
UT WOS:000406086700014
PM 28642033
OA Green Accepted
DA 2022-04-25
ER

PT J
AU Ishima, Y
   Inoue, A
   Fang, J
   Kinoshita, R
   Ikeda, M
   Watanabe, H
   Maeda, H
   Otagiri, M
   Maruyama, T
AF Ishima, Yu
   Inoue, Aki
   Fang, Jun
   Kinoshita, Ryo
   Ikeda, Mayumi
   Watanabe, Hiroshi
   Maeda, Hiroshi
   Otagiri, Masaki
   Maruyama, Toru
TI Poly-S-nitrosated human albumin enhances the antitumor and
   antimetastasis effect of bevacizumab, partly by inhibiting autophagy
   through the generation of nitric oxide
SO CANCER SCIENCE
LA English
DT Article
DE Autophagy; bevacizumab; drug resistance; nitric oxide; SNO-HSA
ID HUMAN SERUM-ALBUMIN; PHASE-II TRIAL; CANCER; TUMOR; MECHANISM; DRUG;
   ANGIOGENESIS; IRINOTECAN; RESISTANCE; DELIVERY
AB Autophagy is one of the major causes of drug resistance. For example, the angiogenesis inhibitor bevacizumab shows only transient and short-term therapeutic effects, whereas long-term therapeutic benefits are rarely observed, probably due to hypoxia-induced autophagy. Nitric oxide (NO) is an important molecule with multiple functions, and it has recently been reported to function as a regulator of autophagy. Therefore, a reasonable therapeutic strategy for overcoming drug resistance by NO would involve it being directly delivered to the tumor. Here, we investigated the inhibitory effect of NO on autophagy by using a macromolecular NO donor S-nitrosated human serum albumin (SNO-HSA) with a high degree of NO loading and tumor targeting potential. In colon 26 (C26) cells, SNO-HSA significantly suppressed hypoxia-induced autophagy by inhibiting the phosphorylation of JNK1 and the expression of its downstream molecule Beclin1. The effect of SNO-HSA was also confirmed in vivo by combining it with Bev. In C26-bearing mice, significant suppression of tumor growth as well as lung metastasis was achieved in the combination group compared to the SNO-HSA or bevacizumab alone group. Similar to the in vitro experiments, the immunostaining of tumor tissues clearly showed that SNO-HSA inhibited the autophagy of tumor cells induced by bevacizumab treatment. In addition to other known antitumor effects of SNO-HSA, that is, the induction of apoptosis and the inhibition of multidrug efflux pumps, these data may open alternate strategies for cancer chemotherapy by taking advantage of the ability of SNO-HSA to suppress autophagy-mediated drug resistance and enhance the efficacy of chemotherapy.
C1 [Ishima, Yu; Inoue, Aki; Kinoshita, Ryo; Ikeda, Mayumi; Watanabe, Hiroshi; Maruyama, Toru] Kumamoto Univ, Grad Sch Pharmaceut Sci, Dept Biopharmaceut, Kumamoto 8620973, Japan.
   [Ishima, Yu; Watanabe, Hiroshi; Maruyama, Toru] Kumamoto Univ, Ctr Clin Pharmaceut Sci, Kumamoto 8620973, Japan.
   [Fang, Jun; Otagiri, Masaki] Sojo Univ, Fac Pharmaceut Sci, Kumamoto, Japan.
   [Maeda, Hiroshi; Otagiri, Masaki] Sojo Univ, DDS Res Inst, Kumamoto, Japan.
RP Maruyama, T (corresponding author), Kumamoto Univ, Grad Sch Pharmaceut Sci, Dept Biopharmaceut, 5-1 Oe Honmachi, Kumamoto 8620973, Japan.
EM tomaru@gpo.kumamoto-u.ac.jp
RI Maeda, Hiroshi/N-4471-2016
OI Ikeda-Imafuku, Mayumi/0000-0002-7254-3050
FU Japan Society for the Promotion of ScienceMinistry of Education,
   Culture, Sports, Science and Technology, Japan (MEXT)Japan Society for
   the Promotion of Science; Ministry of Education, Culture, Sports,
   Science and Technology, JapanMinistry of Education, Culture, Sports,
   Science and Technology, Japan (MEXT) [Kakenhi 25860118, 23390142,
   21390177]; Uehara Memorial FoundationUehara Memorial Foundation; Yasuda
   Medical Foundation
FX This work was supported in part by Grants-in-Aid from the Japan Society
   for the Promotion of Science and Grants-in-Aid from the Ministry of
   Education, Culture, Sports, Science and Technology (Kakenhi 25860118,
   23390142, and 21390177), Japan. The work was also supported in part by
   grants from the Uehara Memorial Foundation and the Yasuda Medical
   Foundation.
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NR 39
TC 18
Z9 19
U1 1
U2 10
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1349-7006
J9 CANCER SCI
JI Cancer Sci.
PD FEB
PY 2015
VL 106
IS 2
BP 194
EP 200
DI 10.1111/cas.12577
PG 7
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA CC2JJ
UT WOS:000350171000009
PM 25457681
OA gold, Green Published
DA 2022-04-25
ER

PT J
AU Zhang, CY
   Sun, J
   Wang, X
   Wang, CF
   Zeng, XD
AF Zhang, Chun-Yang
   Sun, Jie
   Wang, Xing
   Wang, Cui-Fang
   Zeng, Xian-Dong
TI Clinicopathological significance of human leukocyte antigen F-associated
   transcript 10 expression in colorectal cancer
SO WORLD JOURNAL OF GASTROINTESTINAL ONCOLOGY
LA English
DT Article
DE Colorectal cancer; Ubiquitin; Ubiquitin-like proteins; Human leukocyte
   antigen F-associated transcript 10; p53
ID UBIQUITIN-LIKE PROTEIN; ENDOSCOPIC ULTRASOUND; HEPATOCELLULAR-CARCINOMA;
   MODIFIER FAT10; TUMOR; AUTOPHAGY; P53; PHOSPHORYLATION; METASTASIS;
   APOPTOSIS
AB BACKGROUND
   Colorectal cancer (CRC) is a common malignancy of the gastrointestinal tract. The worldwide mortality rate of CRC is about one half of its morbidity. Ubiquitin is a key regulatory factor in the cell cycle and widely exists in eukaryotes. Human leukocyte antigen F-associated transcript 10 (FAT10), known as diubiquitin, is an 18 kDa protein with 29% and 36% homology with the N and C termini of ubiquitin. The function of FAT10 has not been fully elucidated, and some studies have shown that it plays an important role in various cell processes.
   AIM
   To examine FAT10 expression and to analyze the relationship between FAT10 expression and the clinicopathological parameters of CRC.
   METHODS
   FAT10 expression in 61 cases of CRC and para-cancer colorectal tissues was measured by immunohistochemistry and Western blotting. The relationship between FAT10 expression and clinicopathological parameters of CRC was statistically analyzed.
   RESULTS
   Immunohistochemical analysis showed that the positive rate of FAT10 expression in CRC (63.93%) was significantly higher than that in tumor-adjacent tissues (9.84%, P < 0.05) and normal colorectal mucosal tissue (1.64%, P < 0.05). Western blotting also indicated that FAT10 expression was significantly higher in CRC than in tumor-adjacent tissue (P < 0.05). FAT10 expression was closely associated with clinical stage and lymphatic spread of CRC. FAT10 expression also positively correlated with p53 expression.
   CONCLUSION
   FAT10 expression is highly upregulated in CRC. FAT10 expression is closely associated with clinical stage and lymphatic spread of CRC.
C1 [Zhang, Chun-Yang] Shenyang Med Coll, Cent Hosp, Dept Emergency Med, Shenyang 110024, Liaoning, Peoples R China.
   [Sun, Jie; Wang, Xing; Wang, Cui-Fang] Shenyang Med Coll, Cent Hosp, Dept Pathol, Shenyang 110024, Liaoning, Peoples R China.
   [Zeng, Xian-Dong] Shenyang Med Coll, Cent Hosp, Dept Surg Oncol, 5 South Seven West Rd, Shenyang 110024, Liaoning, Peoples R China.
RP Zeng, XD (corresponding author), Shenyang Med Coll, Cent Hosp, Dept Surg Oncol, 5 South Seven West Rd, Shenyang 110024, Liaoning, Peoples R China.
EM 1403973708@qq.com
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NR 38
TC 5
Z9 6
U1 1
U2 2
PU BAISHIDENG PUBLISHING GROUP INC
PI PLEASANTON
PA 8226 REGENCY DR, PLEASANTON, CA 94588 USA
SN 1948-5204
J9 WORLD J GASTRO ONCOL
JI World J. Gastrointest. Oncol.
PD JAN 15
PY 2019
VL 11
IS 1
BP 9
EP 16
DI 10.4251/wjgo.v11.i1.9
PG 8
WC Oncology; Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Gastroenterology & Hepatology
GA HH7NH
UT WOS:000455917100002
PM 30984346
OA Green Published, Green Submitted, hybrid
DA 2022-04-25
ER

PT J
AU Tam, SY
   Wu, VWC
   Law, HKW
AF Tam, Shing Yau
   Wu, Vincent W. C.
   Law, Helen K. W.
TI Dynamics of oxygen level-driven regulators in modulating autophagy in
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SO BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
LA English
DT Article
DE Autophagy; Autophagy regulator; Colorectal cancer cell; Hypoxia; Oxygen
   level
ID HYPOXIA; BNIP3; AMPK
AB Colorectal cancer is a common cancer with metachronous distant metastases still threatening overall survival. Tumor oxygen level influences tumor radiosensitivity in relation to autophagy and apoptosis. The objective of this study is to evaluate the expression and interaction between multiple key regulators in different oxygen levels. Human colorectal adenocarcinoma HT-29 cells were cultured in 1% or 10% oxygen level and irradiated by 2 Gy with different incubation time. Autophagy key regulators, AMPK, HIFs and JNK were evaluated by Western blot. Sequential autophagy key regulator activation was observed in the order of AMPK, HIF-1 alpha, HIF-2 alpha and JNK. 10% oxygen level could promote autophagy with similar degree of autophagy activation as 1% oxygen level in 48-h while irradiation could slightly inhibit autophagy. The results of this study supported prior evaluation of oxygen level and autophagy regulators for improving treatment efficacy and indicated the possible directions in developing individualized radiotherapy by selective targeting of hypoxic regions. (C) 2019 The Authors. Published by Elsevier Inc.
C1 [Tam, Shing Yau; Wu, Vincent W. C.; Law, Helen K. W.] Hong Kong Polytech Univ, Fac Hlth & Social Sci, Dept Hlth Technol & Informat, Hung Hom, Hong Kong, Peoples R China.
RP Wu, VWC; Law, HKW (corresponding author), Hong Kong Polytech Univ, Fac Hlth & Social Sci, Dept Hlth Technol & Informat, Hung Hom, Hong Kong, Peoples R China.
EM shing-yau.tam@connect.polyu.hk; htvinwu@polyu.edu.hk;
   hthelen@polyu.edu.hk
RI Tam, Shing Yau/AAN-4109-2020; Tam, Shing Yau/AAZ-1345-2020
OI Tam, Shing Yau/0000-0002-5899-1041
FU Hong Kong Polytechnic UniversityHong Kong Polytechnic University
FX This research was supported by Postgraduate Studentship to S.T. and
   Internal grants (G-YBPL, and HTI-GRF Seeding Fund for H.L.) from The
   Hong Kong Polytechnic University.
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Z9 5
U1 0
U2 1
PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 0006-291X
EI 1090-2104
J9 BIOCHEM BIOPH RES CO
JI Biochem. Biophys. Res. Commun.
PD SEP 17
PY 2019
VL 517
IS 2
BP 193
EP 200
DI 10.1016/j.bbrc.2019.07.043
PG 8
WC Biochemistry & Molecular Biology; Biophysics
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Biophysics
GA KB2YR
UT WOS:000506366800003
PM 31331640
OA hybrid, Green Published
DA 2022-04-25
ER

PT J
AU Ghasemi, T
   Khalaj-Kondori, M
   Feizi, MAH
   Asadi, P
AF Ghasemi, Tayyebeh
   Khalaj-Kondori, Mohammad
   feizi, Mohammad Ali Hosseinpour
   Asadi, Parviz
TI lncRNA-miRNA-mRNA interaction network for colorectal cancer; An in
   silico analysis
SO COMPUTATIONAL BIOLOGY AND CHEMISTRY
LA English
DT Article
DE lncRNA; Colorectal cancer; Microarray; lncRNA-miRNA-mRNA network
ID LONG NONCODING RNAS; EXPRESSION; FOXP2; INVASION; GENE; IDENTIFICATION;
   BIOMARKERS; SIGNATURE; CARCINOMA; AUTOPHAGY
AB Background: Colorectal cancer (CRC) is one of the most frequent and diagnosed diseases. Accumulating evidences showed that mRNAs and noncoding RNAs play important regulatory roles in tumorigenesis. Identification and determining the relationship between them can help diagnosis and treatment of cancer.
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   Results: By analyzing the three datasets, a total of 21 mRNAs (15 up- and 6 down-regulated) and 24 lncRNAs (18 up- and 6 down-regulated) were identified as common differentially expressed genes between CRC tumor and marginal tissues. Nevertheless, the constructed 1ncRNA-miRNA-mRNA-signaling pathway network revealed a convergence on 6 lncRNAs (3 up- and 3 downregulated), 7 mRNAs (2 up- and 5 downregulated) and 6 miRNAs (3 up- and 3 downregulated). We found that dysregulation of lncRNAs such as PCBP1-AS1, UCA1 and SNHG16 could sequester several miRNAs such as hsa-miR-582-5p and hsa-miR-198 and promote the proliferation, invasion and drug resistance of colorectal cancer cells.
   Conclusions: We introduced a set of lncRNAs, mRNAs and miRNAs differentially expressed in CRC which might be considered for further experimental research as potential biomarkers of CRC development.
C1 [Ghasemi, Tayyebeh; Khalaj-Kondori, Mohammad; feizi, Mohammad Ali Hosseinpour] Univ Tabriz, Fac Nat Sci, Dept Anim Biol, Tabriz, Iran.
   [Asadi, Parviz] Shahid Mahallati Hosp, Gastroenterol Ward, Tabriz, Iran.
RP Khalaj-Kondori, M (corresponding author), Univ Tabriz, Fac Nat Sci, Dept Anim Biol, Tabriz, Iran.
EM khalaj@tabrizu.ac.ir
OI Hosseinpour Feizi, Mohammad Ali/0000-0002-1508-5022
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NR 65
TC 9
Z9 9
U1 1
U2 4
PU ELSEVIER SCI LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND
SN 1476-9271
EI 1476-928X
J9 COMPUT BIOL CHEM
JI Comput. Biol. Chem.
PD DEC
PY 2020
VL 89
AR 107370
DI 10.1016/j.compbiolchem.2020.107370
PG 9
WC Biology; Computer Science, Interdisciplinary Applications
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Life Sciences & Biomedicine - Other Topics; Computer Science
GA PH6UK
UT WOS:000600544900004
PM 32932199
DA 2022-04-25
ER

PT J
AU Liu, JX
   Cai, JP
   Fan, P
   Zhang, NS
   Cao, YG
AF Liu, Jiuxi
   Cai, Jiapei
   Fan, Peng
   Zhang, Naisheng
   Cao, Yongguo
TI The Abilities of Salidroside on Ameliorating Inflammation, Skewing the
   Imbalanced Nucleotide Oligomerization Domain-Like Receptor Family Pyrin
   Domain Containing 3/Autophagy, and Maintaining Intestinal Barrier Are
   Profitable in Colitis
SO FRONTIERS IN PHARMACOLOGY
LA English
DT Article
DE salidroside; colitis; NLRP3 inflammasome; autophagy; intestinal barrier;
   inflammation
ID SODIUM-INDUCED COLITIS; ULCERATIVE-COLITIS; INHIBITION; ACTIVATION;
   AUTOPHAGY; DISEASE; PROTEIN; INJURY; MICE
AB Salidroside (Sal), as a major glycoside extracted from Rhodiola rosea L., has exhibited its mighty anti-aging, anti-oxidant, anti-cancer, anti-inflammation, and neuroprotective effects in many diseases. Recently, it has showed its protective effect in colitis mice by activating the SIRT1/FoxOs pathway. Whereas, it is not known whether Sal has other protective mechanisms on dextran sulfate sodium (DSS)-induced colitis in mice. In this study, we investigated the protective effects and mechanisms of Sal on DSS-induced colitis in mice. The results demonstrated Sal was a competent candidate in the treatment of ulcerative colitis (UC). Sal remitted DSS-induced disease activity index (DAI), colon length shortening, and colonic pathological damage. Simultaneously, Sal alleviated excessive inflammation by reversing the IL-1 beta, TNF-alpha, and IL-10 protein levels in DSS-treated mice. Western blot analysis revealed that Sal inhibited p65 and p38 activation together with peroxisome proliferator-activated receptor (PPAR gamma) up-regulation. In addition, Sal skewed the imbalanced activation of nucleotide oligomerization domain-like receptor family pyrin domain containing 3 inflammasome and autophagy contributing to colitis recovery. The damaged intestinal barrier induced by DSS was also alleviated along with plasma lipopolysaccharides (LPS) reduction after Sal treatment. In vitro, Sal showed PPAR gamma-dependent anti-inflammatory effect in LPS-stimulated RAW264.7 cells. In summary, our results demonstrated that Sal might be an effective factor for UC treatment and its pharmacological value deserved further development.
C1 [Liu, Jiuxi; Cai, Jiapei; Fan, Peng; Zhang, Naisheng; Cao, Yongguo] Jilin Univ, Coll Vet Med, Dept Clin Vet Med, Changchun, Jilin, Peoples R China.
RP Zhang, NS; Cao, YG (corresponding author), Jilin Univ, Coll Vet Med, Dept Clin Vet Med, Changchun, Jilin, Peoples R China.
EM zhangns@jlu.edu.cn; ygcao82@jlu.edu.cn
FU Key Project of Chinese National Programs for Research and Development
   [2016YFD0501009]; National Natural Science Foundation of ChinaNational
   Natural Science Foundation of China (NSFC) [31572582, 31472248]
FX This work was supported by the Key Project of Chinese National Programs
   for Research and Development (no. 2016YFD0501009) and National Natural
   Science Foundation of China (nos. 31572582 and 31472248).
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NR 40
TC 8
Z9 9
U1 5
U2 15
PU FRONTIERS MEDIA SA
PI LAUSANNE
PA AVENUE DU TRIBUNAL FEDERAL 34, LAUSANNE, CH-1015, SWITZERLAND
SN 1663-9812
J9 FRONT PHARMACOL
JI Front. Pharmacol.
PD DEC 2
PY 2019
VL 10
AR 1385
DI 10.3389/fphar.2019.01385
PG 11
WC Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA JW0JR
UT WOS:000502746200001
PM 31849652
OA Green Published, gold
DA 2022-04-25
ER

PT J
AU Elshafay, A
   Tinh, NX
   Salman, S
   Shaheen, YS
   Othman, EB
   Elhady, MT
   Kansakar, AR
   Tran, L
   Van, L
   Hirayama, K
   Huy, NT
AF Elshafay, Abdelrahman
   Ngo Xuan Tinh
   Salman, Samar
   Shaheen, Yara Saber
   Othman, Eman Bashir
   Elhady, Mohamed Tamer
   Kansakar, Aswin Ratna
   Linh Tran
   Le Van
   Hirayama, Kenji
   Nguyen Tien Huy
TI Ginsenoside Rk1 bioactivity: a systematic review
SO PEERJ
LA English
DT Review
DE Ginsenoside; Systematic review; Rk1; Clinical pharmacology
ID PANAX-GINSENG; LUNG-CANCER; INHIBITION; APOPTOSIS; GLYCOSIDES;
   INDUCTION; RESPONSES; SAPONINS; EXTRACTS; RG5RK1
AB Ginsenoside Rk1 (G-Rk1) is a unique component created by processing the ginseng Plant (mainly Sung Ginseng (SG)) at high temperatures. The aim of our study was to systematically review the pharmacological effects G-Rk1. We utilized and manually searched eight data bases to select in vivo and invitro original studies that provided information about biological, pharmaceutical effects of G-Rk1 and were published up to July 2017 with no restriction on language or study design. Out of the 156 papers identified, we retrieved 28 eligible papers in the first skimming phase of research. Several articles largely described the G-Rk1 anti-cancer activity investigating "cell viability","cell proliferation inhibition", "apoptotic activity", and "effects of G-Rk1 on G1 phase and autophagy in tumor cells" either alone or in combination with G-Rg5. Others proved that it has antiplatelet aggregation activities, anti-inflammatory effects, anti-insulin resistance, nephroprotective effect, antimicrobial effect, cognitive function enhancement, lipid accumulation reduction and prevents osteoporosis. In conclusion, G-Rk1 has a significant anti-tumor effect on liver cancer, melanoma, lung cancer, cervical cancer, colon cancer, pancreatic cancer, gastric cancer, and breast adenocarcinoma against in vitro cell lines. In vivo experiments are further warranted to confirm these effects.
C1 [Elshafay, Abdelrahman] Al Azhar Univ, Fac Med, Cairo, Egypt.
   [Ngo Xuan Tinh; Le Van] Univ Med & Pharm, Fac Pharm, Ho Chi Minh, Vietnam.
   [Salman, Samar] Tanta Univ Hosp, Tanta, Egypt.
   [Shaheen, Yara Saber] Cairo Univ, Fac Med, Cairo, Egypt.
   [Othman, Eman Bashir] Tripoli Cent Hosp, Dept Med, Tripoli, Libya.
   [Elhady, Mohamed Tamer] Zagazig Univ, Dept Pediat, Sharkia, Egypt.
   [Kansakar, Aswin Ratna] Dirghayu Guru Hosp, Kathmandu, Nepal.
   [Kansakar, Aswin Ratna] Res Ctr, Kathmandu, Nepal.
   [Linh Tran] Duy Tan Univ, Int Res & Dev, Da Nang, Vietnam.
   [Hirayama, Kenji] Nagasaki Univ, Dept Immunogenet, Inst Trop Med NEKKEN, Grad Sch Biomed Sci, Nagasaki, Japan.
   [Nguyen Tien Huy] Ton Duc Thang Univ, Evidence Based Med Res Grp, Ho Chi Minh City, Vietnam.
   [Nguyen Tien Huy] Ton Duc Thang Univ, Fac Appl Sci, Ho Chi Minh City, Vietnam.
   [Nguyen Tien Huy] Nagasaki Univ, Dept Clin Prod Dev, Inst Trop Med NEKKEN, Leading Grad Sch Program, Nagasaki, Japan.
   [Nguyen Tien Huy] Nagasaki Univ, Grad Sch Biomed Sci, Nagasaki, Japan.
RP Huy, NT (corresponding author), Ton Duc Thang Univ, Evidence Based Med Res Grp, Ho Chi Minh City, Vietnam.; Huy, NT (corresponding author), Ton Duc Thang Univ, Fac Appl Sci, Ho Chi Minh City, Vietnam.; Huy, NT (corresponding author), Nagasaki Univ, Dept Clin Prod Dev, Inst Trop Med NEKKEN, Leading Grad Sch Program, Nagasaki, Japan.; Huy, NT (corresponding author), Nagasaki Univ, Grad Sch Biomed Sci, Nagasaki, Japan.
EM nguyentienhuy@tdt.edu.vn
RI Tran, Linh/O-6874-2018; Huy, Nguyen Tien/B-2573-2010; Hirayama,
   Kenji/AAN-7065-2021
OI Tran, Linh/0000-0001-8667-082X; Huy, Nguyen Tien/0000-0002-9543-9440;
   Kansakar, Aswin Ratna/0000-0003-4410-8964; Tamer Ibrahem,
   Mohamed/0000-0003-1339-1138
FU Ministry of Education, Culture, Sports, Science, and Technology (MEXT)
   of JapanMinistry of Education, Culture, Sports, Science and Technology,
   Japan (MEXT) [16H05844]; Japan Initiative for Global Research Network on
   Infectious Diseases (J-GRID)Ministry of Education, Culture, Sports,
   Science and Technology, Japan (MEXT)
FX This study was supported in part by a "Grant-in-Aid for Scientific
   Research (B)" (16H05844, 2016-2019 for Nguyen Tien Huy) from Ministry of
   Education, Culture, Sports, Science, and Technology (MEXT) of Japan and
   by the Japan Initiative for Global Research Network on Infectious
   Diseases (J-GRID) for Kenji Hirayama. The funders had no role in study
   design, data collection, and analysis, decision to publish, or
   preparation of the manuscript.
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NR 55
TC 14
Z9 14
U1 6
U2 20
PU PEERJ INC
PI LONDON
PA 341-345 OLD ST, THIRD FLR, LONDON, EC1V 9LL, ENGLAND
SN 2167-8359
J9 PEERJ
JI PeerJ
PD NOV 17
PY 2017
VL 5
AR e3993
DI 10.7717/peerj.3993
PG 26
WC Multidisciplinary Sciences
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Science & Technology - Other Topics
GA FM9AB
UT WOS:000415383000009
PM 29158964
OA gold, Green Submitted, Green Published
DA 2022-04-25
ER

PT J
AU Chan, CK
   Tong, KL
   Wong, PF
   Kadir, H
AF Chan, Chim-Kei
   Tong, Kind-Leng
   Wong, Pooi-Fong
   Kadir, Habsah
TI Deoxyelephantopin induces ROS-mediated autophagy and apoptosis in human
   colorectal cancer in vitro and in vivo
SO ASIAN PACIFIC JOURNAL OF TROPICAL BIOMEDICINE
LA English
DT Article
DE Deoxyelephantopin; Autophagy; PI3K; mTOR; Colorectal cancer; MAPK
ID ELEPHANTOPUS-SCABER; SIGNALING PATHWAY; CELLS; ACTIVATION; GROWTH; MTOR;
   P38
AB Objective: To systematically map the stepwise events leading to deoxyelephantopin-induced cell death of HCT116 human colorectal cancer cells and evaluate the effectiveness of deoxyelephantopin in vivo. Methods: HCT116 cells were treated with deoxyelephantopin at various concentrations and time points. Autophagy was confirmed by the detection of autophagosomes and autophagosomal proteins by electron microscopy and Western blotting assays, respectively, and then validated by siRNA knockdown. In addition, apoptosis was confirmed by the detection of apoptosis-related proteins. The intracellular reactive oxygen species (ROS) level was measured using flow cytometry. The growth inhibitory effect of deoxyelephantopin was further evaluated in vivo using a mouse xenograft model. Results: Deoxyelephantopin firstly elevated ROS production, which then triggered autophagic flux with the accumulation of autophagosomal proteins including LC3A/B, ATG5, and ATG7, followed by the induction of apoptosis via the intrinsic and extrinsic pathways. Pre-treatment with N-acetyl-L-cysteine, a ROS inhibitor, reversed both apoptosis and autophagy. The knockdown of LC3 prevented apoptosis induction which confirmed that deoxyelephantopin induced autophagy-dependent apoptosis in HCT116 cells. Accumulation of ROS also activated apoptosis via the mitogen-activated protein kinases signaling pathway. Furthermore, deoxyelephantopin also inhibited the PI3K/AKT/mTOR pathway, which then released the inhibition of autophagy. In vivo study further showed that deoxyelephantopin significantly suppressed the growth of HCT116 subcutaneous xenograft in nude mice. Conclusions: Our findings revealed that deoxyelephantopin elevates oxidative stress and induces ROS-dependent autophagy followed by apoptosis in HCT116 cells via the concerted modulation of multiple signaling pathways. These findings further support the development of deoxyelephantopin as a therapeutic agent for colorectal cancer.
C1 [Chan, Chim-Kei; Kadir, Habsah] Univ Malaya, Fac Sci, Inst Biol Sci, Biomol Res Grp,Biochem Program, Kuala Lumpur 50603, Malaysia.
   [Tong, Kind-Leng; Wong, Pooi-Fong] Univ Malaya, Fac Med, Dept Pharmacol, Kuala Lumpur 50603, Malaysia.
RP Kadir, H (corresponding author), Univ Malaya, Fac Sci, Inst Biol Sci, Biomol Res Grp,Biochem Program, Kuala Lumpur 50603, Malaysia.; Wong, PF (corresponding author), Univ Malaya, Fac Med, Dept Pharmacol, Kuala Lumpur 50603, Malaysia.
EM wongpf@um.edu.my; drhabsah55@gmail.com
RI WONG, POOI-FONG PF/B-5234-2010
OI WONG, POOI-FONG PF/0000-0002-6705-2521
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NR 45
TC 1
Z9 1
U1 2
U2 2
PU WOLTERS KLUWER MEDKNOW PUBLICATIONS
PI MUMBAI
PA WOLTERS KLUWER INDIA PVT LTD , A-202, 2ND FLR, QUBE, C T S  NO 1498A-2
   VILLAGE MAROL, ANDHERI EAST, MUMBAI, 400059, INDIA
SN 2221-1691
EI 2588-9222
J9 ASIAN PAC J TROP BIO
JI Asian Pac. Trop. Biomed.
PD MAR
PY 2020
VL 10
IS 3
BP 120
EP 135
DI 10.4103/2221-1691.276318
PG 16
WC Tropical Medicine
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Tropical Medicine
GA KM9EU
UT WOS:000514445200004
OA gold
DA 2022-04-25
ER

PT J
AU Acharya, B
   Chaijaroenkul, W
   Na-Bangchang, K
AF Acharya, Bishwanath
   Chaijaroenkul, Wanna
   Na-Bangchang, Kesara
TI Atractylodin inhibited the migration and induced autophagy in
   cholangiocarcinoma cells via PI3K/AKT/mTOR and p38MAPK signalling
   pathways
SO JOURNAL OF PHARMACY AND PHARMACOLOGY
LA English
DT Article
DE atractylodin; autophagy; cholangiocarcinoma; PI3K/AKT/mTOR; p38MAPK
ID COLON-CANCER; CYCLE ARREST; APOPTOSIS; SUPPRESSES; INVASION
AB Objectives The effects of atractylodin (ATD), the bioactive compound from Atractylodes lancea, on migration and autophagy status of cholangiocarcinoma cell line were investigated.
   Methods Cytotoxic activity and effects on cell migration and invasion were evaluated by MTT and trans-well assay, respectively. Autophagy and underlying molecular mechanisms were investigated using flow cytometry and western blot analysis.
   Key findings ATD regulated the activity of PI3K/AKT/mTOR and p38MAPK signalling pathways which contributed to autophagy induction. HuCCT-1 cell growth was inhibited by ATD in a time- and dose-dependent manner. ATD inhibited the migration and invasion of HuCCT1 cells in a concentration-dependent manner. It also induced autophagy in HuCCT1 cells in a time- and dose-dependent manner. The SB202190 (autophagy inducer) and 3-MA (autophagy inhibitor) significantly increased and decreased the rate of ATD-induced autophagy, respectively. The 24 h exposure of ATD inhibited the phosphorylation of phosphatidylinositol-3-kinase (PI3K), protein kinase B (AKT), mammalian target of rapamycin (mTOR), mitogen-activated protein kinase (p38MAPK) and increased Beclin-1 expression and LC3 conversion. It also reduced p-AKT/AKT, p-mTOR/mTOR and p-p38MAPK/p38MAPK.
   Conclusions ATD inhibits the proliferation and induces CCA cell autophagy via regulating PI3K/AKT/mTOR and p38MAPK signalling pathways.
C1 [Acharya, Bishwanath; Chaijaroenkul, Wanna; Na-Bangchang, Kesara] Thammasat Univ, Chulabhorn Int Coll Med, Rangsit Ctr, Klongluang, Pathum Thani, Thailand.
   [Na-Bangchang, Kesara] Thammasat Univ, Chulabhorn Int Coll Med, Ctr Excellence Pharmacol & Mol Biol Malaria & Cho, Rangsit Ctr, Klongluang 12120, Pathum Thani, Thailand.
   [Na-Bangchang, Kesara] Thammasat Univ, Drug Discovery & Dev Ctr, Rangsit Ctr, Klongluang, Pathum Thani, Thailand.
RP Na-Bangchang, K (corresponding author), Thammasat Univ, Chulabhorn Int Coll Med, Ctr Excellence Pharmacol & Mol Biol Malaria & Cho, Rangsit Ctr, Klongluang 12120, Pathum Thani, Thailand.
EM kesaratmu@yahoo.com
OI Acharya, Bishwanath/0000-0001-8603-0574
FU Thammasat University (Center of Excellence in Pharmacology and Molecular
   Biology of Malaria and Cholangiocarcinoma), Chulabhorn International
   College of Medicine at Thammasat University, Rangsit Center, Thailand;
   National Research Council of Thailand (Ministry of Higher Education,
   Science, Research, and Innovation) [2020-01]
FX This study was supported by Thammasat University (Center of Excellence
   in Pharmacology and Molecular Biology of Malaria and
   Cholangiocarcinoma), Chulabhorn International College of Medicine at
   Thammasat University, Rangsit Center, Thailand. K.N.-B. is supported by
   the National Research Council of Thailand (Ministry of Higher Education,
   Science, Research, and Innovation) under the Research Team Promotion
   grant [grant number 2020-01].
CR Chen GH, 2017, J PHARMACOL SCI, V134, P59, DOI 10.1016/j.jphs.2017.04.003
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NR 39
TC 2
Z9 2
U1 1
U2 10
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 0022-3573
EI 2042-7158
J9 J PHARM PHARMACOL
JI J. Pharm. Pharmacol.
PD SEP
PY 2021
VL 73
IS 9
BP 1191
EP 1200
DI 10.1093/jpp/rgab036
EA APR 2021
PG 10
WC Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA UQ1GR
UT WOS:000695820100006
PM 33885818
DA 2022-04-25
ER

PT J
AU Lai, K
   Matthews, S
   Wilmott, JS
   Killingsworth, MC
   Yong, JL
   Caixeiro, NJ
   Wykes, J
   Samakeh, A
   Forstner, D
   Lee, M
   McGuinness, J
   Niles, N
   Hong, A
   Ebrahimi, A
   Lee, CS
AF Lai, Kenneth
   Matthews, Slade
   Wilmott, James S.
   Killingsworth, Murray C.
   Yong, Jim L.
   Caixeiro, Nicole J.
   Wykes, James
   Samakeh, Allan
   Forstner, Dion
   Lee, Mark
   McGuinness, John
   Niles, Navin
   Hong, Angela
   Ebrahimi, Ardalan
   Lee, Cheok Soon
TI Differences in LC3B expression and prognostic implications in
   oropharyngeal and oral cavity squamous cell carcinoma patients
SO BMC CANCER
LA English
DT Article
DE Autophagy; LC3B; Oropharyngeal; Oral cavity; SCC; HPV;
   Immunohistochemistry; Survival outcome
ID BREAST-CANCER CELLS; HUMAN-PAPILLOMAVIRUS; AUTOPHAGY INHIBITION;
   COLORECTAL-CANCER; RADIATION-THERAPY; INCIDENCE RATES; POOR-PROGNOSIS;
   COLON-CANCER; RISK-FACTORS; SURVIVAL
AB Background: This study examined the prognostic significance of microtubule-associated protein light chain 3B (LC3B) expression in oropharyngeal and oral cavity squamous cell carcinoma (SCC). The prognostic significance of LC3B expression in relation to human papillomavirus (HPV) status in oropharyngeal SCC was also examined.
   Methods: Tissue microarrays (TMAs) were constructed from formalin-fixed, paraffin-embedded oropharyngeal (n =47) and oral cavity (n = 95) SCC tissue blocks from patients with long-term recurrence and overall survival data (median =47 months). LC3B expression on tumour was assessed by immunohistochemistry and evaluated for associations with clinicopathological variables. LC3B expression was stratified into high and low expression cohorts using ROC curves with Manhattan distance minimisation, followed by Kaplan-Meier and multivariable survival analyses. Interaction terms between HPV status and LC3B expression in oropharyngeal SCC patients were also examined by joint-effects and stratified analyses.
   Results: Kaplan-Meier survival and univariate analyses revealed that high LC3B expression was correlated with poor overall survival in oropharyngeal SCC patients (p = 0.007 and HR = 3.18, 95% CI 1.31 7.71, p = 0.01 respectively). High LC3B expression was also an independent prognostic factor for poor overall survival in oropharyngeal SCC patients (HR = 4.02, 95% CI 1.38 11.47, p = 0.011). In contrast, in oral cavity SCC, only disease-free survival remained statistically significant after univariate analysis (HR = 2.36, 95% CI 1.19 4.67, p = 0.014), although Kaplan-Meier survival analysis showed that high LC3B expression correlated with poor overall and disease-free survival (p = 0.046 and 0.011 respectively), Purthermore, oropharyngeal SCC patients with HPV-negative/high LC3B expression were correlated with poor overall survival in both joint-effects and stratified presentations (p = 0.024 and 0.032 respectively).
   Conclusions: High LC3B expression correlates with poor prognosis in oropharyngeal and oral cavity SCC, which highlights the importance of autophagy in these malignancies. High LC3B expression appears to be an independent prognostic marker for oropharyngeal SCC but not for oral cavity SCC patients. The difference in the prognostic significance of LC3B between oropharyngeal and oral cavity SCCs further supports the biological differences between these malignancies. The possibility that oropharyngeal SCC patients with negative HPV status and high LC3B expression were at particular risk of a poor outcome warrants further investigation in prospective studies with larger numbers.
C1 [Lai, Kenneth; Matthews, Slade; Wilmott, James S.; Hong, Angela; Lee, Cheok Soon] Univ Sydney, Sydney Med Sch, Sydney, NSW, Australia.
   [Lai, Kenneth; Killingsworth, Murray C.; Caixeiro, Nicole J.; Lee, Cheok Soon] Western Sydney Univ, Sch Med, Discipline Pathol, Sydney, NSW, Australia.
   [Lai, Kenneth; Killingsworth, Murray C.; Caixeiro, Nicole J.; Lee, Cheok Soon] Ingham Inst Appl Med Res, Ctr Oncol Educ & Res Translat CONCERT, Sydney, NSW, Australia.
   [Lai, Kenneth; Killingsworth, Murray C.; Yong, Jim L.; Lee, Cheok Soon] Liverpool Hosp, SSWPS, Dept Anat Pathol, Sydney, NSW, Australia.
   [Matthews, Slade] Univ Sydney, Bosch Inst, Sydney, NSW, Australia.
   [Wilmott, James S.] Melanoma Inst Australia, Sydney, NSW, Australia.
   [Killingsworth, Murray C.; Wykes, James; Forstner, Dion] Univ New South Wales, Fac Med, Sydney, NSW, Australia.
   [Wykes, James; Samakeh, Allan; McGuinness, John; Niles, Navin; Ebrahimi, Ardalan] Liverpool Hosp, Dept Head & Neck Surg, Sydney, NSW, Australia.
   [Forstner, Dion] Liverpool Hosp, Dept Radiat Oncol, Sydney, NSW, Australia.
   [Lai, Kenneth] Ingham Inst Appl Med Res, 1 Campbell St, Liverpool, NSW 2170, Australia.
RP Lai, K (corresponding author), Univ Sydney, Sydney Med Sch, Sydney, NSW, Australia.; Lai, K (corresponding author), Western Sydney Univ, Sch Med, Discipline Pathol, Sydney, NSW, Australia.; Lai, K (corresponding author), Ingham Inst Appl Med Res, Ctr Oncol Educ & Res Translat CONCERT, Sydney, NSW, Australia.; Lai, K (corresponding author), Liverpool Hosp, SSWPS, Dept Anat Pathol, Sydney, NSW, Australia.; Lai, K (corresponding author), Ingham Inst Appl Med Res, 1 Campbell St, Liverpool, NSW 2170, Australia.
EM k.lai@uws.edu.au
RI Wilmott, James/AGA-8227-2022; Killingsworth, Murray/O-3736-2019;
   Matthews, Slade/J-4939-2019
OI Wilmott, James/0000-0002-6750-5244; Killingsworth,
   Murray/0000-0002-6125-1183; Matthews, Slade/0000-0002-1652-543X;
   Forstner, dion/0000-0002-6963-6942
FU Centre for Oncology Education and Research Translation (CONCERT) -
   Cancer Institute of New South Wales, Australia
FX This design of the study and collection, analysis, interpretation of
   data and in writing the manuscript was supported by internal funds and
   the Centre for Oncology Education and Research Translation (CONCERT) is
   funded by the Cancer Institute of New South Wales, Australia.
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NR 73
TC 7
Z9 10
U1 0
U2 2
PU BIOMED CENTRAL LTD
PI LONDON
PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND
SN 1471-2407
J9 BMC CANCER
JI BMC Cancer
PD JUN 1
PY 2018
VL 18
AR 624
DI 10.1186/s12885-018-4536-x
PG 12
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA GI2WN
UT WOS:000434232700004
PM 29859041
OA Green Published, gold
DA 2022-04-25
ER

PT J
AU Karasic, TB
   Rosen, MA
   O'Dwyer, PJ
AF Karasic, Thomas B.
   Rosen, Mark A.
   O'Dwyer, Peter J.
TI Antiangiogenic tyrosine kinase inhibitors in colorectal cancer: is there
   a path to making them more effective?
SO CANCER CHEMOTHERAPY AND PHARMACOLOGY
LA English
DT Review
DE Sorafenib; Regorafenib; Antiangiogenesis; Colorectal cancer; VEGFR2
   signaling; DCE-MRI
ID RENAL-CELL CARCINOMA; ENDOTHELIAL GROWTH-FACTOR; PHASE-I TRIAL; ADVANCED
   SOLID TUMORS; OXALIPLATIN-BASED CHEMOTHERAPY; COMBINATION TARGETED
   THERAPY; FACTOR RECEPTOR INHIBITOR; REGORAFENIB BAY 73-4506; GLOBAL
   EVALUATION TRIAL; CONTRAST-ENHANCED MRI
AB Antiangiogenic therapy has a proven survival benefit in metastatic colorectal cancer. Inhibition of the VEGF pathway using a variety of extracellular antibody approaches has clear benefit in combination with chemotherapy, while intracellular blockade using tyrosine kinase inhibitors (TKIs) such as sorafenib and regorafenib has had more limited success. Pharmacodynamic modeling using modalities such as DCE-MRI indicates potent antiangiogenic effects of these TKIs, yet numerous combination therapies, primarily with chemotherapy, have failed to demonstrate an additive benefit. The sole comparative study of a single agent TKI against placebo showed a survival benefit of regorafenib in patients with advanced, refractory disease. Preclinical data demonstrate synergy between antiantiogenic TKIs and targeted interventions including autophagy inhibition, and together with a renewed effort to define markers of susceptibility, such combinations may be a way to improve the limited efficacy of this once-promising drug class.
C1 [Karasic, Thomas B.; O'Dwyer, Peter J.] Univ Penn, Abramson Canc Ctr, 3400 Civic Ctr Blvd, Philadelphia, PA 19146 USA.
   [Rosen, Mark A.] Univ Penn, Dept Radiol, Philadelphia, PA 19104 USA.
RP Karasic, TB (corresponding author), Univ Penn, Abramson Canc Ctr, 3400 Civic Ctr Blvd, Philadelphia, PA 19146 USA.
EM thomas.karasic@uphs.upenn.edu
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NR 98
TC 3
Z9 4
U1 0
U2 11
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0344-5704
EI 1432-0843
J9 CANCER CHEMOTH PHARM
JI Cancer Chemother. Pharmacol.
PD OCT
PY 2017
VL 80
IS 4
BP 661
EP 671
DI 10.1007/s00280-017-3389-3
PG 11
WC Oncology; Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Pharmacology & Pharmacy
GA FH9TS
UT WOS:000411555500001
PM 28721456
DA 2022-04-25
ER

PT J
AU Abdel-Aziz, AK
   Shouman, S
   El-Demerdash, E
   Elgendy, M
   Abdel-Naim, AB
AF Abdel-Aziz, Amal Kamal
   Shouman, Samia
   El-Demerdash, Ebtehal
   Elgendy, Mohamed
   Abdel-Naim, Ashraf B.
TI Chloroquine synergizes sunitinib cytotoxicity via modulating autophagic,
   apoptotic and angiogenic machineries
SO CHEMICO-BIOLOGICAL INTERACTIONS
LA English
DT Article
DE Sunitinib; Chloroquine; Autophagy; Apoptosis; Angiogenesis; Oxidative
   stress
ID BREAST-CANCER CELLS; NITRIC-OXIDE; MICROVESSEL DENSITY; BECLIN 1;
   INHIBITION; SURVIVIN; EXPRESSION; GROWTH; DEATH; DRUG
AB Tyrosine kinases play a pivotal role in oncogenesis. Although tyrosine kinase inhibitors as sunitinib malate are used in cancer therapy, emerging studies report compromised cytotoxicity when used as monotherapy and thus combinations with other anti-cancer agents is recommended. Chloroquine is a clinically available anti-malarial agent which has been shown to exhibit anti-cancer activity. In the current study, we questioned whether chloroquine can modulate sunitinib cytotoxicity. We found that chloroquine synergistically augmented sunitinib cytotoxicity on human breast (MCF-7 and T-47D), cervical (Hela), colorectal (Caco-2 and HCT116), hepatocellular (HepG2), laryngeal (HEp-2) and prostate (PC3) cancer cell lines as indicated by combination and concentration reduction indices. These results were also consistent with that of Ehrlich ascites carcinoma (EAC) Swiss albino mice models as confirmed by tumor volume, weight, histopathological examination and PCNA expression. Sunitinib induced autophagy via upregulating beclin-1 expression which was blocked by chloroquine as evidenced by accumulated SQTSM1/p62 level. Furthermore, chloroquine augmented sunitinib-induced apoptosis by decreasing survivin level and increasing caspase 3 activity. Chloroquine also enhanced the antiangiogenic capacity of sunitinib as indicated by decreased CD34 expression and peritoneal/skin angiogenesis. Sunitinib when combined with chloroquine also increased reactive nitrogen species production via increasing inducible nitric oxide synthase expression and nitric oxide level whilst reduced reactive oxygen species production by increasing GSH level, activities of glutathione peroxidase and catalase and reducing lipid peroxides compared to sunitinib-only treated group. Taken together, these findings suggest that chloroquine enhanced sunitinib cytotoxicity in a synergistic manner via inducing apoptosis while switching off autophagic and angiogenic machineries. Nevertheless, further studies are required to elucidate the efficacy and safety profile of such combination. (C) 2014 Elsevier Ireland Ltd. All rights reserved.
C1 [Abdel-Aziz, Amal Kamal; El-Demerdash, Ebtehal; Abdel-Naim, Ashraf B.] Ain Shams Univ, Fac Pharm, Dept Pharmacol & Toxicol, Cairo, Egypt.
   [Abdel-Aziz, Amal Kamal; Elgendy, Mohamed] European Inst Oncol, Dept Expt Oncol, Milan, Italy.
   [Shouman, Samia] Cairo Univ, Natl Canc Inst, Dept Canc Biol, Cairo, Egypt.
RP Abdel-Naim, AB (corresponding author), Ain Shams Univ, Fac Pharm, Dept Pharmacol & Toxicol, Cairo, Egypt.
EM abnaim@pharma.asu.edu.eg
RI Abdel-Aziz, Amal Kamal/AAB-9050-2019; Abdel-Naim, Ashraf B/J-3199-2012;
   Abdel-Aziz, Amal Kamal/AAA-1360-2021; El-Demerdash,
   Ebtehal/ABE-6729-2020; shouman, samia/F-5395-2018
OI Abdel-Aziz, Amal Kamal/0000-0003-1709-1183; Abdel-Naim, Ashraf
   B/0000-0002-0400-9075; shouman, samia/0000-0002-2883-8775
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NR 56
TC 57
Z9 63
U1 0
U2 24
PU ELSEVIER IRELAND LTD
PI CLARE
PA ELSEVIER HOUSE, BROOKVALE PLAZA, EAST PARK SHANNON, CO, CLARE, 00000,
   IRELAND
SN 0009-2797
EI 1872-7786
J9 CHEM-BIOL INTERACT
JI Chem.-Biol. Interact.
PD JUN 25
PY 2014
VL 217
BP 28
EP 40
DI 10.1016/j.cbi.2014.04.007
PG 13
WC Biochemistry & Molecular Biology; Pharmacology & Pharmacy; Toxicology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Pharmacology & Pharmacy; Toxicology
GA AJ4ML
UT WOS:000337650400004
PM 24751611
DA 2022-04-25
ER

PT J
AU Sutradhar, M
   Rajeshwari
   Barman, TR
   Fernandes, AR
   Paradinha, F
   Roma-Rodrigues, C
   da Silva, MFCG
   Pombeiro, AJL
AF Sutradhar, Manas
   Rajeshwari
   Barman, Tannistha Roy
   Fernandes, Alexandra R.
   Paradinha, Fabiana
   Roma-Rodrigues, Catarina
   da Silva, M. Fatima C. Guedes
   Pombeiro, Armando J. L.
TI Mixed ligand aroylhydrazone and N-donor heterocyclic Lewis base Cu(II)
   complexes as potential antiproliferative agents
SO JOURNAL OF INORGANIC BIOCHEMISTRY
LA English
DT Article
DE Mixed ligand copper(II) complexes; Aroylhydrazone ligand; X-ray
   structure; Antiproliferative agent; Human tumor cell lines
ID MICROWAVE-ASSISTED OXIDATION; BREAST-CANCER CELLS; CATALYST PRECURSORS;
   COBALT COMPLEXES; ALCOHOLS; HYDRAZONE; CHELATORS; APOPTOSIS; CRYSTAL;
   COPPER
AB A series of four mixed ligand aroylhydrazone and N-donor heterocyclic Lewis base Cu(II) complexes [CuL(X)](2) [L refers to the dianionic form of (5-bromo-2-hydroxybenzylidene)-2-hydroxybenzohydrazide; X = pyrazine (Pz; 1), pyridine (Py; 2), imidazole (Imz; 3) and 3-pyridinecarbonitrile (3-PyCN; 4)] has been synthesized and characterized by elemental analysis, various spectroscopic techniques and X-ray crystallography (for 1, 2 and 4). The antiproliferative effect of complexes 1-4 was examined in 4 human tumor cell lines (ovarian carcinoma (A2780), colorectal carcinoma (HCT116), lung adenocarcinoma (A549) and breast adenocarcinoma (MCF7)) and in normal human primary Fibroblasts. Complex 4 exhibits a high cytotoxic activity against ovarian and colorectal carcinoma cells (A2780, HCT116 respectively), with IC50 much lower than those for normal primary fibroblasts. Complex 4 could induce cell death via apoptosis but not autophagy in colorectal carcinoma cells.
C1 [Sutradhar, Manas; Rajeshwari; Barman, Tannistha Roy; Fernandes, Alexandra R.; da Silva, M. Fatima C. Guedes; Pombeiro, Armando J. L.] Univ Lisbon, Ctr Quim Estrut, Inst Super Tecn, Ave Rovisco Pais, P-1049001 Lisbon, Portugal.
   [Fernandes, Alexandra R.; Paradinha, Fabiana; Roma-Rodrigues, Catarina] Univ Nova Lisboa, UCIBIO, Dept Ciencias Vida, Fac Ciencias & Tecnol, Campus Caparica, P-2829516 Caparica, Portugal.
RP Sutradhar, M (corresponding author), Univ Lisbon, Ctr Quim Estrut, Inst Super Tecn, Ave Rovisco Pais, P-1049001 Lisbon, Portugal.
EM manas@tecnico.ulisboa.pt; ma.fernandes@fct.unl.pt;
   fatima.guedes@tecnico.ulisboa.pt
RI Roma-Rodrigues, Catarina/AAT-5658-2021; da Silva, M. Fátima C
   Guedes/H-8274-2012; Fernandes, Alexandra R/C-7465-2011; Pombeiro,
   Armando JL/I-5945-2012; Roma-Rodrigues, Catarina/S-6144-2016; Paradinha,
   Fabiana/L-2307-2018; da Silva, Maria de Fatima Guedes/P-3458-2019;
   Sutradhar, Manas/M-4089-2013; Roy Barman, Tannistha/L-7444-2014
OI Roma-Rodrigues, Catarina/0000-0002-8676-6562; da Silva, M. Fátima C
   Guedes/0000-0003-4836-2409; Fernandes, Alexandra R/0000-0003-2054-4438;
   Pombeiro, Armando JL/0000-0001-8323-888X; Roma-Rodrigues,
   Catarina/0000-0002-8676-6562; Paradinha, Fabiana/0000-0001-8833-677X; da
   Silva, Maria de Fatima Guedes/0000-0003-4836-2409; Sutradhar,
   Manas/0000-0003-3349-9154; Roy Barman, Tannistha/0000-0002-5147-7648
FU Foundation for Science and Technology (FCT), PortugalPortuguese
   Foundation for Science and Technology [PTDC/EQU-EQU/122025/2010,
   UID/QUI/00100/2013]; FCT, PortugalPortuguese Foundation for Science and
   TechnologyEuropean Commission [SFRH/BPD/86067/2012]; Unidade de Ciencias
   Biomoleculares Aplicadas - UCIBIO - FCT/MEC [UID/Multi/04378/2013];
   ERDFEuropean Commission [POCI-01-0145-FEDER-007728]
FX Authors are grateful to the Foundation for Science and Technology (FCT)
   (projects PTDC/EQU-EQU/122025/2010 and UID/QUI/00100/2013), Portugal,
   for financial support. M.S. acknowledges the FCT, Portugal for a
   postdoctoral fellowship (SFRH/BPD/86067/2012). This work was also
   supported by the Unidade de Ciencias Biomoleculares Aplicadas - UCIBIO
   which is financed by national funds from FCT/MEC (UID/Multi/04378/2013)
   and co-financed by the ERDF under the PT2020 Partnership Agreement
   (POCI-01-0145-FEDER-007728). We are also thankful to the Portuguese NMR
   Network (IST-UL Centre) for access to the NMR facility.
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NR 36
TC 23
Z9 23
U1 0
U2 15
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0162-0134
EI 1873-3344
J9 J INORG BIOCHEM
JI J. Inorg. Biochem.
PD OCT
PY 2017
VL 175
BP 267
EP 275
DI 10.1016/j.jinorgbio.2017.07.034
PG 9
WC Biochemistry & Molecular Biology; Chemistry, Inorganic & Nuclear
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Chemistry
GA FI4DD
UT WOS:000411919000030
PM 28806643
DA 2022-04-25
ER

PT J
AU Kuo, YF
   Su, YZ
   Tseng, YH
   Wang, SY
   Wang, HM
   Chueh, PJ
AF Kuo, Yu-Feng
   Su, Ying-Zhen
   Tseng, Yen-Hsueh
   Wang, Sheng-Yang
   Wang, Hsi-Ming
   Chueh, Pin Ju
TI Flavokawain B, a novel chalcone from Alpinia pricei Hayata with potent
   apoptotic activity: Involvement of ROS and GADD153 upstream of
   mitochondria-dependent apoptosis in HCT116 cells
SO FREE RADICAL BIOLOGY AND MEDICINE
LA English
DT Article
DE Apoptosis; Alpinia pricei Hayata; Anticancer; Flavonoid; Flavokawain B;
   GADD153; ROS; Free radicals
ID ENDOPLASMIC-RETICULUM STRESS; UNFOLDED PROTEIN RESPONSE; BLADDER-CANCER
   CELLS; CYCLE ARREST; MEDIATED APOPTOSIS; TRIGGERS APOPTOSIS;
   UP-REGULATION; COLON-CANCER; ER STRESS; P38 MAPK
AB Flavonoids synthesized from chalcone precursors in plants have been shown to possess cytotoxic activities with therapeutic potential. We have isolated the novel chalcone flavokawain B from Alpinia pricei Hayata, a plant native to Taiwan that is used in food and traditional Chinese medicine. Here, we report for the first time that flavokawain B significantly inhibits the growth of colon cancer cells and provide novel insight into the molecular mechanisms that underlie its apoptotic activity. Flavokawain B exerts its apoptotic action through ROS generation and GADD153 up-regulation, which lead to mitochondria-dependent apoptosis characterized by release of cytochrome c and translocation of Bak. The up-regulation of GADD153 in flavokawain B-treated HCT116 cells is associated with mitochondrial dysfunction and altered expression of Bcl-2 family members. Moreover, pretreatment with the ROS scavenger N-acetylcysteine abolishes flavokawain B-induced ROS generation, GADD153 up-regulation, and apoptosis. Similarly, RNAi-mediated gene silencing reduced flavokawain B-enhanced expression of GADD153 and apoptotic Bim, leading to diminished apoptosis. Interestingly, flavokawain B provokes G2/M accumulation as well as autophagy, in addition to apoptosis, suggesting that multiple pathways are activated in flavokawain B-mediated anticancer activity. Taken together, our data provide evidence for a molecular mechanism to explain the apoptotic activity of Alpinia plants, showing that flavokawain B acts through ROS generation and GADD153 up-regulation to regulate the expression of Bcl-2 family members, thereby inducing mitochondrial dysfunction and apoptosis in HCT116 cells. (C) 2010 Elsevier Inc. All rights reserved.
C1 [Kuo, Yu-Feng; Su, Ying-Zhen; Wang, Hsi-Ming; Chueh, Pin Ju] Natl Chung Hsing Univ, Grad Inst Biomed Sci, Taichung 40227, Taiwan.
   [Tseng, Yen-Hsueh; Wang, Sheng-Yang] Natl Chung Hsing Univ, Dept Forestry, Taichung 40227, Taiwan.
RP Chueh, PJ (corresponding author), Natl Chung Hsing Univ, Grad Inst Biomed Sci, Taichung 40227, Taiwan.
EM pjchueh@dragon.nchu.edu.tw
RI Wang, Sheng-Yang/M-9656-2019
OI Wang, Sheng-Yang/0000-0002-8579-3569; Chueh, Pin Ju/0000-0002-3200-7552
FU National Science CouncilMinistry of Science and Technology, Taiwan [NSC
   97-2313-B-005-016-MY3]; Ministry of Education, Taiwan, Republic of
   ChinaMinistry of Education, Taiwan
FX We thank Dr. Tamotsu Yoshimori (Osaka University, Japan) for his
   generous gift of the pEGFP-LC3 construct, Dr. Ping-Shan Lai for his
   technical support with confocal microscopy, Dr. Chia-Che Chang for
   providing wild-type and p53-null HCT116 cells, Dr. Show-Mei Chuang for
   the HFW and A549 cells, and Jun-Hong Xiao for the preparation of
   flavokawain B. This work was supported by grants from the National
   Science Council (NSC 97-2313-B-005-016-MY3) and the Ministry of
   Education, Taiwan, Republic of China, under the ATU plan.
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TC 107
Z9 107
U1 2
U2 24
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0891-5849
EI 1873-4596
J9 FREE RADICAL BIO MED
JI Free Radic. Biol. Med.
PD JUL 15
PY 2010
VL 49
IS 2
BP 214
EP 226
DI 10.1016/j.freeradbiomed.2010.04.005
PG 13
WC Biochemistry & Molecular Biology; Endocrinology & Metabolism
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Endocrinology & Metabolism
GA 613XM
UT WOS:000279017800011
PM 20398749
DA 2022-04-25
ER

PT S
AU Liu, YY
   Hill, RA
   Li, YT
AF Liu, Yong-Yu
   Hill, Ronald A.
   Li, Yu-Teh
BE Norris, JS
TI Ceramide Glycosylation Catalyzed by Glucosylceramide Synthase and Cancer
   Drug Resistance
SO ROLE OF SPHINGOLIPIDS IN CANCER DEVELOPMENT AND THERAPY
SE Advances in Cancer Research
LA English
DT Review; Book Chapter
ID ADENOCARCINOMA CELL-LINE; TUMOR-NECROSIS-FACTOR; BREAST-CANCER;
   STEM-CELLS; MULTIDRUG-RESISTANCE; SPHINGOLIPID METABOLISM;
   MOLECULAR-CLONING; UDP-GALACTOSE; MUTANT P53; GLYCOSPHINGOLIPID
   SYNTHESIS
AB Glucosylceramide synthase (GCS), converting ceramide to glucosylceramide, catalyzes the first reaction of ceramide glycosylation in sphingolipid metabolism. This glycosylation by GCS is a critical step regulating the modulation of cellular activities by controlling ceramide and glycosphingolipids (GSLs). An increase of ceramide in response to stresses, such as chemotherapy, drives cells to proliferation arrest and apoptosis or autophagy; however, ceramide glycosylation promptly eliminates ceramide and consequently, these induced processes, thus protecting cancer cells. Further, persistently enhanced ceramide glycosylation can increase GSLs, participating in selecting cancer cells to drug resistance. GCS is overexpressed in diverse drug-resistant cancer cells and in tumors of breast, colon, and leukemia that display poor response to chemotherapy. As ceramide glycosylation by GCS is a rate-limiting step in GSL synthesis, inhibition of GCS sensitizes cancer cells to anticancer drugs and eradicates cancer stem cells. Mechanistic studies indicate that uncoupling ceramide glycosylation can modulate gene expression, decreasing MDR1 through the cSrc/beta-catenin pathway and restoring p53 expression via RNA splicing. These studies not only expand our knowledge in understanding how ceramide glycosylation affects cancer cells but also provide novel therapeutic approaches for targeting refractory tumors.
C1 [Liu, Yong-Yu; Hill, Ronald A.] Univ Louisiana Monroe, Dept Basic Pharmaceut Sci, Monroe, LA 71209 USA.
   [Li, Yu-Teh] Tulane Univ, Sch Med, Dept Biochem & Mol Biol, New Orleans, LA 70112 USA.
RP Liu, YY (corresponding author), Univ Louisiana Monroe, Dept Basic Pharmaceut Sci, Monroe, LA 71209 USA.
EM yliu@ulm.edu
RI Liu, Yong-Yu/H-8593-2014
OI Liu, Yong-Yu/0000-0002-7968-0162
FU NCI NIH HHSUnited States Department of Health & Human ServicesNational
   Institutes of Health (NIH) - USANIH National Cancer Institute (NCI) [R15
   CA167476] Funding Source: Medline; NCRR NIH HHSUnited States Department
   of Health & Human ServicesNational Institutes of Health (NIH) - USANIH
   National Center for Research Resources (NCRR) [5P20RR016456-11, P20
   RR016456] Funding Source: Medline; NIGMS NIH HHSUnited States Department
   of Health & Human ServicesNational Institutes of Health (NIH) - USANIH
   National Institute of General Medical Sciences (NIGMS) [P20 GM103424, 8
   P20 GM103424-11] Funding Source: Medline; NATIONAL CANCER
   INSTITUTEUnited States Department of Health & Human ServicesNational
   Institutes of Health (NIH) - USANIH National Cancer Institute (NCI)
   [R15CA167476] Funding Source: NIH RePORTER; NATIONAL CENTER FOR RESEARCH
   RESOURCESUnited States Department of Health & Human ServicesNational
   Institutes of Health (NIH) - USANIH National Center for Research
   Resources (NCRR) [P20RR016456] Funding Source: NIH RePORTER; NATIONAL
   INSTITUTE OF GENERAL MEDICAL SCIENCESUnited States Department of Health
   & Human ServicesNational Institutes of Health (NIH) - USANIH National
   Institute of General Medical Sciences (NIGMS) [P20GM103424] Funding
   Source: NIH RePORTER
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NR 160
TC 95
Z9 98
U1 1
U2 30
PU ELSEVIER ACADEMIC PRESS INC
PI SAN DIEGO
PA 525 B STREET, SUITE 1900, SAN DIEGO, CA 92101-4495 USA
SN 0065-230X
BN 978-0-12-394274-6
J9 ADV CANCER RES
JI Adv.Cancer Res.
PY 2013
VL 117
BP 59
EP 89
DI 10.1016/B978-0-12-394274-6.00003-0
PG 31
WC Oncology
WE Book Citation Index – Science (BKCI-S); Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA BDZ27
UT WOS:000315698900004
PM 23290777
OA Green Accepted
DA 2022-04-25
ER

PT J
AU Li, JN
   Vangundy, Z
   Poi, M
AF Li, Junan
   Vangundy, Zachary
   Poi, Ming
TI PTC209, a Specific Inhibitor of BMI1, Promotes Cell Cycle Arrest and
   Apoptosis in Cervical Cancer Cell Lines
SO ANTICANCER RESEARCH
LA English
DT Article
DE PTC209; BMI1; inhibition; cervical cancer; cancer stem cell
ID PROTEIN BMI-1; PTC-209; OVEREXPRESSION; PROLIFERATION; EPIDEMIOLOGY;
   AUTOPHAGY; MYELOMA
AB Background/Aim: Aberrant expression of the BMI1 oncogene has been prevalently found in a variety of human cancers, including cervical cancer. Recent studies have shown that PTC209, a specific BMI1 inhibitor, exhibits high potency in inhibiting the growth of colon, breast, oral cancer cells and cancer-initiating cells, indicative of its chemotherapeutic potential. In the current study, we evaluated the inhibitory abilities of PTC209 in cervical cancer cells. Materials and Methods: Three cervical cell lines, C33A, HeLa, and SiHa were treated with PTC209. The impacts of PTC209 on BMI1 were investigated using quantitative reverse-transcription PCR assay (qRT-PCR) and western blotting; changes in cell viability, cell cycle distribution, and apoptosis were assessed using cell viability testing, colony formation assay and flow cytometry analyses, respectively. Results: PTC209 exhibited considerably high short-term and long-term cytotoxicities in all tested cervical cancer cell lines regardless of their HPV infection status, TP53 and pRb statuses. PTC209 significantly downregulated the expression of BMI1 in cervical cancer cell lines, and such downregulation led to G0/G1 arrest (p<0.05). Moreover, PTC209 drove more cells into apoptosis (p<0.05). Conclusion: PTC209 (BMI1-targeting agents, in general) represents a novel chemotherapeutic agent with potential in cervical cancer therapy.
C1 [Li, Junan; Poi, Ming] Ohio State Univ, Coll Pharm, Div Pharm Practice & Adm, 500 W 12Th Ave, Columbus, OH 43210 USA.
   [Li, Junan; Vangundy, Zachary; Poi, Ming] Ohio State Univ, Ctr Comprehens Canc, Columbus, OH 43210 USA.
   [Vangundy, Zachary; Poi, Ming] Arthur G James Canc Hosp, Dept Pharm, Columbus, OH USA.
   [Vangundy, Zachary; Poi, Ming] Richard J Solove Res Inst, Columbus, OH USA.
RP Li, JN (corresponding author), Ohio State Univ, Coll Pharm, Columbus, OH 43210 USA.
EM li.225@osu.edu
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NR 42
TC 4
Z9 4
U1 1
U2 5
PU INT INST ANTICANCER RESEARCH
PI ATHENS
PA EDITORIAL OFFICE 1ST KM KAPANDRITIOU-KALAMOU RD KAPANDRITI, PO BOX 22,
   ATHENS 19014, GREECE
SN 0250-7005
EI 1791-7530
J9 ANTICANCER RES
JI Anticancer Res.
PD JAN
PY 2020
VL 40
IS 1
BP 133
EP 141
DI 10.21873/anticanres.13934
PG 9
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA KY7BB
UT WOS:000522727700014
PM 31892561
OA Bronze
DA 2022-04-25
ER

PT J
AU Hu, S
   Yin, J
   Yan, S
   Hu, P
   Huang, JZ
   Zhang, G
   Wang, FQ
   Tong, QY
   Zhang, YH
AF Hu, Song
   Yin, Jie
   Yan, Shan
   Hu, Ping
   Huang, Jianzheng
   Zhang, Geng
   Wang, Fuqian
   Tong, Qingyi
   Zhang, Yonghui
TI Chaetocochin J, an epipolythiodioxopiperazine alkaloid, induces
   apoptosis and autophagy in colorectal cancer via AMPK and PI3K/AKT/ mTOR
   pathways
SO BIOORGANIC CHEMISTRY
LA English
DT Article
DE Epipolythiodioxopiperazine; Chaetocochin J; Apoptosis; Autophagy;
   Colorectal cancer
AB Colorectal cancer (CRC) is the third commonly diagnosed malignancy and the second leading cause of cancer death worldwide. Development of novel chemotherapeutics is crucial. Natural products are the main source of drug discovery, and epipolythiodioxopiperazine (ETP) alkaloids are one kind of them have been reported to have potent biological activities. In the present study, we first isolated Chaetocochin J (CJ), an ETP alkaloid from the secondary metabolites of Chaetomium sp, and studied the anti-CRC activity and mechanism of it. The results showed that CJ exhibits potent proliferation inhibition effect, its IC50 to CRC cells are around 0.5 ?M. CJ also induces apoptosis of CRC cells in a dose-dependent manner, and this effect is stronger than topotecan. In addition, CJ treatment triggers autophagic flux in CRC cells, inhibition of autophagy by chloroquine didn?t affect CJ-induced apoptosis and growth inhibition, suggesting CJ may simultaneously induced apoptosis and autophagy in CRC cells. We further explored the mechanism of action, and found that CJ exerts its anti-CRC function via AMPK and PI3K/AKT/mTOR pathways and further regulation of their downstream signaling cascade in CRC cells, including apoptosis and autophagy. These data potently suggest that CJ may be a potential drug candidate for CRC treatment.
C1 [Hu, Song; Zhang, Geng; Wang, Fuqian] Wuhan 1 Hosp, Dept Pharm, 215 Zhongshan Rd, Wuhan 430022, Hubei, Peoples R China.
   [Yin, Jie; Yan, Shan; Huang, Jianzheng; Tong, Qingyi; Zhang, Yonghui] Huazhong Univ Sci & Technol, Tongji Med Coll, Tongji Rongcheng Ctr Biomed, Sch Pharm,Hubei Key Lab Nat Med Chem & Resource E, Wuhan 430030, Hubei, Peoples R China.
   [Hu, Ping] Hubei Univ, State Key Lab Biocatalysis & Enzyme Engn, Natl & Local Joint Engn Res Ctr High Throughput D, Sch Life Sci,Hubei Collaborat Innovat Ctr Green T, Wuhan 430062, Hubei, Peoples R China.
   [Wang, Fuqian] Hubei Univ Chinese Med, Fac Pharm, Wuhan 430065, Hubei, Peoples R China.
RP Wang, FQ; Tong, QY; Zhang, YH (corresponding author), Huazhong Univ Sci & Technol, Tongji Med Coll, Tongji Rongcheng Ctr Biomed, Sch Pharm,Hubei Key Lab Nat Med Chem & Resource E, Wuhan 430030, Hubei, Peoples R China.
EM wangfuqian.c@163.com; qytong@hust.edu.cn; zhangyh@mails.tjmu.edu.cn
RI Zhang, Yonghui/AGY-9072-2022
FU Fundamental Research Funds for the Central UniversitiesFundamental
   Research Funds for the Central Universities [5003514027]; National
   Natural Science Foundation of ChinaNational Natural Science Foundation
   of China (NSFC) [31670351]; Natural Science Foundation of Hubei
   ProvinceNatural Science Foundation of Hubei Province [2020CFB726];
   Scientific Research Project of Wuhan Municipal Health Commission
   [WX20A14]
FX This work was supported by the Fundamental Research Funds for the
   Central Universities (5003514027) , the National Natural Science
   Foundation of China (31670351) , Natural Science Foundation of Hubei
   Province (2020CFB726) , Scientific Research Project of Wuhan Municipal
   Health Commission (WX20A14) .
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TC 3
Z9 4
U1 8
U2 16
PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 0045-2068
EI 1090-2120
J9 BIOORG CHEM
JI Bioorganic Chem.
PD APR
PY 2021
VL 109
AR 104693
DI 10.1016/j.bioorg.2021.104693
EA FEB 2021
PG 8
WC Biochemistry & Molecular Biology; Chemistry, Organic
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Chemistry
GA RL7NE
UT WOS:000639154200005
PM 33609914
DA 2022-04-25
ER

PT J
AU Jo, YK
   Roh, SA
   Lee, H
   Park, NY
   Choi, ES
   Oh, JH
   Park, SJ
   Shin, JH
   Suh, YA
   Lee, EK
   Cho, DH
   Kim, JC
AF Jo, Yoon Kyung
   Roh, Seon Ae
   Lee, Heejin
   Park, Na Yeon
   Choi, Eun Sun
   Oh, Ju-Hee
   Park, So Jung
   Shin, Ji Hyun
   Suh, Young-Ah
   Lee, Eun Kyung
   Cho, Dong-Hyung
   Kim, Jin Cheon
TI Polypyrimidine tract-binding protein 1-mediated down-regulation of ATG10
   facilitates metastasis of colorectal cancer cells
SO CANCER LETTERS
LA English
DT Article
DE ATG10; Autophagy; PTBP1; Metastasis; EMT
ID EPITHELIAL-MESENCHYMAL TRANSITION; POSTTRANSCRIPTIONAL REGULATION;
   TUMOR-SUPPRESSOR; AUTOPHAGY GENE; BREAST-CANCER; N-CADHERIN;
   PROGRESSION; EXPRESSION; DEATH; SURVIVAL
AB Autophagy plays complex roles in tumor initiation and development, and the expression of autophagy-related genes (ATGs) is differentially regulated in various cancer cells, depending on their environment. In this study, we analyzed the expressional relationship between polypyrimidine tract-binding protein 1 (PTBP1) and ATG10 in metastatic colorectal cancer. PTBP1 is associated with tumor metastasis in primary colorectal tumors and colorectal cancer liver metastasis (CLM) tissues. In addition, PTPB1 directly interacts with mRNA of ATG10, and regulates ATG10 expression level in colorectal cancer cells. Ectopic expression of PTBP1 decreased ATG10 expression, whereas down-regulation of PTBP1 increased ATG10 level. In contrast to PTBP1, expression of ATG10 was decreased in CLM tissues. Knock down of ATG10 promoted cell migration and invasion of colorectal cancer cells. Moreover, depletion of ATG10 modulated epithelial-mesenchymal transition-associated proteins in colorectal cancer cells: N-cadherin, TCF-8/ZEB1, and CD44 were up-regulated, whereas E-cadherin was down-regulated. Taken together, our findings suggest that expression of ATG10 negatively regulated by PTBP1 is associated with metastasis of colorectal cancer cells. (C) 2016 Elsevier Ireland Ltd. All rights reserved.
C1 [Jo, Yoon Kyung; Park, Na Yeon; Choi, Eun Sun; Park, So Jung; Shin, Ji Hyun; Cho, Dong-Hyung] Kyung Hee Univ, Grad Sch East West Med Sci, Dept Gerontol, Yongin, South Korea.
   [Roh, Seon Ae; Oh, Ju-Hee; Suh, Young-Ah; Kim, Jin Cheon] Asan Med Ctr, Asan Inst Life Sci, Seoul, South Korea.
   [Lee, Heejin; Lee, Eun Kyung] Catholic Univ Korea, Coll Med, Dept Biochem, Seoul, South Korea.
   [Kim, Jin Cheon] Univ Ulsan, Coll Med, Asan Med Ctr, Dept Surg, 88,Olymp Ro 43 Gil, Seoul 05505, South Korea.
RP Kim, JC (corresponding author), Univ Ulsan, Coll Med, Asan Med Ctr, Dept Surg, 88,Olymp Ro 43 Gil, Seoul 05505, South Korea.; Cho, DH (corresponding author), Kyung Hee Univ, Grad Sch East West Med Sci, 1732,Deogyeong Daero, Yongin 17014, Gyeonggi Do, South Korea.
EM dhcho@khu.ac.kr; jckim@amc.seoul.kr
OI Oh, Ju Hee/0000-0003-2864-7677
FU National Research Foundation, Ministry of Science, ICT and Future
   Planning, Republic of Korea [NRF-2013R1A2A1A03070986, 2013R1A1A1058361]
FX This study was supported by grants from the National Research Foundation
   (NRF-2013R1A2A1A03070986 and 2013R1A1A1058361), Ministry of Science, ICT
   and Future Planning, Republic of Korea.
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PU ELSEVIER IRELAND LTD
PI CLARE
PA ELSEVIER HOUSE, BROOKVALE PLAZA, EAST PARK SHANNON, CO, CLARE, 00000,
   IRELAND
SN 0304-3835
EI 1872-7980
J9 CANCER LETT
JI Cancer Lett.
PD JAN 28
PY 2017
VL 385
BP 21
EP 27
DI 10.1016/j.canlet.2016.11.002
PG 7
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA EF7FV
UT WOS:000390496400003
PM 27836735
DA 2022-04-25
ER

PT J
AU Habibzadeh, P
   Dastsooz, H
   Eshraghi, M
   Los, MJ
   Klionsky, DJ
   Ghavami, S
AF Habibzadeh, Parham
   Dastsooz, Hassan
   Eshraghi, Mehdi
   Los, Marek J.
   Klionsky, Daniel J.
   Ghavami, Saeid
TI Autophagy: The Potential Link between SARS-CoV-2 and Cancer
SO CANCERS
LA English
DT Article
DE colorectal neoplasms; COVID-19; gastrointestinal neoplasms; immune
   checkpoint inhibitors; neoplasms; oncogenic viruses; oncolytic
   virotherapy; post-acute COVID-19 syndrome; reactive oxygen species;
   tumor escape
ID UNFOLDED PROTEIN RESPONSE; BIOLOGICAL FUNCTIONS; METABOLISM; MECHANISMS;
   STRESS; GENES
AB Simple Summary Coronavirus disease 2019 (COVID-19) has led to a global crisis. With the increasing number of individuals infected worldwide, the long-term consequences of this disease have become an active area of research. The constellation of symptoms COVID-19 survivors suffer from is commonly referred to as post-acute COVID-19 syndrome in the scientific literature. In this paper, we discuss the potential long-term complications of this infection resulting from the persistence of the viral particles in body tissues interacting with host cells' autophagy machinery in the context of the development of cancer, cancer progression and metastasis, as well as response to treatment. We also propose a structured framework for future studies to investigate the potential impact of COVID-19 infection on cancer. COVID-19 infection survivors suffer from a constellation of symptoms referred to as post-acute COVID-19 syndrome. However, in the wake of recent evidence highlighting the long-term persistence of SARS-CoV-2 antigens in tissues and emerging information regarding the interaction between SARS-CoV-2 proteins and various components of the host cell macroautophagy/autophagy machinery, the unforeseen long-term consequences of this infection, such as increased risk of malignancies, should be explored. Although SARS-CoV-2 is not considered an oncogenic virus, the possibility of increased risk of cancer among COVID-19 survivors cannot be ruled out. Herein, we provide an overview of the possible mechanisms leading to cancer development, particularly obesity-related cancers (e.g., colorectal cancer), resulting from defects in autophagy and the blockade of the autophagic flux, and also immune escape in COVID-19 survivors. We also highlight the potential long-term implications of COVID-19 infection in the prognosis of patients with cancer and their response to different cancer treatments. Finally, we consider future directions for further investigations on this matter.
C1 [Habibzadeh, Parham] Shiraz Univ Med Sci, Inst Hlth, Res Ctr Hlth Sci, Shiraz 7134814336, Iran.
   [Dastsooz, Hassan] Univ Turin, Dept Life Sci & Syst Biol, Via Accademia,Albertina 13, I-10123 Turin, Italy.
   [Dastsooz, Hassan] IRCCS, IIGM Italian Inst Genom Med, I-10126 Turin, Italy.
   [Dastsooz, Hassan] IRCCS, FPO, Candiolo Canc Inst, I-10060 Turin, Italy.
   [Eshraghi, Mehdi; Ghavami, Saeid] Univ Manitoba, Max Rady Coll Med, Rady Fac Hlth Sci, Dept Human Anat & Cell Sci, Winnipeg, MB R3E 0J9, Canada.
   [Los, Marek J.] Silesian Tech Univ, Biotechnol Ctr, PL-44100 Gliwice, Poland.
   [Klionsky, Daniel J.] Univ Michigan, Life Sci Inst, Ann Arbor, MI 48109 USA.
   [Ghavami, Saeid] Univ Manitoba, Canc Care Manitoba, Res Inst Oncol & Hematol, Winnipeg, MB R3E 0V9, Canada.
   [Ghavami, Saeid] Katowice Sch Technol, Fac Med, Ul Rolna 43, PL-40555 Katowice, Poland.
RP Ghavami, S (corresponding author), Univ Manitoba, Max Rady Coll Med, Rady Fac Hlth Sci, Dept Human Anat & Cell Sci, Winnipeg, MB R3E 0J9, Canada.; Los, MJ (corresponding author), Silesian Tech Univ, Biotechnol Ctr, PL-44100 Gliwice, Poland.; Ghavami, S (corresponding author), Univ Manitoba, Canc Care Manitoba, Res Inst Oncol & Hematol, Winnipeg, MB R3E 0V9, Canada.; Ghavami, S (corresponding author), Katowice Sch Technol, Fac Med, Ul Rolna 43, PL-40555 Katowice, Poland.
EM Parham.Habibzadeh@yahoo.com; Hassan.Dastsooz@unito.it;
   eshraghi.mehdi@gmail.com; Marek.Los@polsl.pl; klionsky@umich.edu;
   saeid.ghavami@umanitoba.ca
RI Habibzadeh, Parham/H-1983-2019
OI Habibzadeh, Parham/0000-0002-2086-0425; Klionsky,
   Daniel/0000-0002-7828-8118; Eshraghi, Mehdi/0000-0002-5321-3849;
   Ghavami, Saeid/0000-0001-5948-508X; Dastsooz, Hassan/0000-0002-0679-4425
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NR 71
TC 2
Z9 2
U1 3
U2 3
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 2072-6694
J9 CANCERS
JI Cancers
PD NOV
PY 2021
VL 13
IS 22
AR 5721
DI 10.3390/cancers13225721
PG 12
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA XJ2ZB
UT WOS:000726661700001
PM 34830876
OA gold, Green Published
DA 2022-04-25
ER

PT J
AU Zhang, JH
   Hunnmersone, M
   Matthews, CS
   Stevens, MFG
   Bradshaw, TD
AF Zhang, Jihong
   Hunnmersone, Marc
   Matthews, Charles S.
   Stevens, Malcolm F. G.
   Bradshaw, Tracey D.
TI N3-Substituted Temozolomide Analogs Overcome Methylguanine-DNA
   Methyltransferase and Mismatch Repair Precipitating Apoptotic and
   Autophagic Cancer Cell Death
SO ONCOLOGY
LA English
DT Article
DE Glioblastoma multiforme; Temozolomide; Methylguanine-DNA
   methyltransferase; Mismatch repair; Apoptosis; Autophagy
ID MALIGNANT GLIOMA-CELLS; MONITORING AUTOPHAGY; INDUCED CYTOTOXICITY;
   ANTICANCER AGENTS; P53 FUNCTION; ALKYLTRANSFERASE; SENSITIVITY;
   INHIBITION; ARREST; LINES
AB Glioblastoma multiforme (GBM) treatment includes temozolomide (TMZ) chemotherapy. O6-Methylguanine lesions are repaired by methylguanine-DNA methyltransferase (MGMT). Response to TMZ requires low MGMT and functional mismatch repair (MMR); resistance, conferred by MGMT or MMR deficiency, represents a barrier to successful treatment. TMZ analogs were synthesized, substituting N3-methyl with propargyl (1) or sulfoxide (2). MTT assays were conducted in SNB19 and U373 isogenic glioma cell lines (V = vector control; M = MGMT-transfected). TMZ potency was reduced >5-fold in SNB19M and U373M cells; in contrast, MGMT-expressing cells were equisensitive as vector controls to analogs 1 and 2. GI(50) values <50 mu m of analogs 1 or 2 were detected in V cells possessing acquired TMZ resistance: SNB19VR (hMSH6 loss) and U373VR (MGMT upregulation). Analogs 1 and 2 inhibited MMR-deficient colorectal carcinoma cell growth (irrespective of p53); G2/M cell cycle arrest preceded apoptosis. gamma H2AX foci inferred the generation of DNA double-strand breaks by analogs 1 and 2. Acridine orange-stained vesicles, intracellular punctate GFP-LC3 protein and double-membraned autophagosomes indicate that TMZ, 1 and 2 induce autophagy in apoptotis-resistant GBM cells. Analogs 1 and 2 elicit in vitro antitumor activity irrespective of MGMT, M MR and p53. Such imidazotetrazines may treat MGMT+ GBM and possess broader spectrum activity causing apoptosis and autophagy in malignancies which evade apoptosis. (C) 2014 S. Karger AG, Basel
C1 [Zhang, Jihong] Kunming Univ Sci & Technol, Fac Med, Kunming, Peoples R China.
   [Hunnmersone, Marc] Pharminox Ltd, Nottingham, England.
   [Matthews, Charles S.; Stevens, Malcolm F. G.; Bradshaw, Tracey D.] Univ Nottingham, Ctr Biomol Sci, Nottingham NG7 2RD, England.
RP Bradshaw, TD (corresponding author), Univ Nottingham, Ctr Biomol Sci, Univ Pk, Nottingham NG7 2RD, England.
EM tracey.bradshaw@nottingham.ac.uk
FU Pharminox Ltd.; National Natural Science Foundation of ChinaNational
   Natural Science Foundation of China (NSFC) [81260501]
FX Financial support for all work described herein was provided by
   Pharminox Ltd. and by the National Natural Science Foundation of China
   (No. 81260501).
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NR 45
TC 16
Z9 16
U1 0
U2 13
PU KARGER
PI BASEL
PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND
SN 0030-2414
EI 1423-0232
J9 ONCOLOGY-BASEL
JI Oncology
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BP 28
EP 48
DI 10.1159/000366131
PG 21
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA AW2KR
UT WOS:000346117000004
PM 25277441
DA 2022-04-25
ER

PT J
AU Koziol, E
   Luca, SV
   Marcourt, L
   Nour, M
   Hnawia, E
   Jakubowicz-Gil, J
   Paduch, R
   Mroczek, T
   Wolfender, JL
   Skalicka-Wozniak, K
AF Koziol, Ewelina
   Luca, Simon Vlad
   Marcourt, Laurence
   Nour, Mohamed
   Hnawia, Edouard
   Jakubowicz-Gil, Joanna
   Paduch, Roman
   Mroczek, Tomasz
   Wolfender, Jean-Luc
   Skalicka-Wozniak, Krystyna
TI Efficient extraction and isolation of skimmianine from New Caledonian
   plant Medicosma leratii and evaluation of its effects on apoptosis,
   necrosis, and autophagy
SO PHYTOCHEMISTRY LETTERS
LA English
DT Article
DE Rutaceae; High-performance countercurrent chromatography; Programmed
   cell death; Acridone alkaloids; Sarcodifurine C
ID QUINOLINE ALKALOIDS; ACRIDONE ALKALOIDS; SORAFENIB; LEAVES; BARK
AB This study was aimed at improving the current knowledge about the new Caledonian plant species Medicosma leratii, by developing efficient methods of extraction and isolation of specialized metabolites. Ultrasound-assisted extraction (UAE) significantly gave higher yields of the furoquinoline alkaloid skimmianine (22.34 mg/100 g) than accelerated solvent extraction (ASE, 1.37-12.36 mg/100 g). High-performance countercurrent chromatographic (HPCCC) separation of the methanol leaf extract with n-hexane-ethyl acetate-methanol-water (6:5:6:5 v/v) afforded skimmianine (1, 7.55 mg, HPLC-DAD purity 99.4%), normelicopidine (3, 1.87 mg, 95.6%), normelicopicine (4, 2.63 mg, 97.3%) and a new furoquinoline alkaloid named sarcodifurine C (2, 1.20 mg, 95.8%). The effect of the crude extract and its main constituent, skimmianine, on apoptosis, autophagy, and necrosis induction in tumor cells has also been investigated. The crude extract and skimmianine were found to be effective apoptosis inducers in HeLa cervical cancer cell line, but not in colon cancer SW620 and HT-29 cells. Additionally, skimmianine effectively potentiated the pro-apoptotic properties of the antincancer agent sorafenib in cervical cancer cells.
C1 [Koziol, Ewelina; Luca, Simon Vlad; Mroczek, Tomasz; Skalicka-Wozniak, Krystyna] Med Univ Lublin, Dept Pharmacognosy, Med Plant Unit, Chodzki 1, PL-20093 Lublin, Poland.
   [Luca, Simon Vlad] Grigore T Pope Univ Med & Pharm Iasi, Dept Pharmacognosy, Univ 16, Iasi 700115, Romania.
   [Marcourt, Laurence; Wolfender, Jean-Luc] Univ Lausanne, Univ Geneva, EPGL, Sch Pharmaceut Sci,CMU, Michel Servet 1, CH-1211 Geneva 4, Switzerland.
   [Nour, Mohamed; Hnawia, Edouard] Univ New Caledonia, EA 4243, LIVE, BP R4, Noumea 98851, New Caledonia.
   [Jakubowicz-Gil, Joanna] Marie Curie Sklodowska Univ, Dept Comparat Anat & Anthropol, Akad 19, PL-20033 Lublin, Poland.
   [Paduch, Roman] Marie Curie Sklodowska Univ, Dept Virol & Immunol, Akad 19, PL-20033 Lublin, Poland.
RP Luca, SV (corresponding author), Grigore T Pope Univ Med & Pharm Iasi, Dept Pharmacognosy, Univ 16, Iasi 700115, Romania.
EM simon-vlad.v.luca@d.umfiasi.ro
RI Luca, Vlad/AAP-6225-2020; Jakubowicz-Gil, Joanna/AAK-3561-2020;
   Skalicka-Woźniak, Krystyna/AAJ-5579-2020; Luca, Simon Vlad/AAF-2613-2019
OI Jakubowicz-Gil, Joanna/0000-0003-2077-804X; Paduch,
   Roman/0000-0001-9779-7252; Skalicka-Wozniak,
   Krystyna/0000-0002-9313-5929; Koziol, Ewelina/0000-0002-8639-4981;
   Mroczek, Tomasz/0000-0002-5267-7182
FU Medical University of Lublin, Poland [DS28]; Swiss National Science
   FoundationSwiss National Science Foundation (SNSF)European Commission
   [316030_164095]
FX This work was financially supported by Medical University of Lublin,
   Poland, grant number DS28. The School of Pharmaceutical Sciences of the
   University of Geneva (Prof. J-L. Wolfender) is thankful to the Swiss
   National Science Foundation for the support in the acquisition of the
   NMR 600 MHz (SNF R'Equip grant 316030_164095).
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Z9 4
U1 1
U2 21
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 1874-3900
EI 1876-7486
J9 PHYTOCHEM LETT
JI Phytochem. Lett.
PD APR
PY 2019
VL 30
BP 224
EP 230
DI 10.1016/j.phytol.2018.12.002
PG 7
WC Plant Sciences; Chemistry, Medicinal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Plant Sciences; Pharmacology & Pharmacy
GA HP0NX
UT WOS:000461363900045
DA 2022-04-25
ER

PT J
AU Russo, M
   Moccia, S
   Bilotto, S
   Spagnuolo, C
   Durante, M
   Lenucci, MS
   Mita, G
   Volpe, MG
   Aquino, RP
   Russo, GL
AF Russo, Maria
   Moccia, Stefania
   Bilotto, Stefania
   Spagnuolo, Carmela
   Durante, Miriana
   Lenucci, Marcello Salvatore
   Mita, Giovanni
   Volpe, Maria Grazia
   Aquino, Rita Patrizia
   Russo, Gian Luigi
TI A Carotenoid Extract from a Southern Italian Cultivar of Pumpkin
   Triggers Nonprotective Autophagy in Malignant Cells
SO OXIDATIVE MEDICINE AND CELLULAR LONGEVITY
LA English
DT Article
ID TRANS-RETINOIC ACID; CHRONIC LYMPHOCYTIC-LEUKEMIA; INDUCED CYTOTOXICITY;
   LINE SAOS-2; CANCER; DIFFERENTIATION; MODULATION; GROWTH;
   PHOSPHORYLATION; MECHANISMS
AB Carotenoids, including beta-carotene, lycopene, and derivatives, such as retinoic acid, have been studied for their significant antiproliferative and differentiating activity on cancer cells in experimental models and in clinics. We are presenting here data on the mechanism of action of a carotenoid-enriched extract obtained from the pumpkin Cucurbita moschata, variety "long of Naples," on two malignant human cell lines, Caco-2 and SAOs, derived from a colon adenocarcinoma and an osteosarcoma, respectively. The carotenoid extract has been obtained from pumpkin pulp and seeds by supercritical CO2 extraction and employed to prepare oil-in-water nanoemulsions. The nanoemulsions, applied at a final carotenoid concentration of 200-400 mu g/ml, were not cytotoxic, but induced a delay in cell growth of about 40% in both SAOs and Caco-2 cell lines. This effect was associated with the activation of a "nonprotective" form of autophagy and, in SAOs cells, to the induction of cell differentiation via a mechanism that involved AMPK activation. Our data suggest the presence of a pool of bioactive compounds in the carotenoid-enriched extract, acting additively, or synergistically, to delay cell growth in cancer cells.
C1 [Russo, Maria; Moccia, Stefania; Bilotto, Stefania; Spagnuolo, Carmela; Volpe, Maria Grazia; Russo, Gian Luigi] CNR, Ist Sci Alimentaz, I-83100 Avellino, Italy.
   [Durante, Miriana; Mita, Giovanni] CNR, Ist Sci Prod Alimentari, I-73100 Lecce, Italy.
   [Lenucci, Marcello Salvatore] Univ Salento, Dipartimento Sci & Tecnol Biol & Ambientali, I-73100 Lecce, Italy.
   [Aquino, Rita Patrizia] Univ Salerno, Dipartimento Farm, Fisciano, Italy.
RP Russo, GL (corresponding author), CNR, Ist Sci Alimentaz, I-83100 Avellino, Italy.
EM glrusso@isa.cnr.it
RI Russo, Gian Luigi/D-6333-2012; moccia, stefania/ABE-3470-2020; Mita,
   Giovanni/B-6575-2015; Durante, Miriana/AAV-9282-2020; Russo,
   Maria/E-8585-2011; Lenucci, Marcello Salvatore/N-7174-2015
OI Russo, Gian Luigi/0000-0001-9321-1613; Mita,
   Giovanni/0000-0002-0850-1681; Russo, Maria/0000-0001-8385-9184; aquino,
   rita patrizia/0000-0002-9754-4244; Lenucci, Marcello
   Salvatore/0000-0002-6493-9549; Volpe, Maria Grazia/0000-0003-0777-0473
FU Italian Ministry of Economy and Finance [191/2009]
FX The authors thank Dr. Giuseppe Mazzarella for the kind assistance in
   using confocal microscopy. This work was supported by the following:
   C.I.S.I.A. project "Innovazione e Sviluppo del Mezzogiorno-Conoscenze
   Integrate per Sostenibilita ed Innovazione del Made in Italy
   Agroalimentare-Legge 191/2009" from the Italian Ministry of Economy and
   Finance to the National Research Council.
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NR 73
TC 12
Z9 13
U1 0
U2 9
PU HINDAWI LTD
PI LONDON
PA ADAM HOUSE, 3RD FLR, 1 FITZROY SQ, LONDON, W1T 5HF, ENGLAND
SN 1942-0900
EI 1942-0994
J9 OXID MED CELL LONGEV
JI Oxidative Med. Cell. Longev.
PY 2017
VL 2017
AR 7468538
DI 10.1155/2017/7468538
PG 15
WC Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Cell Biology
GA FR4SC
UT WOS:000419055000001
PM 29430284
OA Green Published, gold, Green Submitted
DA 2022-04-25
ER

PT J
AU Liu, PF
   Leung, CM
   Chang, YH
   Cheng, JS
   Chen, JJ
   Weng, CJ
   Tsai, KW
   Hsu, CJ
   Liu, YC
   Hsu, PC
   Pan, HW
   Shu, CW
AF Liu, Pei-Feng
   Leung, Chung-Man
   Chang, Yu-Hsiang
   Cheng, Jin-Shiung
   Chen, Jih-Jung
   Weng, Chung-Jeu
   Tsai, Kuo-Wang
   Hsu, Chien-Jen
   Liu, Yen-Chen
   Hsu, Ping-Chi
   Pan, Hung-Wei
   Shu, Chih-Wen
TI ATG4B promotes colorectal cancer growth independent of autophagic flux
SO AUTOPHAGY
LA English
DT Article
DE ATG4B; autophagy; CCND1; colorectal cancer; MTOR; tumor proliferation
ID CYCLIN D1 EXPRESSION; BECLIN 1; TUMORIGENESIS; LC3; PHOSPHORYLATION;
   DEGRADATION; LIPIDATION; P62/SQSTM1; ACTIVATION; INHIBITORS
AB Autophagy is reported to suppress tumor proliferation, whereas deficiency of autophagy is associated with tumorigenesis. ATG4B is a deubiquitin-like protease that plays dual roles in the core machinery of autophagy; however, little is known about the role of ATG4B on autophagy and proliferation in tumor cells. In this study, we found that ATG4B knockdown induced autophagic flux and reduced CCND1 expression to inhibit G(1)/S phase transition of cell cycle in colorectal cancer cell lines, indicating functional dominance of ATG4B on autophagy inhibition and tumor proliferation in cancer cells. Interestingly, based on the genetic and pharmacological ablation of autophagy, the growth arrest induced by silencing ATG4B was independent of autophagic flux. Moreover, dephosphorylation of MTOR was involved in reduced CCND1 expression and G(1)/S phase transition in both cells and xenograft tumors with depletion of ATG4B. Furthermore, ATG4B expression was significantly increased in tumor cells of colorectal cancer patients compared with adjacent normal cells. The elevated expression of ATG4B was highly correlated with CCND1 expression, consistently supporting the notion that ATG4B might contribute to MTOR-CCND1 signaling for G(1)/S phase transition in colorectal cancer cells. Thus, we report that ATG4B independently plays a role as a positive regulator on tumor proliferation and a negative regulator on autophagy in colorectal cancer cells. These results suggest that ATG4B is a potential biomarker and drug target for cancer therapy.
C1 [Liu, Pei-Feng; Tsai, Kuo-Wang; Hsu, Chien-Jen; Liu, Yen-Chen; Pan, Hung-Wei; Shu, Chih-Wen] Kaohsiung Vet Gen Hosp, Dept Med Educ & Res, Kaohsiung, Taiwan.
   [Liu, Pei-Feng] Fooyin Univ, Dept Biotechnol, Kaohsiung, Taiwan.
   [Leung, Chung-Man] Kaohsiung Vet Gen Hosp, Dept Radiat Oncol, Kaohsiung, Taiwan.
   [Leung, Chung-Man; Hsu, Ping-Chi] Natl Kaohsiung First Univ Sci & Technol, Dept Safety Hlth & Environm Engn, Kaohsiung, Taiwan.
   [Chang, Yu-Hsiang] Kaohsiung Vet Gen Hosp, Dept Pediat, Kaohsiung, Taiwan.
   [Chang, Yu-Hsiang] Natl Yang Ming Univ, Sch Med, Taipei 112, Taiwan.
   [Chang, Yu-Hsiang] Tajen Univ, Dept Nursing, Pingtung, Taiwan.
   [Cheng, Jin-Shiung] Kaohsiung Vet Gen Hosp, Dept Internal Med, Kaohsiung, Taiwan.
   [Chen, Jih-Jung] Tajen Univ, Dept Pharm, Pingtung, Taiwan.
   [Chen, Jih-Jung] Tajen Univ, Grad Inst Pharmaceut Technol, Pingtung, Taiwan.
   [Weng, Chung-Jeu] Kaohsiung Armed Forces Gen Hosp, Zuoying Branch, Dept Obstet Gynecol, Kaohsiung, Taiwan.
RP Shu, CW (corresponding author), Kaohsiung Vet Gen Hosp, Dept Med Educ & Res, Kaohsiung, Taiwan.
EM hwpan@vghks.gov.tw; cwshu@vghks.gov.tw
RI Shu, Chih-Wen/AAE-9652-2019
OI Tsai, Kuo-Wang/0000-0002-9028-9834; Hsu, Ping-Chi/0000-0003-2562-1463;
   Shu, Chih-Wen/0000-0002-7774-0002; Liu, Pei-Feng/0000-0002-7849-8940
FU National Science Council (NSC)Ministry of Science and Technology, Taiwan
   [101-2311-B-075B-001, 102-2311-B-075B-001]; Kaohsiung Veterans General
   Hospital [VGHKS102-007, VGHKS103-G01-1, VGHKS100-058]
FX We thank Dr Lopez-Otin for kindly providing Atg4b<SUP>+/+</SUP> and
   atg4b<SUP>-/-</SUP> mouse embryonic fibroblast (MEF) cells from which we
   generated immortalized Atg4b<SUP>+/+</SUP> and atg4b<SUP>-/-</SUP> 3T3
   cells. We also thank Dr Jie Chen and Dr Philip Hinds for sharing
   plasmids FLAG-MTOR and HA-CCND1, respectively. This work was supported
   by National Science Council (NSC 101 and 102-2311-B-075B-001 to C-WS)
   and Kaohsiung Veterans General Hospital (VGHKS102-007 to C-WS,
   VGHKS103-G01-1 to C-JH, and VGHKS100-058 to C-ML).
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NR 56
TC 48
Z9 51
U1 3
U2 15
PU TAYLOR & FRANCIS INC
PI PHILADELPHIA
PA 530 WALNUT STREET, STE 850, PHILADELPHIA, PA 19106 USA
SN 1554-8627
EI 1554-8635
J9 AUTOPHAGY
JI Autophagy
PD AUG
PY 2014
VL 10
IS 8
BP 1454
EP 1465
DI 10.4161/auto.29556
PG 12
WC Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Cell Biology
GA AN0HU
UT WOS:000340266200010
PM 24991826
OA Green Published, Bronze
DA 2022-04-25
ER

PT J
AU Choi, P
   Park, JY
   Kim, T
   Park, SH
   Kim, HK
   Kang, KS
   Ham, J
AF Choi, Pilju
   Park, Jun Yeon
   Kim, Taejung
   Park, Soon-Hye
   Kim, Ho-Kyong
   Kang, Ki Sung
   Ham, Jungyeoh
TI Improved anticancer effect of ginseng extract by microwave-assisted
   processing through the generation of ginsenosides Rg3, Rg5 and Rk1
SO JOURNAL OF FUNCTIONAL FOODS
LA English
DT Article
DE Ginseng; Microwave; Ginsenoside; Cervical cancer; Cell death
ID SCAVENGING ACTIVITY CHANGES; AMERICAN GINSENG; APOPTOSIS; RE;
   ANTIOXIDANT; INHIBITION; INCREASE; MIXTURE
AB In this study, we demonstrated the efficient structural conversion of ginsenosides, which enhances the anticancer activity of ginseng by microwave irradiation. The microwave-irradiated product of ginseng (MG) had a higher content of ginsenosides, Rg3+Rg5+Rk1, particularly Rg5 and Rk1, and, thus, has an increased medicinal effect. To confirm the anticancer effect of MG, it was tested in 5 human cancer cell lines (cervical cancer HeLa, gastric cancer AGS, colon cancer HCT-116, lung cancer A549, and liver cancer HepG2 cells). Anti-proliferation results for 5 human cancer cell lines treated with ginseng extracts indicate that HeLa cells treated with MG showed the highest activity with an IC50 value of 130.1 mu g/mL. MG also suppressed the growth of human cervical cancer cell xenografts in athymic nude mice as an in vivo model. This growth suppression by MG is associated with the induction of cell death and autophagy. Moreover, there were no toxic sign or decrease in renal and hepatic function in mice administered with MG. Therefore, heat processing by microwave irradiation is a useful method to enhance the anticancer effect of ginseng as it increases the content of ginsenosides, Rg3, Rg5, and Rk1. (C) 2015 Elsevier Ltd. All rights reserved.
C1 [Choi, Pilju; Kim, Taejung; Ham, Jungyeoh] Korea Inst Sci & Technol, Gangneung Inst Nat Prod, Kangnung 210340, South Korea.
   [Park, Jun Yeon; Kang, Ki Sung] Gachon Univ, Coll Korean Med, Songnam 461701, South Korea.
   [Park, Soon-Hye; Kim, Ho-Kyong] Richwood Pharmaceut Co LTD, Seoul 100704, South Korea.
RP Kang, KS (corresponding author), Gachon Univ, Coll Korean Med, Songnam 461701, South Korea.
EM kkang@gachon.ac.kr; ham0606@kist.re.kr
FU Korea Institute of Science and Technology institutional program
   [2Z04390]; Ministry of Trade, Industry & Energy (MOTIE, Korea)
   [N0000885]
FX This work was supported by the Korea Institute of Science and Technology
   institutional program (2Z04390). This research was also conducted under
   the industrial infrastructure program for fundamental technologies
   (N0000885) which is funded by the Ministry of Trade, Industry & Energy
   (MOTIE, Korea).
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NR 30
TC 26
Z9 33
U1 3
U2 30
PU ELSEVIER
PI AMSTERDAM
PA RADARWEG 29, 1043 NX AMSTERDAM, NETHERLANDS
SN 1756-4646
EI 2214-9414
J9 J FUNCT FOODS
JI J. Funct. Food.
PD APR
PY 2015
VL 14
BP 613
EP 622
DI 10.1016/j.jff.2015.02.038
PG 10
WC Food Science & Technology; Nutrition & Dietetics
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Food Science & Technology; Nutrition & Dietetics
GA CV8AX
UT WOS:000364500000062
DA 2022-04-25
ER

PT J
AU Jeong, S
   Kim, BG
   Kim, DY
   Kim, BR
   Kim, JL
   Park, SH
   Na, YJ
   Jo, MJ
   Yun, HK
   Jeong, YA
   Kim, HJ
   Lee, SI
   Kim, HD
   Kim, DH
   Oh, SC
   Lee, DH
AF Jeong, Soyeon
   Kim, Bu Gyeom
   Kim, Dae Yeong
   Kim, Bo Ram
   Kim, Jung Lim
   Park, Seong Hye
   Na, Yoo Jin
   Jo, Min Jee
   Yun, Hye Kyeong
   Jeong, Yoon A.
   Kim, Hong Jun
   Lee, Sun Il
   Kim, Han Do
   Kim, Dae Hyun
   Oh, Sang Cheul
   Lee, Dae-Hee
TI Cannabidiol Overcomes Oxaliplatin Resistance by Enhancing NOS3-and
   SOD2-Induced Autophagy in Human Colorectal Cancer Cells
SO CANCERS
LA English
DT Article
DE oxaliplatin resistance; colorectal cancer; CBD; NOS3; autophagy;
   mitochondrial dysfunction
ID NITRIC-OXIDE SYNTHASE; MECHANISMS; STRESS; GROWTH
AB Although oxaliplatin is an effective chemotherapeutic drug for colorectal cancer (CRC) treatment, patients often develop resistance to it. Therefore, a new strategy for CRC treatment is needed. The purpose of this study was to determine the effect of cannabidiol (CBD), one of the components of the cannabis plant, in overcoming oxaliplatin resistance in CRC cells. We established oxaliplatin-resistant cell lines, DLD-1 R and colo205 R, in CRC DLD-1 and colo205 cells. Autophagic cell death was induced when oxaliplatin-resistant cells were treated with both oxaliplatin and CBD. Additionally, phosphorylation of nitric oxide synthase 3 (NOS3) was increased in oxaliplatin-resistant cells compared to that in parent cells. Combined treatment with oxaliplatin and CBD reduced phospho-NOS3 levels and nitric oxide (NO) production and resulted in the production of reactive oxygen species (ROS) by reducing the levels of superoxide dismutase 2, an antioxidant present in the mitochondria, causing mitochondrial dysfunction. Taken together, these results suggest that elevated phosphorylation of NOS3 is essential for oxaliplatin resistance. The combination of oxaliplatin and CBD decreased NOS3 phosphorylation, which resulted in autophagy, by inducing the overproduction of ROS through mitochondrial dysfunction, thus overcoming oxaliplatin resistance.
C1 [Jeong, Soyeon; Kim, Bo Ram; Kim, Jung Lim; Oh, Sang Cheul; Lee, Dae-Hee] Korea Univ, Dept Internal Med, Div Oncol Hematol, Guro Hosp, 148 Gurodong Gil, Seoul 08308, South Korea.
   [Kim, Bu Gyeom; Kim, Dae Yeong; Park, Seong Hye; Na, Yoo Jin; Jo, Min Jee; Yun, Hye Kyeong; Jeong, Yoon A.; Oh, Sang Cheul; Lee, Dae-Hee] Korea Univ, Coll Med, Grad Sch Med, Seoul 08308, South Korea.
   [Kim, Hong Jun] Kyung Hee Univ, Dept Internal Med, Div Oncol, Sch Med, 23 Kyung Hee Dae Ro, Seoul 02447, South Korea.
   [Lee, Sun Il] Korea Univ, Coll Med, Dept Surg, Guro Hosp, Seoul 08308, South Korea.
   [Kim, Han Do; Kim, Dae Hyun] Kaiyon Bio Tech Co Ltd, 226 Gamasan Ro, Seoul 08308, South Korea.
RP Oh, SC; Lee, DH (corresponding author), Korea Univ, Dept Internal Med, Div Oncol Hematol, Guro Hosp, 148 Gurodong Gil, Seoul 08308, South Korea.; Oh, SC; Lee, DH (corresponding author), Korea Univ, Coll Med, Grad Sch Med, Seoul 08308, South Korea.
EM jensyj85@gmail.com; qnrua10047@naver.com; derrickdyblue22@gmail.com;
   ilovewish777@naver.com; clickkjl@naver.com; psh3938@hanmail.net;
   wing1278@naver.com; minjeeyoyo@nate.com; katecoco@hanmail.net;
   leomi2614@naver.com; xpassion84@naver.com; silee@korea.ac.kr;
   howard@kaiyonbiotech.com; dkim238@kaiyonbiotech.com; sachoh@korea.ac.kr;
   neogene@korea.ac.kr
OI Jeong, Soyeon/0000-0002-4568-4579
FU National Research Foundation (NRF) of Korea - Korean government (MSIP)
   [NRF-2017R1A2B2011684, NRF-2017R1D1A1B03030703]; Business for
   Cooperative R&D Between Industry, Academy, and Research Institute -
   Korea Small and Medium Business Administration [C0566291]
FX This work was supported by a National Research Foundation (NRF) of Korea
   grant funded by the Korean government (MSIP, NRF-2017R1A2B2011684 and
   NRF-2017R1D1A1B03030703) and by the Business for Cooperative R&D Between
   Industry, Academy, and Research Institute funded by the Korea Small and
   Medium Business Administration (C0566291).
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NR 41
TC 20
Z9 21
U1 1
U2 4
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
SN 2072-6694
J9 CANCERS
JI Cancers
PD JUN
PY 2019
VL 11
IS 6
AR 781
DI 10.3390/cancers11060781
PG 18
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA II7CZ
UT WOS:000475351200045
PM 31195721
OA gold, Green Submitted, Green Published
DA 2022-04-25
ER

PT J
AU Khan, MZI
   Law, HKW
AF Islam Khan, Md Zahirul
   Law, Helen Ka Wai
TI RAMS11 promotes CRC through mTOR-dependent inhibition of autophagy,
   suppression of apoptosis, and promotion of epithelial-mesenchymal
   transition
SO CANCER CELL INTERNATIONAL
LA English
DT Article
DE LncRNAs; RAMS11; CRC; Autophagy; Apoptosis; EMT
ID LONG NONCODING RNAS; SIGNALING PATHWAY; MECHANISMS
AB Background Long non-coding RNAs (lncRNAs), a class of non-coding RNAs (ncRNAs) associated with diverse biological processes of cells. Over the past decades, cumulating research evidences revealed that abnormal expressions of lncRNAs are associated with colorectal cancer (CRC) initiation, progression, metastasis, and resistance to therapies. Moreover, their usefulness as candidate biomarkers for CRC diagnosis and prognosis are well evident throughout previous literature. In the current study, we examined the role and molecular mechanisms of newly identified lncRNA named RNA associated with metastasis-11 (RAMS11) in CRC development. Methods The expression of RAMS11 in CRC cell lines DLD-1, HT-29, HCT-116, and SW480 and colon normal cells CCD-112-CoN were evaluated by quantitative RT-qPCR. The results showed that the RAMS11 is significantly upregulated in CRC cell lines compared to the normal cells. The CCK-8 proliferation assay, colony formation assay, and migration assay were performed to evaluate the biological and physiological functions of RAMS11 in vitro. To decipher the molecular mechanisms of RAMS11 medicated CRC progression, we further performed western blot analysis of the key pathway proteins (e.g., AMPK, AKT, and mTOR). Results Our results revealed that higher expression of RAMS11 is associated with increased CRC proliferation, migration, and development of metastasis. Knockdown of RAMS11 induced autophagy, apoptosis along with reduction of epithelial-mesenchymal transition (EMT) suggesting that RAMS11 is involved in CRC progression. The molecular mechanisms of RAMS11 indicated that knockdown of RAMS11 significantly inhibited CRC carcinogenesis through mTOR-dependent autophagy induction. Conclusions In sum, our results suggested that RAMS11 is an important oncogene in CRC pathogenesis. Targeting RAMS11 could be a potential therapeutic strategy for CRC management.
C1 [Islam Khan, Md Zahirul; Law, Helen Ka Wai] Hong Kong Polytech Univ, Fac Hlth & Social Sci, Dept Hlth Technol & Informat, Hung Hom, Hong Kong, Peoples R China.
RP Law, HKW (corresponding author), Hong Kong Polytech Univ, Fac Hlth & Social Sci, Dept Hlth Technol & Informat, Hung Hom, Hong Kong, Peoples R China.
EM hthelen@polyu.edu.hk
OI Islam Khan, Md Zahirul/0000-0001-7048-2613
FU Departmental Seeding Fund; Internal Institutional Research Fund
   [P0031318-UAHS]; Hong Kong Polytechnic UniversityHong Kong Polytechnic
   University
FX This project is partially supported by: (1) Research grant to HKL
   including, Departmental Seeding Fund and Internal Institutional Research
   Fund (P0031318-UAHS). (2) Postgraduate studentship from The Hong Kong
   Polytechnic University for ZIK.
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NR 55
TC 4
Z9 4
U1 0
U2 1
PU BMC
PI LONDON
PA CAMPUS, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
EI 1475-2867
J9 CANCER CELL INT
JI Cancer Cell Int.
PD JUN 26
PY 2021
VL 21
IS 1
AR 321
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PG 11
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA TC3ZG
UT WOS:000668579900002
PM 34174900
OA Green Submitted, Green Published, gold
DA 2022-04-25
ER

PT J
AU Prevarskaya, N
   Skryma, R
   Shuba, Y
AF Prevarskaya, Natalia
   Skryma, Roman
   Shuba, Yaroslav
TI Targeting Ca2+ transport in cancer: close reality or long perspective?
SO EXPERT OPINION ON THERAPEUTIC TARGETS
LA English
DT Review
DE angiogenesis; apoptosis; autophagy; Ca2+ channels; Ca2+ pumps; cancer;
   migration; proliferation
ID ENDOPLASMIC-RETICULUM STRESS; PROSTATE-CANCER; CELL-PROLIFERATION;
   CARDIAC-GLYCOSIDES; COLON-CANCER; INTRACELLULAR CALCIUM; ION CHANNELS;
   TRP CHANNELS; APOPTOTIC RESISTANCE; REGULATES APOPTOSIS
AB Introduction: Cancer is caused by defects in the mechanisms underlying cell proliferation, death and migration. Calcium ions are central to all of these phenomena, serving as major signalling agents with the spatial localisation, magnitude and temporal characteristics of calcium signals ultimately determining cell's fate. The transformation of a normal cell into a malignant derivative is associated with a major rearrangement of Ca2+ pumps, Na/Ca exchangers and Ca2+ channels, which leads to enhanced proliferation and invasion under compromised/impaired ability to die.
   Areas covered: This paper examines the changes in Ca2+ signalling and the mechanisms that underlie the passage from normal to pathological cell growth and death control. Understanding these changes and identifying the molecular players involved provide new perspectives for cancer treatment.
   Expert opinion: Despite compelling evidence that the disruption of Ca2+ homeostasis in cancer cells leads to the promotion of certain malignant phenotypes as well as the identification of key Ca2+-transporting molecules whose altered expression and/or function underlies pathological changes, the therapeutic utilisation of these findings for cancer treatment is still at its infancy. However, the rapid development of the field warrants the development of improved molecular Ca2+ transport-targeting tools for cancer diagnosis and treatment.
C1 [Prevarskaya, Natalia] INSERM, U1003, Lab Physiol Cellulaire, Equipe Labellisee Ligue Canc, F-59650 Villeneuve Dascq, France.
   [Skryma, Roman] Univ Lille 1, Lab Excellence Ion Channels Sci & Therapeut, F-59650 Villeneuve Dascq, France.
   [Shuba, Yaroslav] NASU, Bogomoletz Inst Physiol, UA-01024 Kiev 24, Ukraine.
   [Shuba, Yaroslav] NASU, Int Ctr Mol Physiol, UA-01024 Kiev 24, Ukraine.
   [Shuba, Yaroslav] State Key Lab Mol & Cellular Biol, Kiev, Ukraine.
RP Prevarskaya, N (corresponding author), INSERM, U1003, Lab Physiol Cellulaire, Equipe Labellisee Ligue Canc, F-59650 Villeneuve Dascq, France.
EM Natacha.Prevarskaya@univ-lille1.fr
RI Shuba, Yaroslav/AAT-6758-2021
OI Prevarskaya, natacha/0000-0003-0316-197X
FU Inserm (Institut National de la Sante et de la Recherche
   Medicale)Institut National de la Sante et de la Recherche Medicale
   (Inserm); Ligue Nationale Contre le CancerLigue nationale contre le
   cancer; FRM (Fondation de Recherche Medicale)Fondation pour la Recherche
   Medicale; ARC (Association pour la Recherche sur le Cancer)Fondation ARC
   pour la Recherche sur le Cancer; Region Nord/Pas-de-CalaisRegion
   Hauts-de-France; National Academy of Sciences of Ukraine; State Fund for
   Fundamental Research, UkraineState Fund for Fundamental Research (SFFR)
   [F46.2/001]; Universite de Lille1
FX The research of N Prevarskaya and R Skryma is supported by grants from
   Inserm (Institut National de la Sante et de la Recherche Medicale),
   Ligue Nationale Contre le Cancer, FRM (Fondation de Recherche Medicale),
   ARC (Association pour la Recherche sur le Cancer) and Region
   Nord/Pas-de-Calais. The research of Y Shuba is supported by the National
   Academy of Sciences of Ukraine and F46.2/001 grant from State Fund for
   Fundamental Research, Ukraine. Y Shuba is also supported by the visiting
   scientist program of Universite de Lille1. The authors declare no other
   conflicts of interest.
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NR 152
TC 43
Z9 43
U1 0
U2 38
PU TAYLOR & FRANCIS LTD
PI ABINGDON
PA 2-4 PARK SQUARE, MILTON PARK, ABINGDON OR14 4RN, OXON, ENGLAND
SN 1472-8222
EI 1744-7631
J9 EXPERT OPIN THER TAR
JI Expert Opin. Ther. Targets
PD MAR
PY 2013
VL 17
IS 3
BP 225
EP 241
DI 10.1517/14728222.2013.741594
PG 17
WC Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA 088QW
UT WOS:000314851700002
PM 23294334
DA 2022-04-25
ER

PT J
AU Xiao, JX
   Huang, GQ
   Zhang, SH
AF Xiao, Jun-Xia
   Huang, Guo-Qing
   Zhang, Sheng-Hua
TI Soyasaponins inhibit the proliferation of Hela cells by inducing
   apoptosis
SO EXPERIMENTAL AND TOXICOLOGIC PATHOLOGY
LA English
DT Article
DE apoptosis; cell cycle; intracellular Ca2+; mitochondrial transmembrane
   potential; nitric oxide; soyasaponins
ID COLON-CANCER CELLS; CYTOCHROME-C; NITRIC-OXIDE; INDUCTION; CALCIUM;
   MACROAUTOPHAGY; MITOCHONDRIA; SAPONINS; EXTRACT; DEATH
AB This research aimed at investigating the effect of soyasaponins on the proliferation of Hela cells. SS-II, the second fraction of soyasaponins, was separated by column chromatographic method with D101A macroporous resin from soybeans. SS-II could inhibit the proliferation of Hela cells by changing cell cycle distribution and inducing apoptosis. Furthermore, the loss of mitochondrial transmembrane potential was observed by flow cytometry and the increase of intracellular Ca2+ concentration was detected by confocal laser scanning microscope in apoptotic cells. At the same time, the nitric oxide content, nitric oxide synthase (NOS) and inducible NOS activities were also increased. The above results suggested that the inhibitory effect of SS-II on Hela cell proliferation was caused by inducing apoptosis through the mitochondrial pathway. (c) 2007 Elsevier GmbH. All rights reserved.
C1 Huazhong Agr Univ, Sch Food Sci & Technol, Wuhan 430070, Peoples R China.
   Laiyang Agr Univ, Sch Food Sci & Engn, Qingdao 266109, Peoples R China.
RP Zhang, SH (corresponding author), Huazhong Agr Univ, Sch Food Sci & Technol, Wuhan 430070, Peoples R China.
EM zhangsh3411@yahoo.com.cn
OI Huang, Guo-Qing/0000-0002-3343-2008
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NR 26
TC 34
Z9 36
U1 2
U2 7
PU ELSEVIER GMBH, URBAN & FISCHER VERLAG
PI JENA
PA OFFICE JENA, P O BOX 100537, 07705 JENA, GERMANY
SN 0940-2993
EI 1618-1433
J9 EXP TOXICOL PATHOL
JI Exp. Toxicol. Pathol.
PD SEP
PY 2007
VL 59
IS 1
BP 35
EP 42
DI 10.1016/j.etp.2007.02.004
PG 8
WC Pathology; Toxicology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pathology; Toxicology
GA 212PA
UT WOS:000249608100005
PM 17582751
DA 2022-04-25
ER

PT J
AU Sun, ZW
   Zeng, B
   Liu, DD
   Zhao, QT
   Wang, JY
   Xing, HR
AF Sun, Zhiwei
   Zeng, Bin
   Liu, Doudou
   Zhao, Qiting
   Wang, Jianyu
   Xing, H. Rosie
TI S100A8 transported by SEC23A inhibits metastatic colonization via
   autocrine activation of autophagy
SO CELL DEATH & DISEASE
LA English
DT Article
ID REGULATES AUTOPHAGY; TUMOR PROGRESSION; CANCER; CELLS; PROTEIN;
   PERSPECTIVE; APOPTOSIS; RELEASE; PATHWAY
AB Metastasis is the main cause of failure of cancer treatment. Metastatic colonization is regarded the most rate-limiting step of metastasis and is subjected to regulation by a plethora of biological factors and processes. On one hand, regulation of metastatic colonization by autophagy appears to be stage- and context-dependent, whereas mechanistic characterization remains elusive. On the other hand, interactions between the tumor cells and their microenvironment in metastasis have long been appreciated, whether the secretome of tumor cells can effectively reshape the tumor microenvironment has not been elucidated mechanistically. In the present study, we have identified "SEC23A-S1008-BECLIN1-autophagy axis" in the autophagic regulation of metastatic colonization step, a mechanism that tumor cells can exploit autophagy to exert self-restrain for clonogenic proliferation before the favorable tumor microenvironment is established. Specifically, we employed a paired lung-derived oligometastatic cell line (OL) and the homologous polymetastatic cell line (POL) from human melanoma cell line M14 that differ in colonization efficiency. We show that S100A8 transported by SEC23A inhibits metastatic colonization via autocrine activation of autophagy. Furthermore, we verified the clinical relevance of our experimental findings by bioinformatics analysis of the expression of Sec23a and S100A8 and the clinical-pathological associations. We demonstrate that higher Sec23a and Atg5 expression levels appear to be protective factors and favorable diagnostic (TNM staging) and prognostic (overall survival) markers for skin cutaneous melanoma (SKCM) and colon adenocarcinoma (COAD) patients. And we confirm the bioinformatics analysis results with SKCM biopsy samples.
C1 [Sun, Zhiwei; Zeng, Bin; Liu, Doudou; Zhao, Qiting; Wang, Jianyu] Chongqing Med Univ, Inst Life Sci, Chongqing, Peoples R China.
   [Sun, Zhiwei; Zeng, Bin; Liu, Doudou; Zhao, Qiting; Wang, Jianyu; Xing, H. Rosie] Chongqing Med Univ, Lab Translat Canc Stem Cell Res, Chongqing, Peoples R China.
   [Xing, H. Rosie] Chongqing Med Univ, State Key Lab Ultrasound Engn Med Cofounded Chong, Chongqing, Peoples R China.
   [Xing, H. Rosie] Chongqing Med Univ, Minist Sci & Technol, Coll Biomed Engn, Chongqing, Peoples R China.
RP Wang, JY (corresponding author), Chongqing Med Univ, Inst Life Sci, Chongqing, Peoples R China.; Wang, JY; Xing, HR (corresponding author), Chongqing Med Univ, Lab Translat Canc Stem Cell Res, Chongqing, Peoples R China.; Xing, HR (corresponding author), Chongqing Med Univ, State Key Lab Ultrasound Engn Med Cofounded Chong, Chongqing, Peoples R China.
EM wjy2003123@163.com; xinglab310@163.com
FU National Natural Science FundNational Natural Science Foundation of
   China (NSFC) [81672908]; National Natural Science Youth Fund [81602596]
FX This work was supported by the National Natural Science Fund (Grant No.
   81672908) and the National Natural Science Youth Fund (Grant No.
   81602596).
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NR 51
TC 4
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U1 2
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PU SPRINGERNATURE
PI LONDON
PA CAMPUS, 4 CRINAN ST, LONDON, N1 9XW, ENGLAND
SN 2041-4889
J9 CELL DEATH DIS
JI Cell Death Dis.
PD AUG 6
PY 2020
VL 11
IS 8
AR 650
DI 10.1038/s41419-020-02835-w
PG 13
WC Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Cell Biology
GA OD4GX
UT WOS:000579812000001
PM 32811814
OA gold, Green Published
DA 2022-04-25
ER

PT J
AU Wang, XC
   Li, MJ
   Hu, MY
   Wei, P
   Zhu, W
AF Wang, Xingchun
   Li, Minjie
   Hu, Mengyao
   Wei, Ping
   Zhu, Wei
TI BAMBI overexpression together with beta-sitosterol ameliorates NSCLC via
   inhibiting autophagy and inactivating TGF-beta/Smad2/3 pathway
SO ONCOLOGY REPORTS
LA English
DT Article
DE non-small cell lung cancer; BAMBI; beta-sitosterol; autophagy; TGF-beta
ID CELL LUNG-CANCER; TGF-BETA; PSEUDORECEPTOR BAMBI; TUMOR-SUPPRESSOR;
   CHEMO-RESISTANCE; COLON-CANCER; EXPRESSION; APOPTOSIS; BECLIN1;
   CONTRIBUTES
AB Non-small cell lung cancer (NSCLC) has the highest mortality rate among all solid tumors with a poor prognosis. The BMP and activin receptor membrane bound inhibitor (BAMBI) has been identified as a hallmark of NSCLC and beta-sitosterol possesses antitumor potentiality. This study explores the effect of BAMBI overexpression and beta-sitosterol in the context of NSCLC. The results revealed that the transfection of pcDNA-BAMBI and beta-sitosterol treatment significantly reduced the levels of autophagy markers light chain 3 (LC3) II and Beclin 1, whereas the levels of LC3 I and p62 were promoted. The reduced punctate accumulations of GFP-LC3 were detected in pcDNA-BAMBI and beta-sitosterol groups, especially in pcDNA-BAMBI + beta-sitosterol group. BAMBI overexpression and beta-sitosterol induced G0/G1 cell cycle arrest and inhibted cell proliferation in A549 cells. In addition, the levels of transforming growth factor-beta (TGF-beta)/p-Smad2/3/c-Myc pathway proteins were decreased. The TGF-beta overexpression further confirmed that BAMBI overexpression and beta-sitosterol treatment suppressed autohagy and viability of A549 cells was through TGF-beta/Smad2/3/c-Myc pathway. Finally, the tumor growth was suppressed in NSCLC xenografts, and the inhibitory effect was stronger under treatment of pcDNA-BAMBI together with beta-sitosterol. These results indicate that BAMBI overexpression and beta-sitosterol may serve as novel targets for the treatment of NSCLC.
C1 [Wang, Xingchun; Hu, Mengyao; Wei, Ping; Zhu, Wei] Canc Hosp Linyi, Dept Internal Med 1, 6 East St Cemetery, Linyi 276001, Shandong, Peoples R China.
   [Li, Minjie] Canc Hosp Linyi, Dept Internal Med 3, Linyi 276001, Shandong, Peoples R China.
RP Zhu, W (corresponding author), Canc Hosp Linyi, Dept Internal Med 1, 6 East St Cemetery, Linyi 276001, Shandong, Peoples R China.
EM Dr_weizhu@163.com
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NR 44
TC 19
Z9 21
U1 0
U2 6
PU SPANDIDOS PUBL LTD
PI ATHENS
PA POB 18179, ATHENS, 116 10, GREECE
SN 1021-335X
EI 1791-2431
J9 ONCOL REP
JI Oncol. Rep.
PD MAY
PY 2017
VL 37
IS 5
BP 3046
EP 3054
DI 10.3892/or.2017.5508
PG 9
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA ET9LR
UT WOS:000400629500058
PM 28440452
OA Bronze
DA 2022-04-25
ER

PT J
AU Lei, Y
   Lui, VWY
   Grandis, JR
   Egloff, AM
AF Lei, Yu
   Lui, Vivian W. Y.
   Grandis, Jennifer R.
   Egloff, Ann Marie
TI Identification of Mutations in the PYRIN-Containing NLR Genes (NLRP) in
   Head and Neck Squamous Cell Carcinoma
SO PLOS ONE
LA English
DT Article
ID COLON INFLAMMATION; I INTERFERON; INFLAMMASOMES; AUTOPHAGY; CYTOKINES;
   PROTEIN; DISEASE; TUFM
AB Head and Neck Squamous Cell Carcinoma (HNSCC) encompasses malignancies that arise in the mucosa of the upper aerodigestive tract. Recent high throughput DNA sequencing revealed HNSCC genes mutations that contribute to several cancer cell characteristics, including dysregulation of cell proliferation and death, intracellular proinflammatory signaling, and autophagy. The PYRIN-domain containing NLR (Nucleotide-binding domain, Leucine rich Repeats - containing) proteins have recently emerged as pivotal modulators of cell death, autophagy, inflammation, and metabolism. Their close physiologic association with cancer development prompted us to determine whether mutations within the NLRP (PYRIN-containing NLR) gene family were associated with HNSCC genome instability and their clinicopathologic correlations. Catastrophic mutational events underlie cancer cell genome instability and mark a point-of-no-return in cancer cell development and generation of heterogeneity. The mutation profiles of 62 patients with primary conventional type HNSCC excluding other histologic variants were analyzed. Associations were tested using Fisher's Exact test or Mann-Whitney U test. Mutations in NLRP were associated with elevated genome instability as characterized by higher mutation rates. Clinically, NLRP mutations were more frequently found in HNSCC arising in the floor of mouth (50.0%) in comparison with HNSCC at other head and neck locations (14.8%). These mutations were clustered at the leucine rich repeats region of NLRP proteins, and affected NLRP genes were mostly localized at chromosomes 11p15.4 and 19q13.42-19q13.43. Twenty novel NLRP mutations were identified in HNSCC, and mutations in this group of genes were correlated with increased cancer cell genome mutation rates, and such features could be a potential molecular biomarker of HNSCC genome instability.
C1 [Lei, Yu] Univ Pittsburgh, Sch Dent Med, Dept Diagnost Sci, Pittsburgh, PA 15213 USA.
   [Lui, Vivian W. Y.; Grandis, Jennifer R.; Egloff, Ann Marie] Univ Pittsburgh, Sch Med, Dept Otolaryngol, Pittsburgh, PA USA.
   [Lui, Vivian W. Y.; Grandis, Jennifer R.; Egloff, Ann Marie] Univ Pittsburgh, Inst Canc, Pittsburgh, PA USA.
   [Grandis, Jennifer R.] Univ Pittsburgh, Sch Med, Dept Pharmacol & Chem Biol, Pittsburgh, PA USA.
   [Egloff, Ann Marie] Univ Pittsburgh, Sch Med, Dept Microbiol & Mol Genet, Pittsburgh, PA USA.
RP Lei, Y (corresponding author), Univ Pittsburgh, Sch Dent Med, Dept Diagnost Sci, Pittsburgh, PA 15213 USA.
EM leiyuleo@gmail.com
RI Lui, Vivian W. Y./I-5458-2016; Lei, Yu Leo/ABF-1293-2020
OI Lui, Vivian W. Y./0000-0001-6918-1573; Lei, Yu Leo/0000-0002-9868-9824
FU Specialized Program of Research Excellence (SPORE) in Head and Neck
   Cancer neoplasm of the University of Pittsburgh [P50CA097190]; 
   [K07CA137140]; NATIONAL CANCER INSTITUTEUnited States Department of
   Health & Human ServicesNational Institutes of Health (NIH) - USANIH
   National Cancer Institute (NCI) [K07CA137140, P50CA097190] Funding
   Source: NIH RePORTER; NATIONAL INSTITUTE OF DENTAL & CRANIOFACIAL
   RESEARCHUnited States Department of Health & Human ServicesNational
   Institutes of Health (NIH) - USANIH National Institute of Dental &
   Craniofacial Research (NIDCR) [R01DE023685] Funding Source: NIH RePORTER
FX This work was supported by P50CA097190 (JRG) the Specialized Program of
   Research Excellence (SPORE) in Head and Neck Cancer neoplasm of the
   University of Pittsburgh and K07CA137140 (AME). The funders had no role
   in study design, data collection and analysis, decision to publish, or
   preparation of the manuscript.
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NR 40
TC 5
Z9 5
U1 1
U2 9
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 1160 BATTERY STREET, STE 100, SAN FRANCISCO, CA 94111 USA
SN 1932-6203
J9 PLOS ONE
JI PLoS One
PD JAN 21
PY 2014
VL 9
IS 1
AR e85619
DI 10.1371/journal.pone.0085619
PG 9
WC Multidisciplinary Sciences
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Science & Technology - Other Topics
GA 297GT
UT WOS:000330244500084
PM 24465623
OA gold, Green Published, Green Accepted
DA 2022-04-25
ER

PT J
AU Martin, S
   Dudek-Peric, AM
   Maes, H
   Garg, AD
   Gabrysiak, M
   Demirsoy, S
   Swinnen, JV
   Agostinis, P
AF Martin, S.
   Dudek-Peric, A. M.
   Maes, H.
   Garg, A. D.
   Gabrysiak, M.
   Demirsoy, S.
   Swinnen, J. V.
   Agostinis, P.
TI Concurrent MEK and autophagy inhibition is required to restore cell
   death associated danger-signalling in Vemurafenib-resistant melanoma
   cells
SO BIOCHEMICAL PHARMACOLOGY
LA English
DT Article
DE Melanoma; PLX4032; Danger-signalling; Cell death; Autophagy
ID ONCOGENIC B-RAF; BRAF INHIBITORS; TUMOR-CELLS; CALRETICULIN EXPOSURE;
   ANTIMELANOMA ACTIVITY; METASTATIC MELANOMA; ACQUIRED-RESISTANCE;
   IMPROVED SURVIVAL; CANCER-THERAPY; COLON-CANCER
AB Vemurafenib (PLX4032), an inhibitor of BRAF(V600E), has demonstrated significant clinical anti-melanoma effects. However, the majority of treated patients develop resistance, due to a variety of molecular mechanisms including MAPK reactivation through MEK. The induction of a cancer cell death modality associated with danger-signalling resulting in surface mobilization of crucial damage-associated-molecular-patterns (DAMPs), e.g. calreticulin (CRT) and heat shock protein-90 (HSP90), from dying cells, is emerging to be crucial for therapeutic success. Both cell death and danger-signalling are modulated by autophagy, a key adaptation mechanism stimulated during melanoma progression. However, whether melanoma cell death induced by MAPK inhibition is associated with danger-signalling, and the reliance of these mechanisms on autophagy, has not yet been scrutinized.
   Using a panel of isogenic PLX4032-sensitive and resistant melanoma cell lines we show that PLX4032-induced caspase-dependent cell death and DAMPs exposure in the drug-sensitive cells, but failed to do so in the drug-resistant cells, displaying heightened MEK activation. MEK inhibitor, U0126, treatment sensitized PLX4032-resistant cells to death and re-established their danger-signalling capacity. Only melanoma cells exposing death-induced danger-signals were phagocytosed and induced DC maturation. Although the PLX4032-resistant melanoma cells displayed higher basal and drug-induced autophagy, compromising autophagy, pharmacologically or by ATG5 knockdown, was insufficient to re-establish their PLX4032 sensitivity. Interestingly, autophagy abrogation was particularly efficacious in boosting cell death and ecto-CRT/ecto-HSP90 in PLX4032-resistant cells upon blockage of MEK hyper-activation by U0126.
   Thus combination of MEK inhibitors with autophagy blockers may represent a novel treatment regime to increase both cell death and danger-signalling in Vemurafenib-resistant metastatic melanoma. (C) 2015 Elsevier Inc. All rights reserved.
C1 [Martin, S.; Dudek-Peric, A. M.; Maes, H.; Garg, A. D.; Gabrysiak, M.; Demirsoy, S.; Agostinis, P.] Univ Leuven KU Leuven, Dept Cellular & Mol Med, Cell Death Res & Therapy Unit, B-3000 Leuven, Belgium.
   [Swinnen, J. V.] Univ Leuven KU Leuven, Dept Oncol, Lab Lipid Metab & Canc, B-3000 Leuven, Belgium.
RP Agostinis, P (corresponding author), Univ Leuven KU Leuven, Dept Cellular & Mol Med, Lab Cell Death Res & Therapy, Campus Gasthuisberg O&N1,Herestr 49,Box 802, B-3000 Leuven, Belgium.
EM patrizia.agostinis@med.kuleuven.be
RI Agostinis, Patrizia/ABI-1177-2020; Agostinis, Patrizia/AAO-2468-2020;
   Swinnen, Johannes V/AAA-2214-2022; Gabrysiak, Magdalena/AAT-2827-2020;
   Garg, Abhishek D/D-5230-2012
OI Agostinis, Patrizia/0000-0003-1314-2115; Swinnen, Johannes
   V/0000-0002-7720-5077; Garg, Abhishek D/0000-0002-9976-9922; demirsoy,
   seyma/0000-0001-8380-0932; Martin, Seamus/0000-0002-8539-3143
FU KU LeuvenKU Leuven [GOA/11/2009]; FWOFWO [G0584.12]; Vlaamse Liga tegen
   Kanker (VLK); Interuniversity Attraction Poles ProgrammeBelgian Federal
   Science Policy Office [IAP7/32]; Belgian State, Science Policy
   OfficeBelgian Federal Science Policy Office
FX We would like to thank Prof. M. Herlyn for the use of the 451-LU and
   M1617 is ogenic cell lines [10,37,38]. Human immature dendritic cells
   were kindly provided by Dr Gabriela Bomfim Ferreira. Research was
   supported by GOA/11/2009 grant of the KU Leuven to P.A. and J.S. and FWO
   grant G0584.12 to P.A. Aleksandra, M. Dudek-Peric and Hannelore Maes are
   supported by fellowships of the Vlaamse Liga tegen Kanker (VLK).
   Abhishek D. Garg is supported by the FWO Postdoctoral Fellowship. This
   paper represents research results of the IAP7/32 funded by the
   Interuniversity Attraction Poles Programme, initiated by the Belgian
   State, Science Policy Office. We would like to thank Sofie Van Eygen and
   Angela Napolitano for their technical support.
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NR 70
TC 45
Z9 48
U1 0
U2 10
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0006-2952
EI 1873-2968
J9 BIOCHEM PHARMACOL
JI Biochem. Pharmacol.
PD FEB 1
PY 2015
VL 93
IS 3
BP 290
EP 304
DI 10.1016/j.bcp.2014.12.003
PG 15
WC Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA CB2AP
UT WOS:000349429400005
PM 25529535
OA Green Accepted
DA 2022-04-25
ER

PT J
AU Wen, Y
   Zhang, ZJ
   Huang, YP
   Wang, KP
   Liu, K
   Zou, H
   Zhou, JJ
   Zou, ZX
   Luo, SL
   Liu, ZT
   Wu, ZC
   Chen, W
   Xiong, L
AF Wen, Yu
   Zhang, Zi-Jian
   Huang, Yun-Peng
   Wang, Kun-Peng
   Liu, Kai
   Zou, Heng
   Zhou, Jiang-Jiao
   Zou, Zhen-Xing
   Luo, Shi-Lin
   Liu, Zhong-Tao
   Wu, Zheng-Chun
   Chen, Wei
   Xiong, Li
TI Application of the Ethyl Acetate Extract of Cichorium as a Potential
   Photosensitizer in Photodynamic Therapy Induces Apoptosis and Autophagy
   in Colorectal Cancer Cell Lines via the Protein Kinase R-Like
   Endoplasmic Reticulum Kinase Pathway
SO JOURNAL OF BIOMEDICAL NANOTECHNOLOGY
LA English
DT Article
DE Cichorium intybus L.; Colorectal Cancer; Photodynamic Therapy; PERK
ID STRESS; DEATH; TUMOR
AB The present study aims to evaluate the effect of the ethyl acetate extract of Cichorium (EAEC) as a novel photosensitizer in photodynamic therapy (PDT) of colorectal carcinoma (CRC) HCT116 and SW620 cells. The absorption and fluorescence spectra of EAEC were measured using a UV-vis spectrophotometer and fluorescence spectrophotometer, respectively. EAEC-induced reactive oxygen species (ROS) production in HCT116 and SW620 cells was detected using 2',7'-dichlorodihydrofluorescein diacetate (DCFH-DA) and glutathione/glutathione disulfide (GSH/GSSG). The photo- and dark toxicities of EAEC were estimated using the Cell Counting Kit-8 (CCK-8) assay. Cellular uptake and localization of EAEC were detected by confocal laser fluorescence microscopy. Annexin V-FITC/PI staining, Western blotting and immunofluorescence staining were used to assess apoptosis and autophagy. The antitumor activity of EAEC was confirmed in a xenograft model. Finally, effects on the PERK pathway were verified using qRT-PCR and Western blotting. EAEC displayed absorption and fluorescence emission peaks at 660 nm and 678 nm, respectively. EAEC induced ROS production in CRC cells. Assessment of dark toxicity showed that treatment with EAEC alone induced little cytotoxicity in CRC or normal cells but that EAEC-PDT induced significant photocytotoxicity in CRC cells in a time- and dose-dependent manner. After cellular uptake, EAEC was located in the mitochondria. Treatment with EAEC-PDT reduced xenograft tumor size. Further evaluation suggested that activation of the PERK pathway mediates these effects, as the apoptotic rate and autophagy flux increased markedly after EAEC-PDT. EAEC, a natural photosensitizer extracted from Cichorium, displays potential utility in PDT of CRC by targeting the PERK pathway.
C1 [Wen, Yu; Zhang, Zi-Jian; Huang, Yun-Peng; Wang, Kun-Peng; Liu, Kai; Zou, Heng; Zhou, Jiang-Jiao; Liu, Zhong-Tao; Wu, Zheng-Chun; Xiong, Li] Cent S Univ, Xiangya Hosp 2, Dept Gen Surg, Changsha 410011, Hunan, Peoples R China.
   [Zou, Zhen-Xing] Cent S Univ, Xiangya Sch Pharmaceut Sci, Changsha 410011, Hunan, Peoples R China.
   [Luo, Shi-Lin] Cent S Univ, Xiangya Hosp 2, Dept Pharm, Changsha 410011, Hunan, Peoples R China.
   [Chen, Wei] Univ Texas Arlington, Dept Phys, POB 19059, Arlington, TX 76019 USA.
   [Chen, Wei] Univ Texas Arlington, SAVANT Ctr, Arlington, TX 76019 USA.
RP Xiong, L (corresponding author), Cent S Univ, Xiangya Hosp 2, Dept Gen Surg, Changsha 410011, Hunan, Peoples R China.
EM lixionghn@csu.edu.cn
RI wen, yu/AAJ-7482-2021
FU National Natural Science Foundation of ChinaNational Natural Science
   Foundation of China (NSFC) [81773293]; Hunan Province Natural Science
   FoundationNatural Science Foundation of Hunan Province [2017DK2011,
   2017WK2060, 2017SK0121]
FX All animal protocols were approved by the Ethical Review Committee of
   Second Xiangya Hospital of Central South University (the approval number
   of Ethical Review Committee is SYXK2012-003). The authors declare that
   they have no competing interests. This work was supported by the
   National Natural Science Foundation of China (81773293), Hunan Province
   Natural Science Foundation (2017DK2011, 2017WK2060, 2017SK0121). We
   thank the Medical Laboratory Center of the Second Xiangya Hospital for
   providing technical assistance. The confocal microscopy used in this
   study was performed in the College of Chemistry and Chemical Engineering
   of Hunan University by Liu Songyang, Chen Yufeng.
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NR 37
TC 5
Z9 5
U1 2
U2 40
PU AMER SCIENTIFIC PUBLISHERS
PI VALENCIA
PA 26650 THE OLD RD, STE 208, VALENCIA, CA 91381-0751 USA
SN 1550-7033
EI 1550-7041
J9 J BIOMED NANOTECHNOL
JI J. Biomed. Nanotechnol.
PD SEP
PY 2019
VL 15
IS 9
BP 1867
EP 1880
DI 10.1166/jbn.2019.2825
PG 14
WC Nanoscience & Nanotechnology; Materials Science, Biomaterials
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Science & Technology - Other Topics; Materials Science
GA IT1YV
UT WOS:000482645400002
PM 31387675
DA 2022-04-25
ER

PT J
AU Booth, L
   Roberts, JL
   Poklepovic, A
   Dent, P
AF Booth, Laurence
   Roberts, Jane L.
   Poklepovic, Andrew
   Dent, Paul
TI PDE5 inhibitors enhance the lethality of [pemetrexed plus sorafenib]
SO ONCOTARGET
LA English
DT Article
DE sildenafil; autophagy; pemetrexed; chaperone; lung cancer
ID COLON-CANCER CELLS; NITRIC-OXIDE; TYROSINE NITRATION; ACTIVATION;
   PATHWAY; PROTEIN; TARGET; PHOSPHODIESTERASES; CYTOTOXICITY; MECHANISM
AB The combination of pemetrexed and sorafenib has significant clinical activity against a wide variety of tumor types in patients and the present studies were performed to determine whether sildenafil enhances the killing potential of [pemetrexed + sorafenib]. In multiple genetically diverse lung cancer cell lines, sildenafil enhanced the lethality of [pemetrexed + sorafenib]. The three-drug combination reduced the activities of AKT, mTOR and STAT transcription factors; increased the activities of eIF2a and ULK-1; lowered the expression of MCL-1, BCL-XL, thioredoxin and SOD2; and increased the expression of Beclin1. Enhanced cell killing by sildenafil was blocked by inhibition of death receptor signaling and autophagosome formation. Enforced activation of STAT3 and AKT or inhibition of JNK significantly reduced cell killing. The enhanced cell killing caused by sildenafil was more reliant on increased PKG signaling than on the generation of nitric oxide. In vivo sildenafil enhanced the anti-tumor properties of [pemetrexed + sorafenib]. Based on our data we argue that additional clinical studies combining pemetrexed, sorafenib and sildenafil are warranted.
C1 [Booth, Laurence; Roberts, Jane L.; Dent, Paul] Virginia Commonwealth Univ, Dept Biochem & Mol Biol, Med Coll Virginia Campus, Richmond, VA 23298 USA.
   [Poklepovic, Andrew] Virginia Commonwealth Univ, Dept Biochem & Med, Med Coll Virginia Campus, Richmond, VA 23298 USA.
RP Dent, P (corresponding author), Virginia Commonwealth Univ, Dept Biochem & Mol Biol, Med Coll Virginia Campus, Richmond, VA 23298 USA.
EM pdent@vcu.edu
FU Massey Cancer Center; NIH-NCI Cancer Center Support GrantUnited States
   Department of Health & Human ServicesNational Institutes of Health (NIH)
   - USANIH National Cancer Institute (NCI) [P30 CA016059]; Betts family
   fund;  [PHS R01-CA192613]; NATIONAL CANCER INSTITUTEUnited States
   Department of Health & Human ServicesNational Institutes of Health (NIH)
   - USANIH National Cancer Institute (NCI) [P30CA016059, R01CA192613]
   Funding Source: NIH RePORTER
FX Support for the present study was funded from philanthropic funding from
   Massey Cancer Center and PHS R01-CA192613. Services in support of the
   research project were provided by the VCU Massey Cancer Center Tissue
   and Data Acquisition and Analysis Core, supported, in part, with funding
   from NIH-NCI Cancer Center Support Grant P30 CA016059. Thanks to Dr.
   H.F. Young and the Betts family fund for support in the purchase of the
   Hermes Wiscan instrument. PD is the holder of the Universal Inc. Chair
   in Signal Transduction Research. The authors have no conflicts of
   interest to report.
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NR 39
TC 7
Z9 7
U1 0
U2 0
PU IMPACT JOURNALS LLC
PI ORCHARD PARK
PA 6666 E QUAKER ST, STE 1, ORCHARD PARK, NY 14127 USA
EI 1949-2553
J9 ONCOTARGET
JI Oncotarget
PD FEB 21
PY 2017
VL 8
IS 8
BP 13464
EP 13475
DI 10.18632/oncotarget.14562
PG 12
WC Oncology; Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Cell Biology
GA EN0HX
UT WOS:000395692000089
PM 28088782
OA Green Published, Green Submitted, gold
DA 2022-04-25
ER

PT J
AU Luan, F
   He, XR
   Zeng, N
AF Luan, Fei
   He, Xirui
   Zeng, Nan
TI Tetrandrine: a review of its anticancer potentials, clinical settings,
   pharmacokinetics and drug delivery systems
SO JOURNAL OF PHARMACY AND PHARMACOLOGY
LA English
DT Review
DE anticancer; molecular mechanism; natural product; pharmaceutical
   applications; signalling pathway; tetrandrine
ID CELL-CYCLE ARREST; MULTIDRUG-RESISTANCE REVERSAL; BIOACTIVE
   NATURAL-PRODUCTS; COLLAGEN-INDUCED ARTHRITIS; SOLID LIPID NANOPARTICLES;
   JUN NH2-TERMINAL KINASE; SUPPRESSES TUMOR-GROWTH; PROSTATE-CANCER CELLS;
   IN-VITRO; INDUCED APOPTOSIS
AB Objectives Tetrandrine, a natural bisbenzylisoquinoline alkaloid, possesses promising anticancer activities on diverse tumours. This review provides systematically organized information on cancers of tetrandrinein vivoandin vitro, discuss the related molecular mechanisms and put forward some new insights for the future investigations. Key findings Anticancer activities of tetrandrine have been reported comprehensively, including lung cancer, colon cancer, bladder cancer, prostate cancer, ovarian cancer, gastric cancer, breast cancer, pancreatic cancer, cervical cancer and liver cancer. The potential molecular mechanisms corresponding to the anticancer activities of tetrandrine might be related to induce cancer cell apoptosis, autophagy and cell cycle arrest, inhibit cell proliferation, migration and invasion, ameliorate metastasis and suppress tumour cell growth. Pharmaceutical applications of tetrandrine combined with nanoparticle delivery system including liposomes, microspheres and nanoparticles with better therapeutic efficiency have been designed and applied encapsulate tetrandrine to enhance its stability and efficacy in cancer treatment. Tetrandrine was proven to have definite antitumour activities. However, the safety, bioavailability and pharmacokinetic parameter studies on tetrandrine are very limited in animal models, especially in clinical settings. Our present review on anticancer potentials of tetrandrine would be necessary and highly beneficial for providing guidelines and directions for further research of tetrandrine.
C1 [Luan, Fei; Zeng, Nan] Chengdu Univ Tradit Chinese Med, Coll Pharm, Chengdu 611137, Peoples R China.
   [He, Xirui] Zunyi Med Univ, Dept Bioengn, Zhuhai Campus, Zhuhai 519041, Peoples R China.
RP Zeng, N (corresponding author), Chengdu Univ Tradit Chinese Med, Coll Pharm, Chengdu 611137, Peoples R China.; He, XR (corresponding author), Zunyi Med Univ, Dept Bioengn, Zhuhai Campus, Zhuhai 519041, Peoples R China.
EM xiruihe6105194@163.com; zengnan666@aliyun.com
FU National Natural Science Foundation of ChinaNational Natural Science
   Foundation of China (NSFC) [81473399]; Xinglin Scholar Research
   Promotion Project of Chengdu University of Traditional Chinese Medicine
   [CXTD2018014]
FX This project was financially supported by the National Natural Science
   Foundation of China (No. 81473399) and the Xinglin Scholar Research
   Promotion Project of Chengdu University of Traditional Chinese Medicine
   (No. CXTD2018014).
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NR 179
TC 14
Z9 17
U1 5
U2 21
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0022-3573
EI 2042-7158
J9 J PHARM PHARMACOL
JI J. Pharm. Pharmacol.
PD NOV
PY 2020
VL 72
IS 11
BP 1491
EP 1512
DI 10.1111/jphp.13339
EA JUL 2020
PG 22
WC Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA NX7TW
UT WOS:000550756400001
PM 32696989
DA 2022-04-25
ER

PT J
AU Hu, F
   Wu, Y
   Liu, C
   Zhu, YC
   Ye, SZ
   Xi, Y
   Cui, W
   Bu, SZ
AF Hu, Fei
   Wu, Yu
   Liu, Cheng
   Zhu, Yingchao
   Ye, Shazhou
   Xi, Yang
   Cui, Wei
   Bu, Shizhong
TI Penicillin disrupts mitochondrial function and induces autophagy in
   colorectal cancer cell lines
SO ONCOLOGY LETTERS
LA English
DT Article
DE penicillin; colorectal cancer; mitochondrial; autophagy; apoptosis
ID METASTASIS; MECHANISMS; OUTCOMES; SURGERY; ALLERGY; STAGE; LUNG
AB Colorectal cancer is a common malignant tumor of the gastrointestinal tract. Currently, the main treatment is surgical resection, which can be combined with other treatments. However, treatment efficacy is poor, and colorectal cancer is prone to relapse and metastasis; thus, identifying an effective anti-cancer drug is an urgent requirement. The present study examined the antagonistic effect of penicillin on cultured colorectal cancer cells and the related mechanism. A MTT assay was used to assess the growth of the colorectal cancer cells treated with penicillin and to determine the optimal drug concentration. The wound healing and Transwell invasion assays were performed to investigate the effect of penicillin on the migration and invasion of the colorectal cancer cells. Live cell mitochondrial energy metabolism analysis was performed to detect changes in mitochondrial energy metabolism of the colorectal cancer cells, while western blot analysis was used to measure the expression of cytochrome c and autophagy-related protein, LC3. RFP-GFP-LC3 lentivirus was used to detect autophagic flux, and autophagosomes were observed using a transmission electron microscope, while flow cytometry was used to analyze the effect of penicillin on cell cycle progression and apoptosis of the colorectal cancer cells. After penicillin treatment, the growth, migration and invasion ability of the colorectal cancer cells were inhibited. The mitochondrial energy metabolism of the cell was impaired, and the basic respiratory capacity, maximum respiratory capacity, respiratory potential, and ATP production were all reduced. The protein expression levels of the autophagy-related proteins, LC3-II/LC3-I increased in a dose- and time-dependent manner. In addition, autophagy flux and the number of autophagosomes increased, and mitochondrial structural damage was observed. The cell cycle was arrested at the G(1) phase, the number of early apoptotic cells increased and the protein expression level of cleaved caspase-3 increased, while penicillin-induced apoptosis was blocked by the autophagy inhibitor 3-MA. In conclusion, penicillin disrupted mitochondrial function and energy metabolism in the colorectal cancer cells, which resulted in the induction of autophagic apoptosis and ultimately the inhibition of cancer cell growth and metastasis.
C1 [Hu, Fei; Wu, Yu; Liu, Cheng; Zhu, Yingchao; Ye, Shazhou; Xi, Yang; Bu, Shizhong] Ningbo Univ, Sch Med, Diabet Res Ctr, 818 Fenghua Rd, Ningbo 315211, Zhejiang, Peoples R China.
   [Hu, Fei] Wenzhou Med Univ, Cixi Biomed Res Inst, Cixi 315300, Zhejiang, Peoples R China.
   [Cui, Wei] Lihuili Hosp, Ningbo Med Ctr, Dept Colorectal Surg, 57 XingNing Rd, Ningbo 315211, Zhejiang, Peoples R China.
RP Bu, SZ (corresponding author), Ningbo Univ, Sch Med, Diabet Res Ctr, 818 Fenghua Rd, Ningbo 315211, Zhejiang, Peoples R China.; Cui, W (corresponding author), Lihuili Hosp, Ningbo Med Ctr, Dept Colorectal Surg, 57 XingNing Rd, Ningbo 315211, Zhejiang, Peoples R China.
EM cuiwei1111@live.cn; bushizhong@nbu.edu.cn
FU Ningbo Science and Technology Innovation Team Program [2014B82002];
   National Natural Science Foundation of ChinaNational Natural Science
   Foundation of China (NSFC) [81370165]; Fang Runhua Fund of Hong Kong; K.
   C. Wong Magna Fund in Ningbo University
FX This study was supported by Ningbo Science and Technology Innovation
   Team Program (grant no. 2014B82002), the National Natural Science
   Foundation of China (grant no. 81370165), the Fang Runhua Fund of Hong
   Kong and the K. C. Wong Magna Fund in Ningbo University.
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NR 56
TC 0
Z9 1
U1 4
U2 5
PU SPANDIDOS PUBL LTD
PI ATHENS
PA POB 18179, ATHENS, 116 10, GREECE
SN 1792-1074
EI 1792-1082
J9 ONCOL LETT
JI Oncol. Lett.
PD OCT
PY 2021
VL 22
IS 4
AR 691
DI 10.3892/ol.2021.12952
PG 10
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA UA1RQ
UT WOS:000684943400001
PM 34457046
OA gold, Green Published
DA 2022-04-25
ER

PT J
AU Tigu, AB
   Toma, VA
   Mot, AC
   Jurj, A
   Moldovan, CS
   Fischer-Fodor, E
   Berindan-Neagoe, I
   Parvu, M
AF Tigu, Adrian Bogdan
   Toma, Vlad-Alexandru
   Mot, Augustin Catalin
   Jurj, Ancuta
   Moldovan, Cristian Silviu
   Fischer-Fodor, Eva
   Berindan-Neagoe, Ioana
   Parvu, Marcel
TI The Synergistic Antitumor Effect of 5-Fluorouracil Combined with Allicin
   against Lung and Colorectal Carcinoma Cells
SO MOLECULES
LA English
DT Article
DE allicin; 5-FU; apoptosis; colony; synergistic effect; migration
ID CANCER-CELLS; IN-VITRO; APOPTOSIS; PHYTOCHEMICALS; MODULATORS;
   AUTOPHAGY; MIGRATION; DEATH
AB 5-fluorouracil (5-FU) is an anticancer drug used to inhibit the proliferation of many different tumor cells. Since severe events are associated with this compound, its combination with different anticancer drugs or adjuvants would allow the use of a significantly lower dose of 5-FU. In this study, we highlighted that the combination of allicin with 5-FU inhibited the cell migration and proliferation of colorectal and lung cancer cells. 5-FU inhibited cell growth with a similar inhibitory concentration for both normal and tumor cells (similar to 200 mu M), while allicin showed different inhibitory concentrations. With an IC50 of 8.625 mu M, lung cancer cells were the most sensitive to allicin. Compared to 5-FU and allicin single-agent treatments, the co-treatment showed a reduced viability rate, with p < 0.05. The morphological changes were visible on all three cell lines, indicating that the treatment inhibited the proliferation of both normal and tumor cells. We highlighted different cell death mechanisms-apoptosis for lung cancer and a non-apoptotic cell death for colorectal cancer. The synergistic antitumor effect of 5-FU combined with allicin was visible against lung and colorectal carcinoma cells. Better results were obtained when a lower concentration of 5-FU was combined with allicin than the single-agent treatment at IC50.
C1 [Tigu, Adrian Bogdan; Moldovan, Cristian Silviu; Fischer-Fodor, Eva; Berindan-Neagoe, Ioana] Univ Med & Pharm Iuliu Hatieganu, MedFuture Res Ctr Adv Med, Cluj Napoca 400349, Romania.
   [Tigu, Adrian Bogdan; Toma, Vlad-Alexandru; Parvu, Marcel] Babes Bolyai Univ, Fac Biol & Geol, 42 Republicii St, Cluj Napoca 400015, Romania.
   [Toma, Vlad-Alexandru] Inst Biol Res Cluj Napoca, Cluj Napoca 400113, Romania.
   [Toma, Vlad-Alexandru] Natl Inst R&D Isotop & Mol Technol, Dept Mol & Biomol Phys, 67-103 Donat, Cluj Napoca 400293, Romania.
   [Mot, Augustin Catalin] Babes Bolyai Univ, Dept Chem, Fac Chem & Chem Engn, 11 Arany Janos St, Cluj Napoca 400028, Romania.
   [Jurj, Ancuta; Moldovan, Cristian Silviu; Berindan-Neagoe, Ioana] Iuliu Hatieganu Univ Med & Pharm, Res Ctr Funct Genom Biomed & Translat Med, Cluj Napoca 400028, Romania.
   [Fischer-Fodor, Eva] Oncol Inst Prof Dr Ion Chiricuta, Dept Radiobiol & Tumor Biol, Cluj Napoca 400028, Romania.
   [Berindan-Neagoe, Ioana] Oncol Inst Prof Dr Ion Chiricuta, Dept Funct Genom & Expt Pathol, Cluj Napoca 400028, Romania.
RP Parvu, M (corresponding author), Babes Bolyai Univ, Fac Biol & Geol, 42 Republicii St, Cluj Napoca 400015, Romania.
EM adrianbogdantigu@gmail.com; vlad.al.toma@gmail.com;
   gusty_chem@yahoo.com; ancajurj15@gmail.com;
   moldovan.cristian1994@gmail.com; fischer.eva@iocn.ro;
   ioana.neagoe@umfcluj.ro; marcel.parvu@ubbcluj.ro
RI Mot, Augustin C./D-3017-2011; Țigu, Adrian Bogdan/AAI-9446-2020;
   Fischer-Fodor, Eva/C-4506-2011; Mot, Augustin/AAP-4356-2021; Toma,
   Vlad-Alexandru/S-1514-2019; Pârvu, Marcel/AAH-9752-2020; Moldovan,
   Cristian/AAE-2871-2022
OI Mot, Augustin C./0000-0002-1679-0487; Țigu, Adrian
   Bogdan/0000-0001-9397-0791; Fischer-Fodor, Eva/0000-0002-0898-0547; Mot,
   Augustin/0000-0002-1679-0487; Toma, Vlad-Alexandru/0000-0002-1141-2559;
   Pârvu, Marcel/0000-0002-5892-9280; Moldovan,
   Cristian/0000-0003-2927-4622
FU UBB of Cluj-Napoca (Romania) [AGC 30411, AGC 30412, AGC 30413]
FX This research was funded by UBB of Cluj-Napoca (Romania) by a grant to
   support competitiveness: Nr. AGC 30411 from 5.02.2020
   (https://infocercetare.ubbcluj.ro/Proiecte/Proiecte/Edit?id=14721), Nr.
   AGC 30412 from 5.02.2020
   (https://infocercetare.ubbcluj.ro/Proiecte/Proiecte/Edit?id =14722),
   and. Nr. AGC 30413 from 2020
   (https://infocercetare.ubbcluj.ro/Proiecte/Proiecte/Edit?id=14723).
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NR 56
TC 14
Z9 14
U1 3
U2 6
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 1420-3049
J9 MOLECULES
JI Molecules
PD APR 2
PY 2020
VL 25
IS 8
AR 1947
DI 10.3390/molecules25081947
PG 16
WC Biochemistry & Molecular Biology; Chemistry, Multidisciplinary
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Chemistry
GA LP9DX
UT WOS:000534617300106
PM 32331446
OA Green Published, gold
DA 2022-04-25
ER

PT J
AU Wang, CY
   Guo, DW
   Wang, Q
   You, S
   Qiao, ZP
   Liu, Y
   Dai, H
   Tang, H
AF Wang, Chaoyi
   Guo, Dunwei
   Wang, Qiang
   You, Song
   Qiao, Zhongpeng
   Liu, Yong
   Dai, Hang
   Tang, Hua
TI Aliskiren targets multiple systems to alleviate cancer cachexia
SO ONCOLOGY REPORTS
LA English
DT Article
DE cancer cachexia; aliskiren; renin-angiotensin system; inflammation;
   oxidative stress
ID RENIN-ANGIOTENSIN SYSTEM; SKELETAL-MUSCLE; OXIDATIVE STRESS; MURINE
   MYOTUBES; MOUSE MODEL; MICE; AUTOPHAGY; MECHANISMS; INFLAMMATION;
   DEGRADATION
AB To examine the effects of aliskiren, a small-molecule renin inhibitor, on cancer cachexia and to explore the underlying mechanisms. A cancer cachexia model was established by subcutaneously injecting C26 mouse colon carcinoma cells into isogenic BALB/c mice. Aliskiren was administered intragastrically [10 mg/kg body weight (BW)] on day 5 (as a preventive strategy, AP group) or on day 12 (as a therapeutic strategy, AT group) after C26 injection. Mice that received no C26 injection (healthy controls, HC group) or only C26 injection but not aliskiren (cancer, CA group) were used as controls. BW, tumor growth, whole body functions, and survival were monitored daily in half of the mice in each group, whereas serum, tumors, and gastrocnemius muscles were harvested from the other mice after sacrifice on day 20 for further analysis. Aliskiren significantly alleviated multiple cachexia-associated symptoms, including BW loss, tumor burden, muscle wasting, muscular dysfunction, and shortened survival. On the molecular level, aliskiren antagonized cachexia-induced activation of the renin-angiotensin system (RAS), systematic and muscular inflammation, oxidative stress, and autophagy-lysosome as well as ubiquitin-proteasome stimulation. In addition, early administration of aliskiren before cachexia development (AP group) resulted in more robust effects in alleviating cachexia or targeting underlying mechanisms than administration after cachexia development (AT group). Aliskiren exhibited potent anti-cachexia activities. These activities were achieved through the targeting of at least four mechanisms underlying cachexia development: RAS activation, increase in systematic inflammation, upregulation of oxidative stress, and stimulation of autophagy-lysosome pathway (ALP) and ubiquitin-proteasome pathway (UPP).
C1 [Wang, Chaoyi; Guo, Dunwei; Wang, Qiang; You, Song; Qiao, Zhongpeng; Liu, Yong; Dai, Hang; Tang, Hua] Chongqing Med Univ, Affiliated Hosp 1, Dept Gastrointestinal Surg, Chongqing 400016, Peoples R China.
   [Wang, Qiang] Suining Cent Hosp, Dept Gastrointestinal Surg, Suining 629000, Sichuan, Peoples R China.
RP Tang, H (corresponding author), Chongqing Med Univ, Affiliated Hosp 1, Dept Gastrointestinal Surg, Chongqing 400016, Peoples R China.
EM tanglihua6969@sina.com
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NR 39
TC 10
Z9 10
U1 1
U2 5
PU SPANDIDOS PUBL LTD
PI ATHENS
PA POB 18179, ATHENS, 116 10, GREECE
SN 1021-335X
EI 1791-2431
J9 ONCOL REP
JI Oncol. Rep.
PD NOV
PY 2016
VL 36
IS 5
BP 3014
EP 3022
DI 10.3892/or.2016.5118
PG 9
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA DZ6SR
UT WOS:000385992700069
PM 27667116
OA Bronze
DA 2022-04-25
ER

PT J
AU Liu, L
   Meng, T
   Wang, QS
   Jin, HZ
   Sun, ZQ
   Jin, B
   Fang, F
   Wang, HJ
AF Liu, L.
   Meng, T.
   Wang, Q. S.
   Jin, H. Z.
   Sun, Z. Q.
   Jin, B.
   Fang, F.
   Wang, H. J.
TI Association of Beclin-1 and microRNA-30a expression with the severity
   and treatment response of colorectal cancer
SO GENETICS AND MOLECULAR RESEARCH
LA English
DT Article
DE Beclin-1; MicroRNA-30a; Colorectal cancer; Autophagy; Apoptosis;
   Prognosis
ID AUTOPHAGY-RELATED PROTEIN; ADENOCARCINOMA; TUMORIGENESIS; DEGRADATION;
   CARCINOMA; INDUCTION; PROGNOSIS; SURVIVAL; GENE
AB We investigated the associations between Beclin-1 and microRNA-30a (miR-30a) expression and the severity and treatment response in colorectal cancer (CRC). Our sample size consisted of 139 CRC patients who were treated with surgery alone. Immunohistochemistry was used to investigate the expression and prognostic significance of Beclin-1 in CRC, while the weak expression of Beclin-1 in normal tissue was used as the basis for assessing tumors (control group). Real-time reverse transcription-polymerase chain reaction quantified miR-30a levels. The expression levels of Beclin-1 and miR-30a were associated with clinical variables and prognoses. Beclin-1 was expressed more highly in CRC tissues than in controls. This expression was related to gender (P = 0.023), histological grade (P = 0.006), M stage (P = 0.004), tumor node metastasis stage (P = 0.020), vascular invasion, and nodal involvement. Patients with higher Beclin-1 expression levels had higher survival rates (P = 0.08) than patients with lower Beclin-1 expression levels. Beclin-1 was a prognostic indicator (P < 0.05) in a multivariate analysis. Beclin-1 was overexpressed in CRC tissues and was correlated with lower levels of miR-30a (P < 0.05, r = -0. 4189). In conclusion, Beclin-1 was a good prognostic indicator in CRC and was correlated with survival rate. Beclin-1 is important in the growth and metastasis of CRC. Apoptosis in CRC might be due to the increased autophagy induced by decreased levels of miR-30a.
C1 [Liu, L.; Meng, T.; Wang, Q. S.; Jin, H. Z.; Sun, Z. Q.; Jin, B.; Fang, F.; Wang, H. J.] Xinjiang Med Univ, Canc Hosp, Dept Abdomen Surg, Urumqi, Peoples R China.
RP Wang, HJ (corresponding author), Xinjiang Med Univ, Canc Hosp, Dept Abdomen Surg, Urumqi, Peoples R China.
EM wanghaijing_l@163.com
FU Cancer Hospital Affiliated to Xinjiang Medical University
FX Research supported by the Cancer Hospital Affiliated to Xinjiang Medical
   University.
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NR 25
TC 7
Z9 9
U1 0
U2 0
PU FUNPEC-EDITORA
PI RIBEIRAO PRETO
PA RUA FLORIANO PEIXOTO 2444, ALTO DA BOA VISTA, RIBEIRAO PRETO, SP 00000,
   BRAZIL
SN 1676-5680
J9 GENET MOL RES
JI Genet. Mol. Res.
PY 2016
VL 15
IS 2
AR 15027704
DI 10.4238/gmr.15027704
PG 9
WC Biochemistry & Molecular Biology; Genetics & Heredity
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Genetics & Heredity
GA DY1UN
UT WOS:000384880000010
PM 27173217
OA Bronze
DA 2022-04-25
ER

PT J
AU Foglietta, F
   Canaparo, R
   Francovich, A
   Arena, F
   Civera, S
   Cravotto, G
   Frairia, R
   Serpe, L
AF Foglietta, Federica
   Canaparo, Roberto
   Francovich, Andrea
   Arena, Francesca
   Civera, Stefania
   Cravotto, Giancarlo
   Frairia, Roberto
   Serpe, Loredana
TI Sonodynamic Treatment as an Innovative Bimodal Anticancer Approach:
   Shock Wave-mediated Tumor Growth Inhibition in a Syngeneic Breast Cancer
   Model
SO DISCOVERY MEDICINE
LA English
DT Article
ID PHOTODYNAMIC THERAPY; SOLID TUMORS; COLON-CANCER; CELLS; ULTRASOUND;
   APOPTOSIS; MECHANISM; AUTOPHAGY; GENES
AB Despite the great advances in fighting cancer, many therapies still have serious side effects, thus urging the development of highly selective and safe treatments with a wide range of applicability. Sonodynamic therapy (SDT) is an innovative bimodal anticancer approach in which two normally non-toxic components -- one chemical, a sonosensitizer, and one physical, ultrasound -- selectively combine to cause oxidative damage and subsequent cancer cell death. In this study, we investigate the anticancer effect of SDT using shock waves (SWs) to activate protoporphyrin IX (PpIX) cytotoxicity on a Mat B-III syngeneic rat breast cancer model. The SDT-treated group saw a significant decrease (p<0.001) in magnetic resonance imaging (MRI) tumor size measurements 72 hours after treatment with PpIX precursor 5-aminolevulinic acid (ALA) and SWs. This occurred together with significant increase (p<0.01) in apparent diffusion coefficients between pre- and post-treatment MR tumor maps and strong increase in necrotic and apoptotic histological features 72 hours post-treatment. Moreover, significant HIF1A mRNA expression up-regulation was observed along with the prominent selective cleavage of poly (ADP-ribose) polymerase (PARP) and increased autophagy related protein LC3A/B expression in SDT-treated tumors, as compared to untreated tumors 72 hours post-treatment. Thus, the anticancer effect of SDT can be boosted by SWs, making them a valid technology for furthering investigations into this innovative anticancer approach.
C1 [Foglietta, Federica; Canaparo, Roberto; Civera, Stefania; Cravotto, Giancarlo; Serpe, Loredana] Univ Turin, Dept Drug Sci & Technol, I-10125 Turin, Italy.
   [Francovich, Andrea] Univ Fribourg, Inst Physiol, CH-1770 Fribourg, Switzerland.
   [Arena, Francesca] Univ Turin, Ctr Preclin Imaging, I-10010 Colleretto Giacosa, Italy.
   [Frairia, Roberto] Univ Turin, Dept Med Sci, I-10126 Turin, Italy.
RP Serpe, L (corresponding author), Univ Turin, Dept Drug Sci & Technol, Via Pietro Giuria 13, I-10125 Turin, Italy.
EM loredana.serpe@unito.it
RI Cravotto, Giancarlo/AAT-9306-2020; Canaparo, Roberto/I-6431-2019
OI Canaparo, Roberto/0000-0003-2774-6817; Arena,
   Francesca/0000-0003-3644-0609; Frairia, Roberto/0000-0001-9453-772X
FU Italian Ministry of Health; Piemonte Region (grant "Giovani Ricercatori
   ") [GR-2008-1138087]; Associazione Italiana per la Ricerca sul Cancro
   (grant "MFAG") [MFAG-13048]
FX Authors gratefully acknowledge funding from the Italian Ministry of
   Health and Piemonte Region (grant "Giovani Ricercatori 2008,"
   GR-2008-1138087) and from the Associazione Italiana per la Ricerca sul
   Cancro (grant "MFAG 2012," MFAG-13048).
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NR 36
TC 19
Z9 21
U1 0
U2 10
PU DISCOVERY MEDICINE
PI TIMONIUM
PA 10 GERARD AVE, STE 201, TIMONIUM, MD 21093 USA
SN 1539-6509
EI 1944-7930
J9 DISCOV MED
JI Discov. Med.
PD OCT
PY 2015
VL 20
IS 110
BP 197
EP 205
PG 9
WC Medicine, Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Research & Experimental Medicine
GA CY3LI
UT WOS:000366310600005
PM 26562473
DA 2022-04-25
ER

PT J
AU Mohamed, MS
   Kobayashi, A
   Taoka, A
   Watanabe-Nakayama, T
   Kikuchi, Y
   Hazawa, M
   Minamoto, T
   Fukumori, Y
   Kodera, N
   Uchihashi, T
   Ando, T
   Wong, RW
AF Mohamed, Mahmoud Shaaban
   Kobayashi, Akiko
   Taoka, Azuma
   Watanabe-Nakayama, Takahiro
   Kikuchi, Yosuke
   Hazawa, Masaharu
   Minamoto, Toshinari
   Fukumori, Yoshihiro
   Kodera, Noriyuki
   Uchihashi, Takayuki
   Ando, Toshio
   Wong, Richard W.
TI High-Speed Atomic Force Microscopy Reveals Loss of Nuclear Pore
   Resilience as a Dying Code in Colorectal Cancer Cells
SO ACS NANO
LA English
DT Article
DE high-speed atomic force microscopy; live cell imaging; nanopore; nuclear
   pore complex; colon cancer
ID NUCLEOCYTOPLASMIC TRANSPORT; COMPLEX STRUCTURE; NUCLEOPORIN TPR; AURORA
   KINASE; LIVE CELLS; PROTEINS; ENVELOPE; DYNAMICS; NANOPARTICLES;
   VISUALIZATION
AB Nuclear pore complexes (NPCs) are the sole turnstile implanted in the nuclear envelope (NE), acting as a central nanoregulator of transport between the cytosol and the nucleus. NPCs consist of similar to 30 proteins, termed nucleoporins. About one-third of nucleoporins harbor natively unstructured, intrinsically disordered phenylalanine-glycine strings (FG-Nups), which engage in transport selectivity. Because the barriers insert deeply in the NPC, they are nearly inaccessible. Several in vitro barrier models have been proposed; however, the dynamic FG-Nups protein molecules themselves are imperceptible in vivo. We show here that high-speed atomic force microscopy (HS-AFM) can be used to directly visualize nanotopographical changes of the nuclear pore inner channel in colorectal cancer (CRC) cells. Furthermore, using MLN8237/alisertib, an apoptotic and autophagic inducer currently being tested in relapsed cancer clinical trials, we unveiled the functional loss of nucleoporins, particularly the deformation of the FG-Nups barrier, in dying cancer cells. We propose that the loss of this nanoscopic resilience is an irreversible dying code in cells. These findings not only illuminate the potential application of HS-AFM as an intracellular nanoendoscopy but also might aid in the design of future nuclear targeted nanodrug delivery tailored to the individual patient.
C1 [Mohamed, Mahmoud Shaaban; Kobayashi, Akiko; Hazawa, Masaharu; Wong, Richard W.] Kanazawa Univ, Canc Res Inst, Inst Frontier Sci Initiat, Innovat Integrated Biores Core,Cell Bion Res Unit, Kakuma Machi, Kanazawa, Ishikawa 9201192, Japan.
   [Mohamed, Mahmoud Shaaban; Taoka, Azuma; Watanabe-Nakayama, Takahiro; Kodera, Noriyuki; Uchihashi, Takayuki; Ando, Toshio; Wong, Richard W.] Kanazawa Univ, Canc Res Inst, BioAFM Frontier Res Ctr, Kakuma Machi, Kanazawa, Ishikawa 9201192, Japan.
   [Mohamed, Mahmoud Shaaban; Kobayashi, Akiko; Taoka, Azuma; Kikuchi, Yosuke; Hazawa, Masaharu; Fukumori, Yoshihiro; Wong, Richard W.] Kanazawa Univ, Canc Res Inst, Sch Nat Sci & Technol, Div Nat Syst, Kakuma Machi, Kanazawa, Ishikawa 9201192, Japan.
   [Minamoto, Toshinari] Kanazawa Univ, Canc Res Inst, Div Translat & Clin Oncol, Kakuma Machi, Kanazawa, Ishikawa 9201192, Japan.
RP Wong, RW (corresponding author), Kanazawa Univ, Canc Res Inst, Inst Frontier Sci Initiat, Innovat Integrated Biores Core,Cell Bion Res Unit, Kakuma Machi, Kanazawa, Ishikawa 9201192, Japan.; Wong, RW (corresponding author), Kanazawa Univ, Canc Res Inst, BioAFM Frontier Res Ctr, Kakuma Machi, Kanazawa, Ishikawa 9201192, Japan.; Wong, RW (corresponding author), Kanazawa Univ, Canc Res Inst, Sch Nat Sci & Technol, Div Nat Syst, Kakuma Machi, Kanazawa, Ishikawa 9201192, Japan.
EM rwong@staff.kanazawa-u.ac.jp
RI Wong, Richard W./E-9155-2011; Fukumori, Yoshihiro/J-2483-2014; Hazawa,
   M/AAA-2712-2021; Kodera, Noriyuki/AAJ-1797-2020; Taoka,
   Azuma/C-3795-2015; ANDO, Toshio/E-7054-2015; Uchihashi,
   Takayuki/D-5209-2011; HAZAWA, Masaharu/A-6520-2016
OI Kodera, Noriyuki/0000-0003-4880-8423; Taoka, Azuma/0000-0003-2492-7858;
   ANDO, Toshio/0000-0001-8819-154X; Uchihashi,
   Takayuki/0000-0002-0263-5312; Wong, Richard/0000-0002-2131-6595
FU MEXT/JSPSMinistry of Education, Culture, Sports, Science and Technology,
   Japan (MEXT)Japan Society for the Promotion of Science [24227005,
   24117007, 15H04928]; MEXT JapanMinistry of Education, Culture, Sports,
   Science and Technology, Japan (MEXT) [17H05874, 17K08655]; Extramural
   Collaborative Research Grant of Cancer Research Institute, Kanazawa
   University; Uehara Memorial FoundationUehara Memorial Foundation;
   Suzuken Memorial Foundation; Asahi Glass Foundation; Kowa Life Science
   Foundation; Sumitomo Foundation; Mochida Memorial Foundation; Sagawa
   Foundation; Ichiro Kanehara Foundation; Takeda Science FoundationTakeda
   Science Foundation (TSF); Grants-in-Aid for Scientific ResearchMinistry
   of Education, Culture, Sports, Science and Technology, Japan (MEXT)Japan
   Society for the Promotion of ScienceGrants-in-Aid for Scientific
   Research (KAKENHI) [17K19345] Funding Source: KAKEN
FX This work was supported by a MEXT/JSPS KAKENHI Grant Number 24227005 (to
   A.T.); 24117007 (to Y.F.); 15H04928 (to T.M.); and 17H05874, 17K08655
   (to R.W.) from MEXT Japan, and by grants from the Extramural
   Collaborative Research Grant of Cancer Research Institute, Kanazawa
   University, the Uehara Memorial Foundation, the Suzuken Memorial
   Foundation, the Asahi Glass Foundation, the Kowa Life Science
   Foundation, the Sumitomo Foundation, the Mochida Memorial Foundation,
   the Sagawa Foundation, the Ichiro Kanehara Foundation, and the Takeda
   Science Foundation (to R.W.). We are grateful to Jan Lammerding for
   Lamin plasmids. We are especially indebted to Roderick Lim and Bart
   Hoogenboom for insightful discussions at the 4th Kanazawa Bio-AFM
   workshop.
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NR 56
TC 28
Z9 29
U1 0
U2 36
PU AMER CHEMICAL SOC
PI WASHINGTON
PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA
SN 1936-0851
EI 1936-086X
J9 ACS NANO
JI ACS Nano
PD JUN
PY 2017
VL 11
IS 6
BP 5567
EP 5578
DI 10.1021/acsnano.7b00906
PG 12
WC Chemistry, Multidisciplinary; Chemistry, Physical; Nanoscience &
   Nanotechnology; Materials Science, Multidisciplinary
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Chemistry; Science & Technology - Other Topics; Materials Science
GA EZ6DG
UT WOS:000404808000037
PM 28530826
DA 2022-04-25
ER

PT J
AU Jang, D
   Song, J
   Park, JW
   Yoon, SH
   Bae, YS
AF Jang, Da Eun
   Song, Junbin
   Park, Jeong-Woo
   Yoon, Soo-Hyun
   Bae, Young-Seuk
TI Protein kinase CK2 activates Nrf2 via autophagic degradation of Keap1
   and activation of AMPK in human cancer cells
SO BMB REPORTS
LA English
DT Article
DE AMPK; Antioxidants; CK2; Keap1; Nrf2
ID REGULATION-MEDIATED SENESCENCE; TRANSCRIPTION FACTOR NRF2; HUMAN
   COLON-CANCER; DOWN-REGULATION; CELLULAR SENESCENCE; INACTIVATION;
   ACCUMULATION; MECHANISMS; NUTRIENT; STRESS
AB Protein kinase CK2 downregulation induces premature senescence in various human cell types via activation of the reactive oxygen species (ROS)-p53-p21(Cip1/)(WAF1) pathway. The transcription factor "nuclear factor erythroid 2-related factor 2 '' (Nrf2) plays an important role in maintaining intracellular redox homeostasis. In this study, Nrf2 overexpression attenuated CK2 downregulation-induced ROS production and senescence markers including SA-beta-gal staining and activation of p53-p21(Cip1/)(WAF1) in human breast (MCF-7) and colon (HCT116) cancer cells. CK2 downregulation reduced the transcription of Nrf2 target genes, such as glutathione S transferase, glutathione peroxidase 2, and glutathione reductase 1. Furthermore, CK2 downregulation destabilized Nrf2 protein via inhibiting autophagic degradation of Kelch-like ECH-associated protein 1 (Keap1). Finally, CK2 downregulation decreased the nuclear import of Nrf2 by deactivating AMP-activated protein kinase (AMPK). Collectively, our data suggest that both Keap1 stabilization and AMPK inactivation are associated with decreased activity of Nrf2 in CK2 downregulation-induced cellular senescence.
C1 [Jang, Da Eun; Song, Junbin; Park, Jeong-Woo; Bae, Young-Seuk] Kyungpook Natl Univ, Sch Life Sci, BK2 Plus KNU Creat BioRes Grp, Daegu 41566, South Korea.
   [Yoon, Soo-Hyun] Kyungpook Natl Univ, Coll Pharm, Res Inst Pharmaceut Sci, Daegu 41566, South Korea.
RP Bae, YS (corresponding author), Kyungpook Natl Univ, Sch Life Sci, BK2 Plus KNU Creat BioRes Grp, Daegu 41566, South Korea.
EM ysbae@knu.ac.kr
FU Basic Science Research Program through the National Research Foundation
   of Korea (NRF) - Ministry of Science, ICT and Future Planning
   [NRF-2019R1A2C1005219]
FX This research was supported by the Basic Science Research Program
   through the National Research Foundation of Korea (NRF) funded by the
   Ministry of Science, ICT and Future Planning (NRF-2019R1A2C1005219).
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NR 23
TC 6
Z9 8
U1 0
U2 1
PU KOREAN SOCIETY BIOCHEMISTRY & MOLECULAR BIOLOGY
PI SEOUL
PA KOREA SCIENCE & TECHNOLOGY CENTER, # 801,  635-4 , YEOKSAM-DONG,
   KANGNAM-KU, SEOUL, 135-703, SOUTH KOREA
SN 1976-6696
EI 1976-670X
J9 BMB REP
JI BMB Rep.
PD MAY 31
PY 2020
VL 53
IS 5
BP 272
EP 277
DI 10.5483/BMBRep.2020.53.5.044
PG 6
WC Biochemistry & Molecular Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology
GA LU4TN
UT WOS:000537749800006
PM 32317087
OA Green Published, gold
DA 2022-04-25
ER

PT J
AU Yuan, L
   Zhang, X
   Cheng, K
   Li, LP
   Guo, ZM
   Zeng, L
AF Yuan, Li
   Zhang, Xiao
   Cheng, Kai
   Li, Liping
   Guo, Zhongming
   Zeng, Liang
TI IRF1 Inhibits Autophagy-Mediated Proliferation of Colorectal Cancer via
   Targeting ATG13
SO CANCER INVESTIGATION
LA English
DT Article
DE Colorectal cancer; IRF1; growth; autophagy
ID ULK1 COMPLEX
AB IRF1 is a nuclear transcription factor that mediates interferon effects and appears to have anti-tumor activity. To determine the roles of IRF1 in colorectal cancer (CRC), we investigated the effects of IRF1 in CRC cells. We found that IRF1 inhibit cell proliferation and tumor growth. Under starvation conditions, IRF1 enhanced apoptosis and reduced autophagic flux. ATG13, an important factor of autophagy complex, was confirmed as a target of IRF1. These findings indicated that IRF1 function as a tumor suppressor in CRC and inhibit autophagy through ATG13, targeting this pathway may provide new insights into the molecular mechanisms of CRC progression.
C1 [Yuan, Li; Cheng, Kai; Li, Liping; Guo, Zhongming; Zeng, Liang] Guangzhou Med Univ, Guangzhou Women & Childrens Med Ctr, Dept Pathol, 9 Jinsui Rd, Guangzhou 510623, Peoples R China.
   [Zhang, Xiao] Guangzhou Med Univ, Affiliated Hosp 1, Dept Gastrointestinal Surg, Guangzhou, Peoples R China.
RP Yuan, L (corresponding author), Guangzhou Med Univ, Guangzhou Women & Childrens Med Ctr, Dept Pathol, 9 Jinsui Rd, Guangzhou 510623, Peoples R China.
EM lizzyklarck@126.com
FU National Natural Science Foundation of ChinaNational Natural Science
   Foundation of China (NSFC) [81802346]; Guangzhou Women and Children's
   Medical Center/Guangzhou Institute of Pediatrics
FX This work is supported by the National Natural Science Foundation of
   China [No. 81802346], and the fund from Guangzhou Women and Children's
   Medical Center/Guangzhou Institute of Pediatrics [No. YIP-2018-004].
CR Choo A, 2006, CURR GENE THER, V6, P543, DOI 10.2174/156652306778520683
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NR 27
TC 2
Z9 2
U1 3
U2 5
PU TAYLOR & FRANCIS INC
PI PHILADELPHIA
PA 530 WALNUT STREET, STE 850, PHILADELPHIA, PA 19106 USA
SN 0735-7907
EI 1532-4192
J9 CANCER INVEST
JI Cancer Invest.
PD JAN 2
PY 2022
VL 40
IS 1
BP 35
EP 45
DI 10.1080/07357907.2021.1961265
EA AUG 2021
PG 11
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA XZ2YD
UT WOS:000685816400001
PM 34313498
DA 2022-04-25
ER

PT J
AU Dubey, A
   Jeong, YJ
   Jo, JH
   Woo, S
   Kim, DH
   Kim, H
   Kang, SC
   Stang, PJ
   Chi, KW
AF Dubey, Abhishek
   Jeong, Yong Joon
   Jo, Jae Ho
   Woo, Sangkook
   Kim, Dong Hwan
   Kim, Hyunuk
   Kang, Se Chan
   Stang, Peter J.
   Chi, Ki-Whan
TI Anticancer Activity and Autophagy Involvement of Self-Assembled
   Arene-Ruthenium Metallacycles
SO ORGANOMETALLICS
LA English
DT Article
ID HOLLOW-FIBER ASSAY; CANCER-CELLS; TISSUE TRANSGLUTAMINASE;
   BIOLOGICAL-ACTIVITY; IN-VIVO; COORDINATION-COMPLEXES;
   MOLECULAR-RECTANGLES; PANCREATIC-CANCER; DNA-DAMAGE; DRUG
AB A suite of six metallacycles (16) was generated via coordination-driven self-assembly using the three dicarboxylate-bridged areneRu precursors [Ru-2(mu-eta(4)-OO boolean AND OO)(eta(6)-p-iPrC(6)H4Me)(2)][CF3SO3](2); (OO boolean AND OO = oxalate (A1), 2,5-dihydroxy-1,4-benzoquinonato (dobq) (A2), 5,8-dihydroxy-1,4-naphthoquinonato (donq) (A3); CF3SO3 = triflate) with one of two dipyridyl ligands (L1 and L2). The metallacycles were isolated in excellent yield (8692%) as triflate salts and characterized by proton (H-1) and carbon-13 (C-13) nuclear magnetic resonance (NMR) and electrospray ionizationmass spectrometry (ESI-MS) to confirm their structural assignments. Single-crystal X-ray crystal analysis of 1 revealed that two L1 ligands bridged two A1 acceptors to form a rectangular architecture. The 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay was conducted to evaluate the in vitro cytotoxicities relative to two chemotherapeutic agents: namely, cisplatin and doxorubicin. Metallacycles 3 and 6 potently inhibited the growth of HCT-15 human colon and AGS human gastric cancer cells. The hollow fiber (HF) assay was performed to investigate the in vivo antitumor activities of metallacycles 3 and 6. Metallacycle 6 was more effective in inhibiting HCT-15 cells than metallacycle 3 in both in vitro and in vivo studies. Moreover, 3 and 6 induced autophagic activity in HCT-15 cells. These results suggested that the autophagic response elicited by metallacycles 3 and 6 could mediate the anticancer effects observed in human colorectal cancer cells.
C1 [Dubey, Abhishek; Jo, Jae Ho; Woo, Sangkook; Kim, Dong Hwan; Chi, Ki-Whan] Univ Ulsan, Dept Chem, Ulsan 680749, South Korea.
   [Jeong, Yong Joon; Kang, Se Chan] Gachon Univ, Dept Life Sci, Songnam 461701, South Korea.
   [Kim, Hyunuk] Korea Inst Energy Res, Energy Mat Lab, Taejon 305343, South Korea.
   [Stang, Peter J.] Univ Utah, Dept Chem, Salt Lake City, UT 84112 USA.
RP Kang, SC (corresponding author), Gachon Univ, Dept Life Sci, Songnam 461701, South Korea.
EM sckang73@gachon.ac.kr; kwchi@ulsan.ac.kr
RI Dubey, Abhishek/M-5118-2016; Stang, Peter J./Y-2744-2019
OI Dubey, Abhishek/0000-0002-8984-8109; chi, ki-whan/0000-0002-7816-801X
FU Basic Science Research program through the National Research Foundation
   of Korea [NRF-2013R1A1A2006859]; Priority Research Center Program
   through the National Research Foundation of Korea [2009-0093818];
   National Institutes of Health (NIH)United States Department of Health &
   Human ServicesNational Institutes of Health (NIH) - USA [GM-57052];
   Research and Development Program of the Korea Institute of Energy
   Research (KIER) [B5-2513]
FX K.-W.C. gratefully acknowledges the generous financial support of the
   Basic Science Research program (NRF-2013R1A1A2006859) and the Priority
   Research Center Program (2009-0093818) through the National Research
   Foundation of Korea and the X-ray diffraction experiments performed at
   the Pohang Accelerator Laboratory in Korea. P.J.S. thanks the National
   Institutes of Health (NIH) for financial support (GM-57052). H.K. thanks
   the Research and Development Program of the Korea Institute of Energy
   Research (KIER, B5-2513).
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NR 85
TC 25
Z9 25
U1 4
U2 47
PU AMER CHEMICAL SOC
PI WASHINGTON
PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA
SN 0276-7333
EI 1520-6041
J9 ORGANOMETALLICS
JI Organometallics
PD SEP 28
PY 2015
VL 34
IS 18
BP 4507
EP 4514
DI 10.1021/acs.organomet.5b00512
PG 8
WC Chemistry, Inorganic & Nuclear; Chemistry, Organic
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Chemistry
GA CS4OW
UT WOS:000362056400008
DA 2022-04-25
ER

PT J
AU Senichkin, VV
   Kopeina, GS
   Zamaraev, AV
   Lavrik, IN
   Zhivotovsky, BD
AF Senichkin, V. V.
   Kopeina, G. S.
   Zamaraev, A. V.
   Lavrik, I. N.
   Zhivotovsky, B. D.
TI Nutrient Restriction in Combinatory Therapy of Tumors
SO MOLECULAR BIOLOGY
LA English
DT Review
DE Calorie restriction; chemotherapy; apoptosis; autophagy mechanisms
ID ACTIVATED PROTEIN-KINASE; PROGRAMMED CELL-DEATH; BCL-2 FAMILY PROTEINS;
   COLON-CANCER CELLS; CALORIC RESTRICTION; DIETARY RESTRICTION; OXIDATIVE
   STRESS; MEDIATED CLEAVAGE; GROWTH-HORMONE; BRAIN-TUMOR
AB The main objective of anticancer treatment is the elimination of degenerated cells by the induction of programmed cell death. Various chemotherapy drugs and radiation are able to activate cell death mechanisms in tumors. However, unfortunately, monotherapy will always be insufficiently effective because of the variety and virulence of tumors, as well as their ability to develop resistance to drugs. Moreover, monotherapy might constrain many negative side effects. Therefore, the combination of different approaches and/or drugs will increase the efficiency of treatment. One such promising approach is the combination of nutrient restriction (NR) and various chemotherapeutic drugs. This approach may not only affect the autophagy but also influence apoptotic cell death. This review is focused on the potential of NR use in anticancer therapy, as well as the molecular mechanisms underlying this approach.
C1 [Senichkin, V. V.; Kopeina, G. S.; Zamaraev, A. V.; Lavrik, I. N.; Zhivotovsky, B. D.] Moscow MV Lomonosov State Univ, Fac Basic Med, Moscow 119991, Russia.
   [Lavrik, I. N.] Otto Von Guericke Univ, Dept Translat Inflammat Res, D-39120 Magdeburg, Germany.
   [Zhivotovsky, B. D.] Karolinska Inst, Div Toxicol, Inst Environm Med, S-17177 Stockholm, Sweden.
RP Zhivotovsky, BD (corresponding author), Moscow MV Lomonosov State Univ, Fac Basic Med, Moscow 119991, Russia.; Zhivotovsky, BD (corresponding author), Karolinska Inst, Div Toxicol, Inst Environm Med, S-17177 Stockholm, Sweden.
EM Boris.Zhivotovsky@ki.se
RI Zhivotovsky, Boris/A-4346-2014; Kopeina, Gelina/AAD-5713-2022; Zamaraev,
   Alexey V/O-6268-2017; Lavrik, Inna N/C-1700-2009; Senichkin, Viacheslav
   V/P-4602-2017
OI Zhivotovsky, Boris/0000-0002-2238-3482; Lavrik, Inna
   N/0000-0002-9324-309X; Senichkin, Viacheslav V/0000-0001-6781-8331;
   Gelina, Kopeina/0000-0002-7143-6923; Zamaraev,
   Alexey/0000-0003-0509-6323
FU Russian Science FoundationRussian Science Foundation (RSF)
   [14-25-00056]; Russian Foundation for Basic ResearchRussian Foundation
   for Basic Research (RFBR) [14-04-31090 mol_a, 14-04-00699 A, 16-04-00113
   A]; Dynasty Foundation
FX This work was supported by grant from the Russian Science Foundation
   (14-25-00056). The work in the authors' laboratories is also supported
   by grants from the Russian Foundation for Basic Research (14-04-31090
   mol_a, 14-04-00699 A and 16-04-00113 A) and the Dynasty Foundation. We
   apologize to those authors whose primary works could not be cited owing
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NR 155
TC 4
Z9 4
U1 1
U2 13
PU MAIK NAUKA/INTERPERIODICA/SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013-1578 USA
SN 0026-8933
EI 1608-3245
J9 MOL BIOL+
JI Mol. Biol.
PD MAY
PY 2016
VL 50
IS 3
BP 362
EP 378
DI 10.1134/S0026893316030109
PG 17
WC Biochemistry & Molecular Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology
GA DO9XE
UT WOS:000378140500004
DA 2022-04-25
ER

PT J
AU Cui, H
   Yang, S
   Jiang, Y
   Li, C
   Zhao, Y
   Shi, Y
   Hao, Y
   Qian, F
   Tang, B
   Yu, P
AF Cui, H.
   Yang, S.
   Jiang, Y.
   Li, C.
   Zhao, Y.
   Shi, Y.
   Hao, Y.
   Qian, F.
   Tang, B.
   Yu, P.
TI The glycosyltransferase ST6Gal-I is enriched in cancer stem-like cells
   in colorectal carcinoma and contributes to their chemo-resistance
SO CLINICAL & TRANSLATIONAL ONCOLOGY
LA English
DT Article
DE Cancer stem cells (CSCs); Colorectal carcinoma (CRC); ST6
   beta-galactoside alpha-2,6-sialyltransferase 1 (ST6Gal-I)
ID BECLIN 1; AUTOPHAGY; CD44; APOPTOSIS; TARGET; 5-FLUOROURACIL;
   EXPRESSION; PATHWAY
AB Presence of cancer stem cells (CSCs) contributes to tumor outgrowth, chemo-resistance and relapse in some cancers including colorectal carcinoma (CRC). The current characterization methods of CSCs in CRC only allows enrichment of CSCs but not their purification. Recent reports showed that ST6 beta-galactoside alpha-2,6-sialyltransferase 1 (ST6Gal-I) plays an essential role in protecting tumor cells against harsh environment like oxidative stress and nutrient deprivation. Therefore, whether ST6Gal-I may be highly expressed in CSCs or whether it may enhance resistance of tumor cells to chemotherapy deserves exploration.
   ST6Gal-I levels were determined in CRC specimens, compared to paired normal colorectal tissue, and examined in CD133+ vs CD133- CRC cells, and CD44+ vs CD44- CRC cells. ST6Gal-I levels and their association with patient survival were examined. In vivo, 2 CRC cell lines Caco-2 and SW48 were transduced with two lentiviruses, one lentivirus carrying a green fluorescent protein reporter and a luciferase reporter under a cytomegalovirus promoter to allow tracing tumor cells by both fluorescence and luciferase activity, and one lentivirus carrying a nuclear red fluorescent protein under the control of ST6Gal-I promoter to allow separation of ST6Gal-I+ vs ST6Gal-I- CRC cells. Tumor sphere formation, resistance to fluorouracil-induced apoptosis, and frequency of tumor formation after serial adoptive transplantation were done on ST6Gal-I+ vs ST6Gal-I- CRC cells.
   ST6Gal-I levels were significantly upregulated in clinically obtained CRC specimens, compared to paired normal colorectal tissue. Poorer patient survival was detected in ST6Gal-I-high CRC, compared to ST6Gal-I-low subjects. Higher levels of ST6Gal-I were detected in CD133+ CRC cells than CD133- CRC cells, and in CD44+ CRC cells than in CD44- CRC cells. Compared to ST6Gal-I- CRC cells, ST6Gal-I+ CRC cells generated significantly more tumor spheres in culture, were more resistant to fluorouracil-induced apoptosis likely through upregulating cell autophagy, and generated tumor more frequently after serial adoptive transplantation.
   ST6Gal-I may be highly expressed in the cancer stem-like cells in CRC and enhances cancer cell resistance to chemotherapy.
C1 [Cui, H.; Yang, S.; Jiang, Y.; Li, C.; Zhao, Y.; Shi, Y.; Hao, Y.; Qian, F.; Tang, B.; Yu, P.] Third Mil Med Univ, Southwest Hosp, Dept Gen Surg, 30 Gaotanyanzheng St, Chongqing 400038, Peoples R China.
   [Cui, H.; Yang, S.; Jiang, Y.; Li, C.; Zhao, Y.; Shi, Y.; Hao, Y.; Qian, F.; Tang, B.; Yu, P.] Third Mil Med Univ, Southwest Hosp, Ctr Minimal Invas Gastrointestinal Surg, 30 Gaotanyanzheng St, Chongqing 400038, Peoples R China.
RP Tang, B; Yu, P (corresponding author), Third Mil Med Univ, Southwest Hosp, Dept Gen Surg, 30 Gaotanyanzheng St, Chongqing 400038, Peoples R China.; Tang, B; Yu, P (corresponding author), Third Mil Med Univ, Southwest Hosp, Ctr Minimal Invas Gastrointestinal Surg, 30 Gaotanyanzheng St, Chongqing 400038, Peoples R China.
EM taNTbo@sina.cn; yupeiwu01@yeah.net
OI Yu, Peiwu/0000-0002-4364-3589
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Z9 7
U1 1
U2 2
PU SPRINGER-VERLAG ITALIA SRL
PI MILAN
PA VIA DECEMBRIO, 28, MILAN, 20137, ITALY
SN 1699-048X
EI 1699-3055
J9 CLIN TRANSL ONCOL
JI Clin. Transl. Oncol.
PD SEP
PY 2018
VL 20
IS 9
BP 1175
EP 1184
DI 10.1007/s12094-018-1840-5
PG 10
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA GR0SM
UT WOS:000442233000010
PM 29423671
DA 2022-04-25
ER

PT J
AU Sato, K
   Tsuchihara, K
   Fujii, S
   Sugiyama, M
   Goya, T
   Atomi, Y
   Ueno, T
   Ochiai, A
   Esumi, H
AF Sato, Kazunori
   Tsuchihara, Katsuya
   Fujii, Satoshi
   Sugiyama, Masanori
   Goya, Tomoyuki
   Atomi, Yutaka
   Ueno, Takashi
   Ochiai, Atsushi
   Esumi, Hiroyasu
TI Autophagy is activated in colorectal cancer cells and contributes to the
   tolerance to nutrient deprivation
SO CANCER RESEARCH
LA English
DT Article
ID PROTEIN-KINASE; GLUCOSE STARVATION; HYPOXIA; INHIBITION; LC3;
   TUMORIGENESIS; PROTEOLYSIS; MATURATION; APOPTOSIS; BECLIN-1
AB Several types of cancer cells, including colorectal cancerderived cell lines' show austerity, the resistance to nutrient starvation, but exactly how cancer cells obtain energy sources under conditions in which their external nutrient supply is extremely limited remains to be clarified. Because autophagy is a catabolic process by which cells supply amino acids from self-digested organelles, cancer cells are likely to use autophagy to obtain amino acids as alternative energy sources. Amino acid deprivation-induced autophagy was assessed in DLD-1 and other colorectal cancer-derived cell lines. The autophagosome-incorporated LC3-II protein level increased after treatment with a combination of atitolysosome inhibitors, which interferes with the consumption of autophagosomes. Autophagosome formation was also morphologically confirmed using ectopically expressed green fluorescent protein-LC3 fusion proteins in DLD-1 and SW480 cells. These data suggest that autophagosomes were actively produced and promptly consumed in colorectal cancer cells under nutrient starvation. Autolysosome inhibitors and 3-methyl adenine, which suppresses autophagosome formation, remarkably enhanced apoptosis under amino acid-deprived and glucosedeprived condition. Similar results were obtained in the cells with decreased ATG7 level by the RNA interference. These data suggest that autophagy is pivotal for the survival of colorectal cancer cells that have acquired austerity. Furthermore, autophagosome formation was seen only in the tumor cells but not in the adjacent noncancerous epithelial cells of colorectal cancer specimens. Taken together, autophagy is activated in colorectal cancers in vitro and in vivo, and autophagy may contribute to the survival of the cancer cells in their microenvironment.
C1 Natl Canc Ctr Hosp E, Canc Physiol Project, Chiba 2778577, Japan.
   Natl Canc Ctr Hosp E, Res Ctr Innovat Oncol, Div Pathol, Chiba, Japan.
   Juntendo Univ, Sch Med, Dept Biochem, Tokyo 113, Japan.
   Kyorin Univ, Sch Med, Dept Surg, Tokyo, Japan.
RP Esumi, H (corresponding author), Natl Canc Ctr Hosp E, Canc Physiol Project, 6-5-1 Kashiwanoha, Chiba 2778577, Japan.
EM hesumi@east.ncc.go.jp
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NR 31
TC 284
Z9 303
U1 0
U2 26
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
J9 CANCER RES
JI Cancer Res.
PD OCT 15
PY 2007
VL 67
IS 20
BP 9677
EP 9684
DI 10.1158/0008-5472.CAN-07-1462
PG 8
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA 222HG
UT WOS:000250286300011
PM 17942897
DA 2022-04-25
ER

PT J
AU Xie, YD
   Zhao, YF
   Shi, L
   Li, W
   Chen, K
   Li, M
   Chen, X
   Zhang, HW
   Li, TT
   Matsuzawa-Ishimoto, Y
   Yao, XM
   Shao, DH
   Ke, ZF
   Li, J
   Chen, Y
   Zhang, XM
   Cui, J
   Cui, SZ
   Leng, QB
   Cadwell, K
   Li, XX
   Wei, H
   Zhang, HB
   Li, HB
   Xiao, H
AF Xie, Yadong
   Zhao, Yifan
   Shi, Lei
   Li, Wei
   Chen, Kun
   Li, Min
   Chen, Xia
   Zhang, Haiwei
   Li, Tiantian
   Matsuzawa-Ishimoto, Yu
   Yao, Xiaomin
   Shao, Dianhui
   Ke, Zunfu
   Li, Jian
   Chen, Yan
   Zhang, Xiaoming
   Cui, Jun
   Cui, Shuzhong
   Leng, Qibin
   Cadwell, Ken
   Li, Xiaoxia
   Wei, Hong
   Zhang, Haibing
   Li, Huabin
   Xiao, Hui
TI Gut epithelial TSC1/mTOR controls RIPK3-dependent necroptosis in
   intestinal inflammation and cancer
SO JOURNAL OF CLINICAL INVESTIGATION
LA English
DT Article
ID PROGRAMMED NECROSIS; BOWEL-DISEASE; ADAPTER RIPK3; CELL-DEATH; KINASE;
   HOMEOSTASIS; MTOR; PHOSPHORYLATION; EXPRESSION; AUTOPHAGY
AB Although Western diet and dysbios is are the most prominent environmental factors associated with inflammatory bowel diseases (Ins), the corresponding host factors and cellular mechanisms remain poorly defined. Here we report that the TSC1/mTOR pathway in the gut epithelium represents a metabolic and innate immune checkpoint for intestinal dysfunction and inflammation. mTOR hyperactivation triggered by Western diet or Tsc1 ablation led to epithelium necroptosis, barrier disruption, and predisposition to dextran sulfate sodium-induced colitis and inflammation-associated colon cancer. Mechanistically, our results uncovered a critical role for TSC1/mTOR in restraining the expression and activation of RIPK3 in the gut epithelium through TRIM11-mediated ubiquitination and autophagy-dependent degradation. Notably, microbiota depletion by antibiotics or gnotobiotics attenuated RIPK3 expression and activation, thereby alleviating epithelial necroptosis and colitis driven by mTOR hyperactivation. mTOR primarily impinged on RIPK3 to potentiate necroptosis induced by TNF and by microbial pathogen-associated molecular patterns (PAMPs), and hyperactive mTOR and aberrant necroptosis were intertwined in human Ins. Together, our data reveal a previously unsuspected link between the Western diet, microbiota, and necroptosis and identify the mTOR/RIPK3/necroptosis axis as a driving force for intestinal inflammation and cancer.
C1 [Xie, Yadong; Zhao, Yifan; Shi, Lei; Li, Wei; Chen, Xia; Li, Tiantian; Shao, Dianhui; Zhang, Xiaoming; Xiao, Hui] Chinese Acad Sci, Ctr Microbes Dev & Hlth, Key Lab Mol Virol & Immunol, Inst Pasteur Shanghai, Shanghai, Peoples R China.
   [Xie, Yadong; Zhao, Yifan; Shi, Lei; Li, Wei; Chen, Xia; Li, Tiantian; Shao, Dianhui; Zhang, Xiaoming; Xiao, Hui] CAS Ctr Excellence Mol Cell Sci, Shanghai, Peoples R China.
   [Xie, Yadong; Zhao, Yifan; Shi, Lei; Li, Wei; Chen, Xia; Li, Tiantian; Shao, Dianhui; Zhang, Xiaoming; Xiao, Hui] Chinese Acad Sci, Univ Chinese Acad Sci, Shanghai, Peoples R China.
   [Xie, Yadong; Chen, Kun; Li, Min; Li, Huabin] Fudan Univ, Affiliated Eye Ear Nose & Throat Hosp, Ctr Allerg & Inflammatory Dis, Shanghai, Peoples R China.
   [Xie, Yadong; Chen, Kun; Li, Min; Li, Huabin] Fudan Univ, Affiliated Eye Ear Nose & Throat Hosp, Dept Otolaryngol Head & Neck Surg, Shanghai, Peoples R China.
   [Zhang, Haiwei; Chen, Yan; Zhang, Haibing] Chinese Acad Sci, Shanghai Inst Nutr & Hlth, CAS Key Lab Nutr Metab & Food Safety, Univ Chinese Acad Sci, Shanghai, Peoples R China.
   [Matsuzawa-Ishimoto, Yu; Yao, Xiaomin; Cadwell, Ken] NYU, Kimmel Ctr Biol & Med, Skirball Inst Biomol Med, Sch Med, New York, NY USA.
   [Ke, Zunfu; Li, Huabin] Sun Yat Sen Univ, Dept Pathol, Affiliated Hosp 1, Guangzhou, Guangdong, Peoples R China.
   [Li, Jian; Wei, Hong] Third Mil Med Univ, Coll Basic Med Sci, Dept Lab Anim Sci, Chongqing, Peoples R China.
   [Cui, Jun] Sun Yat Sen Univ, Sch Life Sci, Key Lab Gene Engn, State Key Lab Biocontrol,Minist Educ, Guangzhou, Guangdong, Peoples R China.
   [Cui, Shuzhong; Leng, Qibin] Guangzhou Med Univ, Affiliated Canc Hosp, State Key Lab Resp Dis, Guangzhou, Guangdong, Peoples R China.
   [Li, Xiaoxia] Cleveland Clin, Lerner Res Inst, Dept Inflammat & Immun, Cleveland, OH 44106 USA.
RP Xiao, H (corresponding author), Inst Pasteur Shanghai, 320 Yueyang Rd, Shanghai 200031, Peoples R China.; Li, HB (corresponding author), Fudan Univ, Affiliated Eye Ear Nose & Throat Hosp, 83 Fenyang Rd, Shanghai 200031, Peoples R China.
EM allergyli@163.com; huixiao@ips.ac.cn
OI Xiao, Hui/0000-0001-5304-243X; Cadwell, Ken/0000-0002-5860-0661
FU National Natural Science Foundation of ChinaNational Natural Science
   Foundation of China (NSFC) [81720108019, 81725004, 91542206, 31470847,
   31700784]; Strategic Priority Research Program of the Chinese Academy of
   SciencesChinese Academy of Sciences [XDB29030302]; Shanghai Municipal
   Science and Technology Major Project [2019SHZDZX02]; Key development and
   research project [2016YFA0502100]
FX This study was supported by the National Natural Science Foundation of
   China (81720108019, 81725004, 91542206, 31470847, and 31700784), the Key
   development and research project 2016YFA0502100, the Strategic Priority
   Research Program of the Chinese Academy of Sciences (XDB29030302), and
   the Shanghai Municipal Science and Technology Major Project
   (2019SHZDZX02).
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NR 79
TC 41
Z9 42
U1 9
U2 20
PU AMER SOC CLINICAL INVESTIGATION INC
PI ANN ARBOR
PA 2015 MANCHESTER RD, ANN ARBOR, MI 48104 USA
SN 0021-9738
EI 1558-8238
J9 J CLIN INVEST
JI J. Clin. Invest.
PD APR 1
PY 2020
VL 130
IS 4
BP 2111
EP 2128
DI 10.1172/JCI133264
PG 18
WC Medicine, Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Research & Experimental Medicine
GA LJ3XK
UT WOS:000530101000051
PM 31961824
OA Green Published, Bronze
DA 2022-04-25
ER

PT J
AU Rui, LX
   Shu, SY
   Jun, WJ
   Mo, CZ
   Wu, SZ
   Min, LS
   Yuan, L
   Yong, PJ
   Cheng, SZ
   Sheng, WS
   Yao, TZ
AF Rui, Li Xiao
   Shu, Song Yu
   Jun, Wu Jing
   Mo, Chen Zi
   Wu, Sun Zheng
   Min, Liu Shu
   Yuan, Lin
   Yong, Peng Jin
   Cheng, Song Zhi
   Sheng, Wang Shi
   Yao, Tang Ze
TI The dual induction of apoptosis and autophagy by SZC014, a synthetic
   oleanolic acid derivative, in gastric cancer cells via NF-kappa B
   pathway
SO TUMOR BIOLOGY
LA English
DT Article
DE SZC014; Oleanolic acid derivative; Apoptosis; Autophagy; NF-kappa B
   pathway; Gastric cancer cells
ID URSOLIC ACID; CARCINOMA; PROGRESSION; DEATH; COLON; CYCLE
AB Oleanolic acid (OA) possesses various pharmacological activities, such as antitumor and anti-inflammation; however, its clinical applications are limited by its relatively weak activities and low bioavailability. In this study, we evaluated the cytotoxic activity of seven novel OA derivatives, one of which, SZC014 [2-(pyrrolidine-1-yl) methyl-3-oxo-olean-12-en-28-oic acid], exhibited the strongest antitumor activity; its anticancer effect on gastric cancer cells and action mechanisms were investigated. The viability of OA and seven synthesized derivatives treating gastric cancer cells was detected using tetrazolium (MTT). Among them, SZC014 exhibited the strongest cytotoxic activity against gastric cancer cells (SGC7901, MGC803, and MKN-45). The effect of SZC014 on cell cycle was identified by propidium iodide (PI) staining assay. The cellular apoptosis induced by SZC014 was tested by annexin V/PI. The cellular morphological changes and ultrastructural structures affected by SZC014 were observed and imaged through inverted phase contrast microscope and transmission electron microscopy. Western blotting was performed to explore the expression of proteins associated with apoptosis (caspase 3, caspase 9, Bax, Bcl-2, and Bcl-xL), autophagy (Beclin 1 and ATG 5), and nuclear factor-kappa B (NF-kappa B) signal pathway, respectively. The cytotoxic activities of all the seven synthesized OA derivatives were stronger than that of OA against gastric cancer cells. SZC014 exhibited stronger cytotoxic activity than other OA derivatives, inhibited the proliferation of gastric cancer cells, besides, induced G2/M phase cell cycle arrest in SGC7901 cells. Both apoptosis and autophagy were found simultaneously in SZC014-treated SGC7901 cells. Caspase-dependent apoptosis induced by SZC014 was confirmed to be associated with upregulation of Bax and downregulation of Bcl-2 and Bcl-xL, while upregulation of Beclin 1 and ATG 5 was inferred to be involved in SZC014-induced autophagy. Moreover, treating cells with SZC014 resulted in a decrease in phosphorylation of I kappa B alpha and NF-kappa B/p65 and NF-kappa B/p65 nuclear translocation. The cytotoxic activities of seven OA derivatives were generally stronger than that of OA, among which, SZC014 possessed the most potent anticancer activity in SGC7901 cells and would be a promising chemotherapic agent for the treatment of gastric cancer.
C1 [Rui, Li Xiao; Shu, Song Yu; Jun, Wu Jing; Mo, Chen Zi; Wu, Sun Zheng; Min, Liu Shu; Yuan, Lin; Yong, Peng Jin; Yao, Tang Ze] Dalian Med Univ, Dept Pharmacol, Dalian, Peoples R China.
   [Cheng, Song Zhi; Sheng, Wang Shi] Dalian Univ Technol, Coll Pharmaceut Sci & Technol, Dalian, Peoples R China.
RP Yao, TZ (corresponding author), Dalian Med Univ, Dept Pharmacol, Dalian, Peoples R China.; Sheng, WS (corresponding author), Dalian Univ Technol, Coll Pharmaceut Sci & Technol, Dalian, Peoples R China.
EM wangss@dlut.edu.cn; zeyaotang@163.com
RI Sun, Zhengwu/AAJ-3126-2021
FU Natural Science Foundation of ChinaNational Natural Science Foundation
   of China (NSFC) [30772601]; University Innovation Team Project
   Foundation of Education Department of Liaoning Province [LT2013019]
FX This work was supported by the Natural Science Foundation of China (no.
   30772601) and the University Innovation Team Project Foundation of
   Education Department of Liaoning Province (no. LT2013019).
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NR 34
TC 16
Z9 17
U1 1
U2 19
PU SAGE PUBLICATIONS LTD
PI LONDON
PA 1 OLIVERS YARD, 55 CITY ROAD, LONDON EC1Y 1SP, ENGLAND
SN 1010-4283
EI 1423-0380
J9 TUMOR BIOL
JI Tumor Biol.
PD APR
PY 2016
VL 37
IS 4
BP 5133
EP 5144
DI 10.1007/s13277-015-4293-2
PG 12
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA DK4QS
UT WOS:000374904500095
PM 26547583
DA 2022-04-25
ER

PT J
AU Kaushik, G
   Ramalingam, S
   Subramaniam, D
   Rangarajanb, P
   Protti, P
   Rammamoorthy, P
   Anant, S
   Mammen, JMV
AF Kaushik, Gaurav
   Ramalingam, Satish
   Subramaniam, Dharmalingam
   Rangarajanb, Parthasarthy
   Protti, Piero
   Rammamoorthy, Prabhu
   Anant, Shrikant
   Mammen, Joshua M. V.
TI Honokiol induces cytotoxic and cytostatic effects in malignant melanoma
   cancer cells
SO AMERICAN JOURNAL OF SURGERY
LA English
DT Article
DE Melanoma; AKT; Cyclin D1; Cell-cycle arrest; AKT; mTOR; gamma-secretase
ID TUMOR-INITIATING CELLS; CYCLIN D1; COLON-CANCER; CUTANEOUS MELANOMA;
   EPITHELIAL-CELLS; KINASE; EXPRESSION; INHIBITORS; COMBINATION;
   ACTIVATION
AB BACKGROUND: Melanomas are aggressive neoplasms with limited therapeutic options. Therefore, developing new therapies with low toxicity is of utmost importance. Honokiol is a natural compound that recently has shown promise as an effective anticancer agent.
   METHODS: The effect of honokiol on melanoma cancer cells was assessed in vitro. Proliferation and physiologic changes were determined using hexosaminidase assay and transmission electron microscopy. Protein expression was assessed by immunoblotting.
   RESULTS: Honokiol treatment inhibited cell proliferation and induced death. Electron microscopy showed autophagosome formation. Reduced levels of cyclin D1 accompanied cell-cycle arrest. Honokiol also decreased phosphorylation of AKT (known as protein kinase B) and mammalian target of rapamycin, and inhibited gamma-secretase activity by down-regulating the expression of gamma-secretase complex proteins, especially anterior pharynx-defective 1.
   CONCLUSIONS: Honokiol is highly effective in inhibiting melanoma cancer cells by attenuating AKT/mammalian target of rapamycin and Notch signaling. These studies warrant further clinical evaluation for honokiol alone or with present chemotherapeutic regimens for the treatment of melanomas. (C) 2012 Elsevier Inc. All rights reserved.
C1 [Ramalingam, Satish; Subramaniam, Dharmalingam; Rangarajanb, Parthasarthy; Rammamoorthy, Prabhu; Anant, Shrikant; Mammen, Joshua M. V.] Univ Kansas, Med Ctr, Dept Mol & Integrat Physiol, Kansas City, KS 66103 USA.
   [Ramalingam, Satish; Subramaniam, Dharmalingam; Rangarajanb, Parthasarthy; Rammamoorthy, Prabhu; Anant, Shrikant; Mammen, Joshua M. V.] Univ Kansas, Ctr Canc, Kansas City, KS 66160 USA.
   [Kaushik, Gaurav; Protti, Piero; Mammen, Joshua M. V.] Univ Kansas, Med Ctr, Dept Surg, Kansas City, KS 66103 USA.
RP Anant, S (corresponding author), Univ Kansas, Med Ctr, Dept Mol & Integrat Physiol, Kansas City, KS 66103 USA.
EM sanant@kumc.edu
RI Anant, Shrikant/AAF-8020-2020; Ramalingam, Satish/H-1577-2018
OI Ramalingam, Satish/0000-0002-3076-279X
FU National Institutes of HealthUnited States Department of Health & Human
   ServicesNational Institutes of Health (NIH) - USA; Department of Surgery
   at the University of Kansas Medical Center; NATIONAL CANCER
   INSTITUTEUnited States Department of Health & Human ServicesNational
   Institutes of Health (NIH) - USANIH National Cancer Institute (NCI)
   [R01CA109269, R01CA135559] Funding Source: NIH RePORTER
FX Supported by grants from the National Institutes of Health (S.A.) and
   from the Department of Surgery at the University of Kansas Medical
   Center (J.M.V.M.).
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NR 33
TC 34
Z9 37
U1 0
U2 5
PU EXCERPTA MEDICA INC-ELSEVIER SCIENCE INC
PI BRIDGEWATER
PA 685 ROUTE 202-206 STE 3, BRIDGEWATER, NJ 08807 USA
SN 0002-9610
J9 AM J SURG
JI Am. J. Surg.
PD DEC
PY 2012
VL 204
IS 6
BP 868
EP 873
DI 10.1016/j.amjsurg.2012.09.001
PG 6
WC Surgery
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Surgery
GA 060UG
UT WOS:000312803000012
PM 23231930
OA Green Accepted
DA 2022-04-25
ER

PT J
AU Liu, YF
   Wu, L
   Li, K
   Liu, FR
   Wang, L
   Zhang, DL
   Zhou, J
   Ma, X
   Wang, SY
   Yang, SY
AF Liu, Yanfeng
   Wu, Lei
   Li, Kai
   Liu, Fengrui
   Wang, Li
   Zhang, Dongling
   Zhou, Jing
   Ma, Xuan
   Wang, Shengyu
   Yang, Shuanying
TI Ornithine aminotransferase promoted the proliferation and metastasis of
   non-small cell lung cancer via upregulation of miR-21
SO JOURNAL OF CELLULAR PHYSIOLOGY
LA English
DT Article
DE GSK-3; invasion and migration; miR-21; non-small cell lung cancer;
   ornithine aminotransferase; proliferation
ID ROS-DEPENDENT APOPTOSIS; COLON-CANCER; DIHYDROTANSHINONE; MECHANISMS;
   RESISTANCE; CRYPTOTANSHINONE; SENSITIVITY; MUTATIONS; CARCINOMA;
   AUTOPHAGY
AB The incidence and mortality of lung cancer ranked the first among all types of cancer in China, and non-small cell lung cancer (NSCLC) is the most common type of lung cancer accounting for 85% of all lung cancers. Given that the survival rate of patients with advanced NSCLC is still poor nowadays, identification of novel therapeutic targets and the development of effective therapies are desired for the treatment of NSCLC in clinics. In this study, we reported the upregulation of ornithine aminotransferase (OAT) in NSCLC cells and clinical tumor samples as well as its association with the advanced TNM stage, metastasis, and poor tumor differentiation of lung cancer. Using different NSCLC cell lines, we demonstrated that OAT promoted the proliferation, invasion, and migration, inhibited the apoptosis, and altered cell cycle of NSCLC cells; besides, the involvement of OAT-miR-21-glycogen synthase kinase-3 signaling in the functional role of OAT in NSCLC was also revealed. Importantly, in the absence of OAT, the growth and metastasis of tumor lung cancer xenograft was significantly suppressed in the nude mice. Based on our findings, OAT may be a potential novel biomarker for the diagnosis and therapeutic outcome monitoring of NSCLC. Inhibition of OAT may also represent a new therapeutic strategy of NSCLC.
C1 [Liu, Yanfeng; Yang, Shuanying] Xi An Jiao Tong Univ, Dept Resp Med, Affiliated Hosp 2, Xian, Shaanxi, Peoples R China.
   [Liu, Yanfeng; Li, Kai; Liu, Fengrui; Wang, Li; Zhang, Dongling] Xi An Jiao Tong Univ, Dept Emergency, Affiliated Hosp 1, Xian, Shaanxi, Peoples R China.
   [Wu, Lei] Xi An Jiao Tong Univ, Dept Med Affairs, Affiliated Hosp 1, Xian, Shaanxi, Peoples R China.
   [Zhou, Jing; Ma, Xuan; Wang, Shengyu] Xi An Jiao Tong Univ, Dept Resp Med, Affiliated Hosp 1, Xian, Shaanxi, Peoples R China.
RP Yang, SY (corresponding author), Xi An Jiao Tong Univ, Dept Resp Med, Affiliated Hosp 2, Xian, Shaanxi, Peoples R China.
EM yangshuanying66@163.com
FU Natural Science Basic Research Plan in Shaanxi Province of China
   [2017JM8094]; National Natural Science Foundation of ChinaNational
   Natural Science Foundation of China (NSFC) [81350032, 81672300]
FX Natural Science Basic Research Plan in Shaanxi Province of China,
   Grant/Award Number: 2017JM8094; National Natural Science Foundation of
   China, Grant/Award Numbers: 81350032, 81672300
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NR 29
TC 10
Z9 10
U1 2
U2 15
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0021-9541
EI 1097-4652
J9 J CELL PHYSIOL
JI J. Cell. Physiol.
PD AUG
PY 2019
VL 234
IS 8
BP 12828
EP 12838
DI 10.1002/jcp.27939
PG 11
WC Cell Biology; Physiology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Cell Biology; Physiology
GA HX2SA
UT WOS:000467240800061
PM 30549035
DA 2022-04-25
ER

PT J
AU Zhang, C
   Shi, J
   Mao, SY
   Xu, YS
   Zhang, D
   Feng, LY
   Zhang, B
   Yan, YY
   Wang, SC
   Pan, JP
   Yang, YP
   Lin, NM
AF Zhang, Chong
   Shi, Jing
   Mao, Shi-ying
   Xu, Ya-si
   Zhang, Dan
   Feng, Lin-yi
   Zhang, Bo
   Yan, You-you
   Wang, Si-cong
   Pan, Jian-ping
   Yang, You-ping
   Lin, Neng-ming
TI Role of p38 MAPK in enhanced human cancer cells killing by the
   combination of aspirin and ABT-737
SO JOURNAL OF CELLULAR AND MOLECULAR MEDICINE
LA English
DT Article
DE aspirin; ABT-737; combination; p38
ID DOUBLE-EDGED-SWORD; COLORECTAL-CANCER; LUNG-CANCER; IN-VITRO; AUTOPHAGY;
   APOPTOSIS; MCL-1; RISK; ACTIVATION; MULTIPLE
AB Regular use of aspirin after diagnosis is associated with longer survival among patients with mutated-PIK3CA colorectal cancer, but not among patients with wild-type PIK3CA cancer. In this study, we showed that clinically achievable concentrations of aspirin and ABT-737 in combination could induce a synergistic growth arrest in several human PIK3CA wild-type cancer cells. In addition, our results also demonstrated that long-term combination treatment with aspirin and ABT-737 could synergistically induce apoptosis both in A549 and H1299 cells. In the meanwhile, short-term aspirin plus ABT-737 combination treatment induced a greater autophagic response than did either drug alone and the combination-induced autophagy switched from a cytoprotective signal to a death-promoting signal. Furthermore, we showed that p38 acted as a switch between two different types of cell death (autophagy and apoptosis) induced by aspirin plus ABT-737. Moreover, the increased anti-cancer efficacy of aspirin combined with ABT-737 was further validated in a human lung cancer A549 xenograft model. We hope that this synergy may contribute to failure of aspirin cancer therapy and ultimately lead to efficacious regimens for cancer therapy.
C1 [Zhang, Chong; Mao, Shi-ying; Feng, Lin-yi; Wang, Si-cong; Pan, Jian-ping; Yang, You-ping] Zhejiang Univ City Coll, Sch Med, Hangzhou 310003, Zhejiang, Peoples R China.
   [Shi, Jing] Zhejiang Med Coll, Dept Pharm, Hangzhou, Zhejiang, Peoples R China.
   [Xu, Ya-si; Zhang, Dan; Zhang, Bo; Yan, You-you; Lin, Neng-ming] Hangzhou First Peoples Hosp, Inst Individualized Med, 261 Huansha Rd, Hangzhou 310006, Zhejiang, Peoples R China.
   [Zhang, Dan; Lin, Neng-ming] Zhejiang Chinese Med Univ, Affiliated Hangzhou Peoples Hosp 1, Hangzhou, Zhejiang, Peoples R China.
   [Lin, Neng-ming] Zhejiang Canc Hosp, Lab Clin Pharm, Hangzhou, Zhejiang, Peoples R China.
RP Lin, NM (corresponding author), Hangzhou First Peoples Hosp, Inst Individualized Med, 261 Huansha Rd, Hangzhou 310006, Zhejiang, Peoples R China.
EM lnm1013@163.com
RI zhang, chong/D-1812-2016
FU National Natural Science Foundation of ChinaNational Natural Science
   Foundation of China (NSFC) [81272473, 30872325, 81302806]; Zhejiang
   Provincial Foundation of National Science [LQ12H31001, LY12H16005];
   Science Research Foundation of Zhejiang Health Bureau; Ministry of
   Health [WKJ2012-2-022]; Science Research Foundation of Zhejiang Health
   Bureau [2012KYA068]; Zhejiang Provincial Program for the Cultivation of
   High-level Innovative Health talents [2010-190-4]; Excellent Young
   Teacher Project of Education Department of Zhejiang Province
   [Ij2013015]; Student Research Fund of Zhejiang University City College
   [X2014562119]; Scientific and Technological Developing Scheme of
   Hangzhou City [20130633B34, 20130633B33]
FX The authors gratefully acknowledge financial support from National
   Natural Science Foundation of China (81272473, 30872325, 81302806),
   Zhejiang Provincial Foundation of National Science (LQ12H31001,
   LY12H16005), Science Research Foundation of Zhejiang Health Bureau & the
   Ministry of Health (WKJ2012-2-022), Science Research Foundation of
   Zhejiang Health Bureau (2012KYA068), Zhejiang Provincial Program for the
   Cultivation of High-level Innovative Health talents (2010-190-4),
   Excellent Young Teacher Project of Education Department of Zhejiang
   Province (Ij2013015), Student Research Fund of Zhejiang University City
   College (X2014562119), Scientific and Technological Developing Scheme of
   Hangzhou City (20130633B34, 20130633B33). Chong Zhang, Jing Shi,
   Shi-ying Mao, Lin-yi Feng and You-ping Yang performed the research;
   Neng-ming Lin and Jian-ping Pan designed the research study; You-you Yan
   and Si-cong Wang contributed essential reagents or tools; Bo Zhang,
   Ya-si Xu and Dan Zhang analysed the data; Chong Zhang and Bo Zhang wrote
   the paper.
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NR 27
TC 27
Z9 28
U1 3
U2 19
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
EI 1582-4934
J9 J CELL MOL MED
JI J. Cell. Mol. Med.
PD FEB
PY 2015
VL 19
IS 2
BP 408
EP 417
DI 10.1111/jcmm.12461
PG 10
WC Cell Biology; Medicine, Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Cell Biology; Research & Experimental Medicine
GA CA7NQ
UT WOS:000349104500012
PM 25388762
OA gold, Green Published
DA 2022-04-25
ER

PT J
AU Koustas, E
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   Mihailidou, C
   Schizas, D
   Papavassiliou, AG
AF Koustas, Evangelos
   Karamouzis, Michalis V.
   Mihailidou, Chrysovalantou
   Schizas, Dimitrios
   Papavassiliou, Athanasios G.
TI Co-targeting of EGFR and autophagy signaling is an emerging treatment
   strategy in metastatic colorectal cancer
SO CANCER LETTERS
LA English
DT Review
DE Colorectal cancer; Epidermal growth factor receptor; Autophagy;
   Endocytosis; Panitumumab; Cetuximab
ID GROWTH-FACTOR RECEPTOR; ACQUIRED-RESISTANCE; MONOCLONAL-ANTIBODY;
   NUCLEAR TRANSLOCATION; PREDICTIVE BIOMARKER; CELL-SURVIVAL; RAB GTPASES;
   CETUXIMAB; PROTEIN; MECHANISMS
AB The epidermal growth factor receptor (EGFR) and its associated pathway is a critical key regulator of CRC development and progression. The monoclonal antibodies (MoAbs) cetuximab and panitumumab, directed against EGFR, represent a major step forward in the treatment of metastatic colorectal cancer (mCRC), in terms of progression-free survival and overall survival in several clinical trials. However, the activity of anti-EGFR MoAbs appears to be limited to a subset of patients with mCRC. Studies have highlighted that acquired-resistance to anti-EGFR MoAbs biochemically converge into Ras/Raf/Mek/Erk and PI3K/Akt/mTOR pathways. Recent data also suggest that acquired-resistance to anti-EGFR MoAbs is accompanied by inhibition of EGFR internalization, ubiqutinization, degradation and prolonged down regulation. It is well established that autophagy, a self-cannibalization process, is considered to be associated with resistance to the anti-EGFR MoAbs therapy. Additionally, autophagy induced by anti-EGFR MoAbs acts as a protective response in cancer cells. Thus, inhibition of autophagy after treatment with EGFR MoAbs can result in autophagic cell death. A combination therapy comprising of anti-EGFR MoAbs and autophagy inhibitors would represent a multi-pronged approach that could be evolved into an active therapeutic strategy in mCRC patients. (C) 2017 Elsevier B.V. All rights reserved.
C1 [Koustas, Evangelos; Karamouzis, Michalis V.; Mihailidou, Chrysovalantou; Papavassiliou, Athanasios G.] Univ Athens, Mol Oncol Unit, Dept Biol Chem, Med Sch, Athens 11527, Greece.
   [Schizas, Dimitrios] Univ Athens, Dept Surg 1, Med Sch, Athens 11527, Greece.
RP Karamouzis, MV; Papavassiliou, AG (corresponding author), Univ Athens, Dept Biol Chem, Med Sch, 75,M Asias St, Athens 11527, Greece.
EM mkaramouz@med.uoa.gr; papavas@med.uoa.gr
RI Karamouzis, Michalis/AAD-2860-2020; SCHIZAS, DIMITRIOS/Z-3323-2019;
   Koustas, Evangelos/ABE-9336-2020
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NR 101
TC 41
Z9 42
U1 1
U2 38
PU ELSEVIER IRELAND LTD
PI CLARE
PA ELSEVIER HOUSE, BROOKVALE PLAZA, EAST PARK SHANNON, CO, CLARE, 00000,
   IRELAND
SN 0304-3835
EI 1872-7980
J9 CANCER LETT
JI Cancer Lett.
PD JUN 28
PY 2017
VL 396
BP 94
EP 102
DI 10.1016/j.canlet.2017.03.023
PG 9
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA EU0QB
UT WOS:000400715200010
PM 28323034
DA 2022-04-25
ER

PT J
AU Jin, H
   Seo, GS
   Lee, SH
AF Jin, Hao
   Seo, Geom Seog
   Lee, Sung Hee
TI Isoliquiritigenin-mediated p62/SQSTM1 induction regulates apoptotic
   potential through attenuation of caspase-8 activation in colorectal
   cancer cells
SO EUROPEAN JOURNAL OF PHARMACOLOGY
LA English
DT Article
DE Isoliquiritigenin; Colorectal cancer cell; Apoptosis; p62/SQSTM1;
   Caspase-8; 5-Fluorouracil
ID UP-REGULATION; AUTOPHAGY; TUMORIGENESIS; EXPRESSION; LICORICE; SURVIVAL
AB Isoliquiritigenin (ISL) is a natural flavonoid that exhibits anticancer properties in various carcinoma cell types. However, the precise mechanism responsible for its anticancer activity has not been elucidated fully. In the present study, we examined ISL-mediated apoptotic mechanisms in colorectal cancer (CRC) cells. ISL induced apoptosis in human HCT-116 cells and caused marked induction of p62/SQSTM1 mRNA and protein expression. Similarly, ISL potently inhibited in vivo tumor growth and induced p62/SQSTM1 expression in xenograft tumor tissues. In a p62/SQSTM1 siRNA transfection study, ISL-induced p62/SQSTM1 expression attenuated ISL-mediated apoptosis by reducing caspase-8 activation. ISL potentiated the apoptotic effects of 5-fluorouracil (5-FU) on HCT-116 cells. However, ISL-induced p62/SQSTM1 expression also attenuated the potency of apoptosis induced by the combination of 5-FU and ISL. Our results demonstrate that ISL-induced p62/SQSTM1 upregulation affects ISL-mediated apoptotic potential through attenuation of caspase-8 activation in CRC cells. These findings broaden the understanding of the molecular basis of ISL-mediated apoptosis.
C1 [Jin, Hao; Lee, Sung Hee] Wonkwang Univ, Coll Pharm, Inst Pharmaceut Res & Dev, Jeonbuk 54538, South Korea.
   [Seo, Geom Seog] Wonkwang Univ, Coll Med, Digest Dis Res Inst, Jeonbuk 54538, South Korea.
RP Lee, SH (corresponding author), Wonkwang Univ, Coll Pharm, 460 Iksandae Ro, Iksan 54538, South Korea.
EM gsseo@wku.ac.kr
FU National Research Foundation of Korea (NRF) - Korea government (Ministry
   of Science, ICT & Future Planning) [2016R1A2B4009121]
FX This work was supported by the National Research Foundation of Korea
   (NRF) grant funded by the Korea government (Ministry of Science, ICT &
   Future Planning) (2016R1A2B4009121).
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NR 30
TC 9
Z9 11
U1 4
U2 17
PU ELSEVIER
PI AMSTERDAM
PA RADARWEG 29, 1043 NX AMSTERDAM, NETHERLANDS
SN 0014-2999
EI 1879-0712
J9 EUR J PHARMACOL
JI Eur. J. Pharmacol.
PD DEC 15
PY 2018
VL 841
BP 90
EP 97
DI 10.1016/j.ejphar.2018.10.015
PG 8
WC Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA HA5MK
UT WOS:000450316400011
PM 30339814
DA 2022-04-25
ER

PT J
AU Chang, JZ
   Chen, SD
   Zheng, H
   Zhang, HP
AF Chang, Jin-Zhe
   Chen, Shu-Dong
   Zheng, Hui
   Zhang, Hua-Ping
TI Downregulation of transcription factor EB inhibits the growth and
   metastasis of colorectal carcinomas
SO EUROPEAN JOURNAL OF INFLAMMATION
LA English
DT Article
DE colorectal carcinoma; metastasis; TFEB; xenograft tumor model
ID LYSOSOMAL BIOGENESIS; CANCER STATISTICS; MITF/TFE FAMILY; TFEB;
   AUTOPHAGY
AB To determine the roles of transcription factor EB (TFEB) in colorectal cancer (CRC), we collected samples of tumor tissues and normal tissues from 40 patients with CRC. The expression of TFEB in these samples was analyzed by using quantitative real-time polymerase chain reaction (qRT-PCR) and Western blot. Furthermore, we explored the expression of TFEB mRNA in CCD-18Co normal cells and HT-29, HCT-8, C2BBe1 cancer cells. HT-29, HCT-8, and C2BBe1 cancer cells were transfected with a TFEB-specific small interference RNA (siRNA) and scrambled siRNA, then the TFEB expression was confirmed by Western blot. The migration and invasion abilities of cells transfected with TFEB-siRNA were examined by transwell method and wound-healing assay. The subsequent effect of TFEB silencing on the tumor growth was also detected in mice xenograft model in vivo. Our study found that TFEB expression was significantly increased (P < 0.05) in colorectal tumor tissues compared with normal tissues. Consistent with TFEB expression in tissues, compared with the normal CCD-18Co cells, TFEB mRNA expression was also significantly augmented in CRC cells. TFEB protein expression was markedly reduced in HT-29, HCT-8, and C2BBe1 cells after TFEB-siRNA transfection. In addition, inhibition of TFEB expression resulted in decrease of cells migration and invasion abilities. In vivo study, compared with the negative control group, the tumor weight, and volume were also reduced after inhibiting the TFEB expression. Our research suggested that TFEB expression is related to the occurrence and development of colorectal adenocarcinoma. The migration and invasion abilities of cancer cells, the weight and volume of tumor were all decreased when inhibiting TFEB expression. Thus, TFEB serves as an important factor in the development of CRC by modulating cancer cell migration and invasion, showing the potential therapeutic target of CRC in clinical.
C1 [Chang, Jin-Zhe] Guangrao Cty Peoples Hosp, Dept Gen Surg, Dongying, Peoples R China.
   [Chen, Shu-Dong; Zheng, Hui; Zhang, Hua-Ping] Qingdao Univ, Yuhuangding Hosp, 2 Gastrointestinal Surg, 20 Yuhuangding East Rd, Yantai 264000, Peoples R China.
RP Zhang, HP (corresponding author), Qingdao Univ, Yuhuangding Hosp, 2 Gastrointestinal Surg, 20 Yuhuangding East Rd, Yantai 264000, Peoples R China.
EM zhanghuapinghpp@163.com
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NR 23
TC 0
Z9 0
U1 0
U2 0
PU SAGE PUBLICATIONS INC
PI THOUSAND OAKS
PA 2455 TELLER RD, THOUSAND OAKS, CA 91320 USA
SN 1721-727X
EI 2058-7392
J9 EUR J INFLAMM
JI Eur. J. Inflamm.
PD OCT 17
PY 2018
VL 16
AR 2058739218805333
DI 10.1177/2058739218805333
PG 9
WC Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology
GA HE8ZV
UT WOS:000453737400001
OA gold
DA 2022-04-25
ER

PT J
AU Kijima, T
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   Omoto, I
   Kita, Y
   Muto, M
   Bass, AJ
   Diehl, JA
   Ginsberg, GG
   Doki, Y
   Mori, M
   Uchikado, Y
   Arigami, T
   Avadhani, NG
   Basu, D
   Rustgi, AK
   Natsugoe, S
AF Kijima, Takashi
   Nakagawa, Hiroshi
   Shimonosono, Masataka
   Chandramouleeswaran, Prasanna M.
   Hara, Takeo
   Sahu, Varun
   Kasagi, Yuta
   Kikuchi, Osamu
   Tanaka, Koji
   Giroux, Veronique
   Muir, Amanda B.
   Whelan, Kelly A.
   Ohashi, Shinya
   Naganuma, Seiji
   Klein-Szanto, Andres J.
   Shinden, Yoshiaki
   Sasaki, Ken
   Omoto, Itaru
   Kita, Yoshiaki
   Muto, Manabu
   Bass, Adam J.
   Diehl, J. Alan
   Ginsberg, Gregory G.
   Doki, Yuichiro
   Mori, Masaki
   Uchikado, Yasuto
   Arigami, Takaaki
   Avadhani, Narayan G.
   Basu, Devraj
   Rustgi, Anil K.
   Natsugoe, Shoji
TI Three-Dimensional Organoids Reveal Therapy Resistance of Esophageal and
   Oropharyngeal Squamous Cell Carcinoma Cells
SO CELLULAR AND MOLECULAR GASTROENTEROLOGY AND HEPATOLOGY
LA English
DT Article
DE 3D Organoids; Autophagy; CD44; 5-Fluorouracil
ID CANCER; SURGERY; PROTEIN; MODELS; COLON
AB We have established 3 dimensional organoids from patients with esophageal and oropharyngeal squamous cell carcinomas. We show that 3-dimensional organoids reveal resistance mechanisms and provide a robust platform to predict therapy response in the setting of personalized medicine.
   BACKGROUND & AIMS: Oropharyngeal and esophageal squamous cell carcinomas, especially the latter, are a lethal disease, featuring intratumoral cancer cell heterogeneity and therapy resistance. To facilitate cancer therapy in personalized medicine, three-dimensional (3D) organoids may be useful for functional characterization of cancer cells ex vivo. We investigated the feasibility and the utility of patient-derived 3D organoids of esophageal and oropharyngeal squamous cell carcinomas.
   METHODS: We generated 3D organoids from paired biopsies representing tumors and adjacent normal mucosa from therapy-naive patients and cell lines. We evaluated growth and structures of 3D organoids treated with 5-fluorouracil ex vivo.
   RESULTS: Tumor-derived 3D organoids were grown successfully from 15 out of 21 patients (71.4%) and passaged with recapitulation of the histopathology of the original tumors. Successful formation of tumor-derived 3D organoids was associated significantly with poor response to presurgical neoadjuvant chemotherapy or chemoradiation therapy in informative patients (P = 0.0357, progressive and stable diseases, n = 10 vs. partial response, n = 6). The 3D organoid formation capability and 5-fluorouracil resistance were accounted for by cancer cells with high CD44 expression and autophagy, respectively. Such cancer cells were found to be enriched in patient-derived 3D organoids surviving 5-fluorouracil treatment.
   CONCLUSIONS: The single cell-based 3D organoid system may serve as a highly efficient platform to explore cancer therapeutics and therapy resistance mechanisms in conjunction with morphological and functional assays with implications for translation in personalized medicine.
C1 [Kijima, Takashi; Shimonosono, Masataka; Shinden, Yoshiaki; Sasaki, Ken; Omoto, Itaru; Kita, Yoshiaki; Uchikado, Yasuto; Arigami, Takaaki; Natsugoe, Shoji] Kagoshima Univ, Grad Sch Med & Dent Sci, Dept Digest Surg Breast & Thyroid Surg, 8-35-1 Sakuragaoka, Kagoshima 8908520, Japan.
   [Kijima, Takashi; Avadhani, Narayan G.] Univ Penn, Sch Vet Med, Dept Biomed Sci, Philadelphia, PA 19104 USA.
   [Nakagawa, Hiroshi; Shimonosono, Masataka; Chandramouleeswaran, Prasanna M.; Tanaka, Koji; Giroux, Veronique; Whelan, Kelly A.; Ginsberg, Gregory G.; Rustgi, Anil K.] Univ Penn, Perelman Sch Med, Dept Med, Div Gastroenterol, 951 Biomed Res Bldg,421 Curie Blvd, Philadelphia, PA 19104 USA.
   [Nakagawa, Hiroshi; Shimonosono, Masataka; Chandramouleeswaran, Prasanna M.; Tanaka, Koji; Giroux, Veronique; Whelan, Kelly A.; Ginsberg, Gregory G.; Rustgi, Anil K.] Univ Penn, Abramson Canc Ctr, Philadelphia, PA 19104 USA.
   [Hara, Takeo; Tanaka, Koji; Doki, Yuichiro; Mori, Masaki] Osaka Univ, Grad Sch Med, Dept Gastroenterol Surg, Osaka, Japan.
   [Sahu, Varun; Basu, Devraj] Univ Penn, Perelman Sch Med, Dept Otorhinolaryngol, Philadelphia, PA 19104 USA.
   [Kasagi, Yuta; Muir, Amanda B.] Childrens Hosp Philadelphia, Div Pediat Gastroenterol Hepatol & Nutr, Philadelphia, PA 19104 USA.
   [Kikuchi, Osamu; Ohashi, Shinya; Muto, Manabu] Kyoto Univ, Grad Sch Med, Dept Therapeut Oncol, Kyoto, Japan.
   [Kikuchi, Osamu; Bass, Adam J.] Harvard Med Sch, Dept Med, Dana Farber Canc Inst, Boston, MA USA.
   [Whelan, Kelly A.] Temple Univ, Lewis Katz Sch Med, Fels Inst Canc Res & Mol Biol, Philadelphia, PA 19122 USA.
   [Naganuma, Seiji] Kochi Univ, Dept Pathol, Sch Med, Nankoku, Kochi, Japan.
   [Klein-Szanto, Andres J.] Fox Chase Canc Ctr, Histopathol Facil & Canc Biol Program, 7701 Burholme Ave, Philadelphia, PA 19111 USA.
   [Diehl, J. Alan] Med Univ South Carolina, Hollings Canc Ctr, Dept Biochem & Mol Biol, Charleston, SC 29425 USA.
RP Natsugoe, S (corresponding author), Kagoshima Univ, Grad Sch Med & Dent Sci, Dept Digest Surg Breast & Thyroid Surg, 8-35-1 Sakuragaoka, Kagoshima 8908520, Japan.; Rustgi, AK (corresponding author), Univ Penn, Perelman Sch Med, Dept Med, Div Gastroenterol, 951 Biomed Res Bldg,421 Curie Blvd, Philadelphia, PA 19104 USA.; Nakagawa, H (corresponding author), Univ Penn, Perelman Sch Med, Dept Med, Cell Culture & iPS Core,Div Gastroenterol, 956 Biomed Res Bldg,421 Curie Blvd, Philadelphia, PA 19104 USA.
EM nakagawh@pennmedicine.upenn.edu; anil2@pennmedicine.upenn.edu;
   natsugoe@m2.kufm.kagoshima-u.ac.jp
RI Ohashi, Shinya/AAD-8920-2022
OI Nakagawa, Hiroshi/0000-0001-7330-4863; Kijima,
   Takashi/0000-0003-1681-7069; Hara, Takeo/0000-0001-6591-0759; Kikuchi,
   Osamu/0000-0001-5012-5897
FU Ministry of Education, Culture, Sports, Science and Technology of
   JapanMinistry of Education, Culture, Sports, Science and Technology,
   Japan (MEXT) [17H04285, 15K10108]; NIHUnited States Department of Health
   & Human ServicesNational Institutes of Health (NIH) - USA [P01CA098101,
   U54CA163004, R01DK114436, R01AA026297, R01AA022986]; University of
   Pennsylvania Center of Excellence in Environmental Toxicology
   [K01DK103953, F32CA174176, T32DK007066, K08DK106444, P30ES013508];
   American Cancer SocietyAmerican Cancer Society [RP-10-033-01-CCE];
   NIH/NIDDK Center of Molecular Studies in Digestive and Liver Diseases
   [P30DK050306]; Japan Society for the Promotion of Science Postdoctoral
   FellowshipMinistry of Education, Culture, Sports, Science and
   Technology, Japan (MEXT)Japan Society for the Promotion of Science;
   Fonds de Recherche du Quebec - Sante Postdoctoral Fellowship
   [P-Giroux-27692, P-Giroux-31601]; Molecular Pathology and Imaging,
   Molecular Biology/Gene Expression, Cell Culture/iPS and Mouse Core
   Facilities; NATIONAL CANCER INSTITUTEUnited States Department of Health
   & Human ServicesNational Institutes of Health (NIH) - USANIH National
   Cancer Institute (NCI) [P01CA098101, U54CA163004] Funding Source: NIH
   RePORTER; NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY
   DISEASESUnited States Department of Health & Human ServicesNational
   Institutes of Health (NIH) - USANIH National Institute of Diabetes &
   Digestive & Kidney Diseases (NIDDK) [K08DK106444, R01DK114436,
   K01DK103953, P30DK050306, T32DK007066] Funding Source: NIH RePORTER;
   NATIONAL INSTITUTE OF ENVIRONMENTAL HEALTH SCIENCESUnited States
   Department of Health & Human ServicesNational Institutes of Health (NIH)
   - USANIH National Institute of Environmental Health Sciences (NIEHS)
   [P30ES013508] Funding Source: NIH RePORTER; NATIONAL INSTITUTE ON
   ALCOHOL ABUSE AND ALCOHOLISMUnited States Department of Health & Human
   ServicesNational Institutes of Health (NIH) - USANIH National Institute
   on Alcohol Abuse & Alcoholism (NIAAA) [R01AA026297, R01AA022986] Funding
   Source: NIH RePORTER
FX This study was supported by the Grant-in-Aid for challenging Exploratory
   Research, Grant in Aid for Scientific Research B and Grant in Aid for
   Scientific Research C from the Ministry of Education, Culture, Sports,
   Science and Technology of Japan (17H04285 to SN; and 15K10108 to YK).
   This study was also supported by the following NIH Grants: P01CA098101
   (HN, KT, KAW, VG, AJK, AB, JAD, AKR), U54CA163004 (HN, GGG, AKR),
   R01DK114436 (HN), R01AA026297 (HN), R01AA022986 (NGA), P30ES013508
   University of Pennsylvania Center of Excellence in Environmental
   Toxicology (HN and AKR), K01DK103953 (KAW), F32CA174176 (KAW),
   T32DK007066 (KAW), K08DK106444 (ABM), the American Cancer Society
   RP-10-033-01-CCE (AKR), NIH/NIDDK P30DK050306 Center of Molecular
   Studies in Digestive and Liver Diseases, The Molecular Pathology and
   Imaging, Molecular Biology/Gene Expression, Cell Culture/iPS and Mouse
   Core Facilities. KT is a recipient of the Japan Society for the
   Promotion of Science Postdoctoral Fellowship. VG is a recipient of the
   Fonds de Recherche du Quebec - Sante Postdoctoral Fellowship
   (P-Giroux-27692 and P-Giroux-31601).
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NR 48
TC 52
Z9 53
U1 5
U2 13
PU ELSEVIER INC
PI SAN DIEGO
PA 525 B STREET, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 2352-345X
J9 CELL MOL GASTROENTER
JI Cell. Mol. Gastroenterol. Hepatol.
PY 2019
VL 7
IS 1
BP 73
EP 91
DI 10.1016/j.jcmgh.2018.09.003
PG 19
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA HF4DF
UT WOS:000454182700005
PM 30510992
OA gold, Green Published
DA 2022-04-25
ER

PT J
AU Zhang, W
   Yuan, WT
   Song, JM
   Wang, SJ
   Gu, XM
AF Zhang, Wei
   Yuan, Weitang
   Song, Junmin
   Wang, Shijun
   Gu, Xiaoming
TI LncRNA CPS1-IT1 suppresses EMT and metastasis of colorectal cancer by
   inhibiting hypoxia-induced autophagy through inactivation of HIF-1 alpha
SO BIOCHIMIE
LA English
DT Article
DE CPS1 intronic transcript 1 (CPS1-IT1); Colorectal carcinoma (CRC);
   Hypoxia-inducible factor-1 alpha (HIF-1 alpha); Epithelial-mesenchymal
   transition (EMT); Autophagy
ID INDUCIBLE FACTOR-1-ALPHA; POOR-PROGNOSIS; NECK-CANCER; EXPRESSION; RNA;
   CELLS; HIF-1; GENE; HEAD; COEXPRESSION
AB Objective: Hypoxia is a common phenomenon in solid tumor microenvironment. Thereby, the aim of this study was to investigate the molecular mechanisms of tumor metastasis and epithelial-mesenchymal transition (EMT) regulated by lncRNA CPS1 intronic transcript 1 (CPS1-IT1) under hypoxia in CRC.
   Methods: Expression of lncRNA CPS1-IT1, hypoxia-inducible factor-1 alpha (HIF-1 alpha) and autophagy related protein (LC3) were initially assessed in human CRC tissues and in a series of CRC cell lines. The relationship of CPS1-IT1, HIF-1 alpha and autophagy were analyzed in CRC were performed through in vitro and in vivo functional assays.
   Results: Expression of CPS1-IT1 were significantly reduced, while HIF-1 alpha and LC3-II were increased in CRC tissues and cell lines. Then, in vitro assays revealed that CPS1-IT1 suppresses EMT and autophagy by inhibiting the activation of HIF-1 alpha in CRC. An in vivo animal model also demonstrated the tumor suppressor mechanism of CPS1-IT1.
   Conclusion: In this study, we found that hypoxia induce autophagy, and inhibition of autophagy could suppress tumor metastasis and EMT in CRC. Additionally, lncRNA CPS1-IT might suppresses metastasis and EMT by inhibiting hypoxia-induced autophagy through inactivation of HIF-1 alpha in CRC. (C) 2017 Elsevier B.V. and Societe Francaise de Biochimie et Biologie Moleculaire (SFBBM). All rights reserved.
C1 [Zhang, Wei; Yuan, Weitang; Song, Junmin; Wang, Shijun; Gu, Xiaoming] Zhengzhou Univ, Affiliated Hosp 1, Dept Colorectal & Anal Surg, 1 Jianshe East Rd, Zhengzhou 450052, Henan, Peoples R China.
RP Zhang, W (corresponding author), Zhengzhou Univ, Affiliated Hosp 1, Dept Colorectal & Anal Surg, 1 Jianshe East Rd, Zhengzhou 450052, Henan, Peoples R China.
EM weiwei509@yeah.net
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NR 39
TC 55
Z9 57
U1 1
U2 11
PU ELSEVIER FRANCE-EDITIONS SCIENTIFIQUES MEDICALES ELSEVIER
PI ISSY-LES-MOULINEAUX
PA 65 RUE CAMILLE DESMOULINS, CS50083, 92442 ISSY-LES-MOULINEAUX, FRANCE
SN 0300-9084
EI 1638-6183
J9 BIOCHIMIE
JI Biochimie
PD JAN
PY 2018
VL 144
BP 21
EP 27
DI 10.1016/j.biochi.2017.10.002
PG 7
WC Biochemistry & Molecular Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology
GA FQ6TH
UT WOS:000418496400003
PM 29017924
DA 2022-04-25
ER

PT J
AU Papadia, P
   Barozzi, F
   Hoeschele, JD
   Piro, G
   Margiotta, N
   Di Sansebastiano, GP
AF Papadia, Paride
   Barozzi, Fabrizio
   Hoeschele, James D.
   Piro, Gabriella
   Margiotta, Nicola
   Di Sansebastiano, Gian-Pietro
TI Cisplatin, Oxaliplatin, and Kiteplatin Subcellular Effects Compared in a
   Plant Model
SO INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
LA English
DT Article
DE cytoskeleton; vacuoles; transgenic Arabidopsis; cisplatin; kiteplatin;
   oxaliplatin
ID ANTITUMOR-ACTIVITY; ARABIDOPSIS-THALIANA; AUTOPHAGY; CANCER; PROTEIN;
   DRUGS; COMPLEXES; ANTICANCER; RESISTANCE; TRANSPORT
AB The immediate visual comparison of platinum chemotherapeutics' effects in eukaryotic cells using accessible plant models of transgenic Arabidopsis thaliana is reported. The leading anticancer drug cisplatin, a third generation drug used for colon cancer, oxaliplatin and kiteplatin, promising Pt-based anticancer drugs effective against resistant lines, were administered to transgenic A. thaliana plants monitoring their effects on cells from different tissues. The transgenic plants' cell cytoskeletons were labelled by the green fluorescent protein (GFP)-tagged microtubule-protein TUA6 (TUA6-GFP), while the vacuolar organization was evidenced by two soluble chimerical GFPs (GFPChi and AleuGFP) and one transmembrane GFP-tagged tonoplast intrinsic protein 1-1 (TIP1.1-GFP). The three drugs showed easily recognizable effects on plant subcellular organization, thereby providing evidence for a differentiated drug targeting. Genetically modified A. thaliana are confirmed as a possible rapid and low-cost screening tool for better understanding the mechanism of action of human anticancer drugs.
C1 [Papadia, Paride; Barozzi, Fabrizio; Piro, Gabriella; Di Sansebastiano, Gian-Pietro] Univ Salento, Dept Biotechnol & Environm Sci, Via Monteroni Ctr Ecotekne, I-73100 Lecce, Italy.
   [Hoeschele, James D.] Eastern Michigan Univ, Dept Chem, Ypsilanti, MI 48197 USA.
   [Margiotta, Nicola] Univ Bari Aldo Moro, Dept Chem, Via E Orabona 4, I-70125 Bari, Italy.
RP Di Sansebastiano, GP (corresponding author), Univ Salento, Dept Biotechnol & Environm Sci, Via Monteroni Ctr Ecotekne, I-73100 Lecce, Italy.; Margiotta, N (corresponding author), Univ Bari Aldo Moro, Dept Chem, Via E Orabona 4, I-70125 Bari, Italy.
EM paride.papadia@unisalento.it; fabrizio.barozzi@unisalento.it;
   hoeschel@chemistry.msu.edu; gabriella.piro@unisalento.it;
   nicola.margiotta@uniba.it; gp.disansebastiano@unisalento.it
RI Papadia, Paride/AAC-9472-2021; Barozzi, Fabrizio/AAY-9844-2021; Di
   Sansebastiano, Gian Pietro/I-7193-2012; Margiotta, Nicola/AAE-3975-2021
OI Papadia, Paride/0000-0001-9611-3824; Barozzi,
   Fabrizio/0000-0003-1409-2324; Di Sansebastiano, Gian
   Pietro/0000-0001-5388-0695; Margiotta, Nicola/0000-0003-4034-875X
FU Italian Ministero dell'Universita e della; European UnionEuropean
   Commission [COST CM1105]
FX Paride Papadia would like to thank the Italian Ministero dell'Universita
   e della Ricerca for ex-60% funds. Gian-Pietro Di Sansebastiano would
   like to thank project no14 "Reti di Laboratori Pubblici di ricerca,
   SELGE", Regione Puglia. Nicola Margiotta would like to thank the
   University of Bari (Italy), the Italian Ministero dell'Universita e
   della Ricerca, the Inter-University Consortium for Research on the
   Chemistry of Metal Ions in Biological Systems (C.I.R.C.M.S.B.), and the
   European Union (COST CM1105: Functional metal complexes that bind to
   biomolecules) for support.
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NR 54
TC 3
Z9 4
U1 0
U2 9
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 1422-0067
J9 INT J MOL SCI
JI Int. J. Mol. Sci.
PD FEB
PY 2017
VL 18
IS 2
AR 306
DI 10.3390/ijms18020306
PG 13
WC Biochemistry & Molecular Biology; Chemistry, Multidisciplinary
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Chemistry
GA EM6YD
UT WOS:000395457700075
PM 28146116
OA Green Published, Green Submitted, gold
DA 2022-04-25
ER

PT J
AU Xie, GY
   Sun, LX
   Li, YL
   Chen, BC
   Wang, C
AF Xie, Gangyin
   Sun, Linxiao
   Li, Yonglin
   Chen, Bicheng
   Wang, Cheng
TI Periplocin inhibits the growth of pancreatic cancer by inducing
   apoptosis via AMPK-mTOR signaling
SO CANCER MEDICINE
LA English
DT Article
DE apoptosis; pancreatic cancer; Periplocin; proliferation
ID ACTIVATED PROTEIN-KINASE; COLON-CANCER; CELL-GROWTH; IN-VITRO;
   AUTOPHAGY; DEATH; VIVO; PATHWAY
AB Background Periplocin is a monomeric compound that exhibits anti-tumor activities. It is extracted from Cortex Periplocae.
   Objective This study aimed at determining the effect of periplocin treatment on the apoptosis and proliferation of human pancreatic cancer cells, and to elucidate on its mechanisms of action.
   Methods PANC1 and cfpac1 cells were treated with periplocin. Cell proliferation was detected by RTCA, Ki67 immunofluorescence, and a clonogenic assay. The transwell assay was used to examine cell migration and invasion functions. The expression of apoptosis-associated proteins was detected by flow cytometry and western blotting. Total RNA was extracted from the treated and untreated group of PANC1 cells for RNA-seq detection and analysis. Differentially expressed genes were screened for GO biological process and KEGG pathway analysis. Finally, CFPAC1 cells were subcutaneously inoculated into BALB / c nude mice to assess tumor growth.
   Results Periplocin inhibited the proliferation of PANC1 and CFPAC1 cells and induced their apoptosis by activating the AMPK/mTOR pathway and inhibiting p70 S6K. It also attenuated the cell migration, invasion, and inhibited the growth of cfpac1 xenografts in nude mice.
   Conclusions Periplocin inhibits human pancreatic cancer cell proliferation and induces their apoptosis by activating the AMPK / mTOR pathway.
C1 [Xie, Gangyin; Sun, Linxiao; Li, Yonglin; Chen, Bicheng; Wang, Cheng] Wenzhou Med Univ, Affiliated Hosp 1, Key Lab Diag & Treatment Severe Hepatopancreat Di, Zhejiang Prov Top Key Discipline Surg, Wenzhou, Zhejiang, Peoples R China.
RP Chen, BC; Wang, C (corresponding author), Wenzhou Med Univ, Affiliated Hosp 1, Key Lab Diag & Treatment Severe Hepatopancreat Di, Zhejiang Prov Top Key Discipline Surg, Wenzhou, Zhejiang, Peoples R China.
EM bichengchen@hotmail.com; wangchengmandy@126.com
FU Wenzhou Municipal Science and Technology Bureau [Y20190073]; Natural
   Science Foundation of Zhejiang ProvinceNatural Science Foundation of
   Zhejiang Province [LQ20H030004]
FX This study was supported by grants from the Wenzhou Municipal Science
   and Technology Bureau (Y20190073) and Natural Science Foundation of
   Zhejiang Province (LQ20H030004)
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NR 37
TC 6
Z9 6
U1 2
U2 6
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 2045-7634
J9 CANCER MED-US
JI Cancer Med.
PD JAN
PY 2021
VL 10
IS 1
BP 325
EP 336
DI 10.1002/cam4.3611
EA NOV 2020
PG 12
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA QB0TG
UT WOS:000591693500001
PM 33231372
OA Green Published, gold
DA 2022-04-25
ER

PT J
AU Schneider, NFZ
   Cerella, C
   Lee, JY
   Mazumder, A
   Kim, KR
   de Carvalho, A
   Munkert, J
   Padua, RM
   Kreis, W
   Kim, KW
   Christov, C
   Dicato, M
   Kim, HJ
   Han, BW
   Braga, FC
   Simoes, CMO
   Diederich, M
AF Schneider, Naira F. Z.
   Cerella, Claudia
   Lee, Jin-Young
   Mazumder, Aloran
   Kim, Kyung Rok
   de Carvalho, Annelise
   Munkert, Jennifer
   Padua, Rodrigo M.
   Kreis, Wolfgang
   Kim, Kyu-Won
   Christov, Christo
   Dicato, Mario
   Kim, Hyun-Jung
   Han, Byung Woo
   Braga, Fernao C.
   Simoes, Claudia M. O.
   Diederich, Marc
TI Cardiac Glycoside Glucoevatromonoside Induces Cancer Type-Specific Cell
   Death
SO FRONTIERS IN PHARMACOLOGY
LA English
DT Article
DE cardiac glycoside; glucoevatromonoside; apoptosis; non-canonical cell
   death; lung cancer
ID LUNG-CANCER; CYCLIN B1; CARDIOTONIC STEROIDS; SOLID TUMORS; DNA-DAMAGE;
   BRAZILIAN CULTIVAR; SIGNALING PATHWAYS; ANTITUMOR-ACTIVITY;
   COLORECTAL-CANCER; DIGITALIS-LANATA
AB Cardiac glycosides (CGs) are natural compounds used traditionally to treat congestive heart diseases. Recent investigations repositioned CGs as potential anticancer agents. To discover novel cytotoxic CG scaffolds, we selected the cardenolide glucoevatromonoside (GEV) out of 46 CGs for its low nanomolar anti-lung cancer activity. GEV presented reduced toxicity toward non-cancerous cell types (lung MRC-5 and PBMC) and high-affinity binding to the Na+/K+-ATPase a subunit, assessed by computational docking. GEV-induced cell death was caspase-independent, as investigated by a multiparametric approach, and culminates in severe morphological alterations in A549 cells, monitored by transmission electron microscopy, live cell imaging and flow cytometry. This non-canonical cell death was not preceded or accompanied by exacerbation of autophagy. In the presence of GEV, markers of autophagic flux (e.g. LC3I-II conversion) were impacted, even in presence of bafilomycin A1. Cell death induction remained unaffected by calpain, cathepsin, parthanatos, or necroptosis inhibitors. Interestingly, GEV triggered caspase-dependent apoptosis in U937 acute myeloid leukemia cells, witnessing cancer-type specific cell death induction. Differential cell cycle modulation by this CG led to a G2/M arrest, cyclin B1 and p53 downregulation in A549, but not in U937 cells. We further extended the anti-cancer potential of GEV to 3D cell culture using clonogenic and spheroid formation assays and validated our findings in vivo by zebrafish xenografts. Altogether, GEV shows an interesting anticancer profile with the ability to exert cytotoxic effects via induction of different cell death modalities.
C1 [Schneider, Naira F. Z.; de Carvalho, Annelise; Simoes, Claudia M. O.] Univ Fed Santa Catarina, Ctr Ciencias Saude, Dept Ciencias Farmaceut, Lab Virol Applicada, Florianopolis, SC, Brazil.
   [Cerella, Claudia; Dicato, Mario] Hop Kirchberg, Lab Biol Mol & Cellulaire Canc, Luxembourg, Luxembourg.
   [Cerella, Claudia; Lee, Jin-Young; Mazumder, Aloran; Kim, Kyung Rok; Han, Byung Woo; Diederich, Marc] Seoul Natl Univ, Coll Pharm, Res Inst Pharmaceut Sci, Dept Pharm, Seoul, South Korea.
   [Munkert, Jennifer; Kreis, Wolfgang] Friedrich Alexander Univ, Dept Biol, Erlangen, Germany.
   [Padua, Rodrigo M.; Braga, Fernao C.] Univ Fed Minas Gerais, Fac Farm, Dept Prod Farmaceut, Belo Horizonte, MG, Brazil.
   [Kim, Kyu-Won] Seoul Natl Univ, Coll Pharm, SNU Harvard Neurovasc Protect Ctr, Seoul, South Korea.
   [Kim, Kyu-Won] Seoul Natl Univ, Res Inst Pharmaceut Sci, Seoul, South Korea.
   [Christov, Christo] Univ Lorraine, Fac Med, Nancy, France.
   [Kim, Hyun-Jung] Chung Ang Univ, Coll Pharm, Seoul, South Korea.
RP Diederich, M (corresponding author), Seoul Natl Univ, Coll Pharm, Res Inst Pharmaceut Sci, Dept Pharm, Seoul, South Korea.
EM marcdiederich@snu.ac.kr
RI Braga, Fernão/AAO-3888-2020; Kim, Kyu Won/AAJ-7213-2020; Schneider,
   Naira FZ/L-9215-2013; Braga, Fernão C/E-3236-2016; Diederich,
   Marc/O-7335-2015; de Padua, Rodrigo Maia/H-5341-2018
OI Braga, Fernão/0000-0001-9468-376X; Braga, Fernão C/0000-0001-9468-376X;
   Diederich, Marc/0000-0003-0115-4725; de Padua, Rodrigo
   Maia/0000-0002-9939-6900
FU Waxweiler grant for cancer prevention research from the Action Lions
   Vaincre le Cancer; BK21 and Televie; CAPES PDSE programCoordenacao de
   Aperfeicoamento de Pessoal de Nivel Superior (CAPES)
   [99999.014368/2013-07]; CAPES/MEC (Ministry of Education); CNPq/MCTI
   (Ministry of Science, Technology and Innovation); CNPqConselho Nacional
   de Desenvolvimento Cientifico e Tecnologico (CNPQ) [472544/2013-6,
   490057/2011-0]; CAPESCoordenacao de Aperfeicoamento de Pessoal de Nivel
   Superior (CAPES) [PNPD 2257/2011]; Marie Curie Foundation/IRSES/European
   Community [295251]; BK21Ministry of Education & Human Resources
   Development (MOEHRD), Republic of Korea; Recherches Scientifiques
   Luxembourg (RSL); National Research Foundation (NRF); MEST of Korea for
   Tumor Microenvironment Global Core Research Center (GCRC)
   [NRF-2011-0030001]; Seoul National University Research Grant; Brain
   Korea (BK21) PLUS program; Recherche Cancer et Sang foundation;
   Recherches Scientifiques Luxembourg association; Een Haerz fir
   kriibskrank Kanner association; Action LIONS Vaincre le Cancer
   association; Televie Luxembourg
FX ClC was supported by a Waxweiler grant for cancer prevention research
   from the Action Lions Vaincre le Cancer, by BK21 and Televie. NS was
   supported by CAPES PDSE program 99999.014368/2013-07. The Brazilian
   authors would like to thank the funding agencies CAPES/MEC (Ministry of
   Education) and CNPq/MCTI (Ministry of Science, Technology and
   Innovation) for their research scholarships. This work was also
   supported by CNPq (Grants 472544/2013-6 and 490057/2011-0), CAPES (Grant
   PNPD 2257/2011), and Marie Curie Foundation/IRSES/European Community
   (Grant 295251). J-YL and AM were supported by BK21 and Recherches
   Scientifiques Luxembourg (RSL). Research at SNU is supported by the
   National Research Foundation (NRF) by the MEST of Korea for Tumor
   Microenvironment Global Core Research Center (GCRC) grant [grant number
   NRF-2011-0030001; by the Seoul National University Research Grant and by
   Brain Korea (BK21) PLUS program]. LBMCC was supported by the Recherche
   Cancer et Sang foundation, the Recherches Scientifiques Luxembourg
   association, by the Een Haerz fir kriibskrank Kanner association, by the
   Action LIONS Vaincre le Cancer association and by Televie Luxembourg.
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NR 61
TC 20
Z9 21
U1 4
U2 15
PU FRONTIERS MEDIA SA
PI LAUSANNE
PA PO BOX 110, EPFL INNOVATION PARK, BUILDING I, LAUSANNE, 1015,
   SWITZERLAND
SN 1663-9812
J9 FRONT PHARMACOL
JI Front. Pharmacol.
PD MAR 1
PY 2018
VL 9
AR 70
DI 10.3389/fphar.2018.00070
PG 17
WC Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA FX8VS
UT WOS:000426374400001
PM 29545747
OA Green Published, gold
DA 2022-04-25
ER

PT J
AU He, Y
   Zhang, L
   Tan, F
   Wang, LF
   Liu, DH
   Wang, RJ
   Yin, XZ
AF He, Yong
   Zhang, Ling
   Tan, Fei
   Wang, Li-Fang
   Liu, De-Hui
   Wang, Rong-Juan
   Yin, Xiong-Zhang
TI MiR-153-5p promotes sensibility of colorectal cancer cells to
   oxaliplatin via targeting Bcl-2-mediated autophagy pathway
SO BIOSCIENCE BIOTECHNOLOGY AND BIOCHEMISTRY
LA English
DT Article
DE Colorectal cancer; L-OHP resistant; miR-153-5p; Bcl-2; autophagy
AB Oxaliplatin (L-OHP) is one of the effective chemotherapeutic drugs for colorectal cancer (CRC). Further investigation into the molecular mechanism of chemoresistance could improve outcomes for patients with colorectal cancer. Recently, microRNAs have been reported as a key in drug resistance of tumors. In this study, we aimed to investigate the effects of miR-153-5p in L-OHP-resistant CRC cells, and its underlying mechanism. Downregulation of miR-153-5p was observed in CRC cells, while upregulation of miR-153-5p enhances the chemosensitivity of CRC/L-OHP cells. The autophagy of CRC/L-OHP cells was markedly increased after exposure to L-OHP but abolished by the upregulation of miR-153-5p. Dual-luciferase reporter assays validated that Bcl-2 was a direct target of miR-153-5p. In conclusion, our data suggested that miR-153-5p was a mediator of cisplatin resistance in colorectal cancer by affecting Bcl-2-mediated autophagy, indicating a new therapeutic target for CRC treatment.
C1 [He, Yong; Tan, Fei; Wang, Li-Fang; Liu, De-Hui; Wang, Rong-Juan] Ganzhou Peoples Hosp, Intravenous Drugs Dispensing Ctr, Ganzhou, Jiangxi, Peoples R China.
   [Zhang, Ling] FirstPeoples Hosp Xiantao, Dept Pharm, Xiantao, Hubei, Peoples R China.
   [Yin, Xiong-Zhang] Huazhong Univ Sci & Technol, Tongji Med Coll, Tongji Hosp, Dept Pharm, Wuhan, Hubei, Peoples R China.
RP Yin, XZ (corresponding author), Huazhong Univ Sci & Technol, Tongji Med Coll, Tongji Hosp, Dept Pharm, Wuhan, Hubei, Peoples R China.
EM xiongzhang027@163.com
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NR 22
TC 6
Z9 6
U1 0
U2 2
PU TAYLOR & FRANCIS LTD
PI ABINGDON
PA 2-4 PARK SQUARE, MILTON PARK, ABINGDON OR14 4RN, OXON, ENGLAND
SN 0916-8451
EI 1347-6947
J9 BIOSCI BIOTECH BIOCH
JI Biosci. Biotechnol. Biochem.
PD AUG 2
PY 2020
VL 84
IS 8
BP 1645
EP 1651
DI 10.1080/09168451.2020.1760784
EA MAY 2020
PG 7
WC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology;
   Chemistry, Applied; Food Science & Technology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology;
   Chemistry; Food Science & Technology
GA MM4LQ
UT WOS:000538613600001
PM 32380907
OA Bronze
DA 2022-04-25
ER

PT J
AU Lee, HJ
   Kim, JH
   Hong, S
   Hwang, I
   Park, SJ
   Kim, TI
   Kim, WH
   Yu, JW
   Kim, SW
   Cheon, JH
AF Lee, Hyun Jung
   Kim, Jae Hyeon
   Hong, Sujeong
   Hwang, Inhwa
   Park, Soo Jung
   Kim, Tae Il
   Kim, Won Ho
   Yu, Je-Wook
   Kim, Seung Won
   Cheon, Jae Hee
TI Proteomics-based functional studies reveal that galectin-3 plays a
   protective role in the pathogenesis of intestinal Behcet's disease
SO SCIENTIFIC REPORTS
LA English
DT Article
ID INFLAMMATORY-BOWEL-DISEASE; CROHNS-DISEASE; ER STRESS; AUTOPHAGY;
   COLITIS; SUSCEPTIBILITY; POLYMORPHISMS; INFLAMMASOMES; ASSOCIATIONS;
   IL-1-BETA
AB The pathogenesis of intestinal Behcet's disease (BD) remains poorly understood. Therefore, we aimed to discover and validate biomarkers using proteomics analysis and subsequent functional studies. After two-dimensional electrophoresis, candidate proteins were identified using matrix-assisted laser desorption/ionization tandem time-of-flight mass spectrometry (MALDI-TOF/TOF MS). We validated these results by evaluating the protein levels and their functions in vitro using HT-29 colorectal cancer cells, colon tissues from patients and mice, and murine bone marrow derived macrophages (BMDMs). Of the 30 proteins differentially expressed in intestinal BD tissues, we identified seven using MALDI-TOF/TOF MS. Focusing on galectin-3, we found that TGF-B and IL-10 expression was significantly lower in shLGALS3-transfected cells. Expression of GRP78 and XBP1s and apoptosis rates were all higher in shLGALS3-transfected cells upon the induction of endoplasmic reticulum stress. In response to lipopolysaccharide stimulation, microtubule-associated protein 1 light chain 3B accumulated and lysosomes decreased in these cells. Finally, Salmonella typhimurium infection induced caspase-1 activation and increased IL-1 beta production, which facilitated activation of the NLRC4 inflammasome, in Lgals3(-/-) murine BMDMs compared to wild type BMDMs. Our data suggest that galectin-3 may play a protective role in the pathogenesis of intestinal BD via modulation of ER stress, autophagy, and inflammasome activation.
C1 [Lee, Hyun Jung; Kim, Jae Hyeon; Park, Soo Jung; Kim, Tae Il; Kim, Won Ho; Kim, Seung Won; Cheon, Jae Hee] Yonsei Univ, Coll Med, Dept Internal Med, Seoul, South Korea.
   [Lee, Hyun Jung; Kim, Jae Hyeon; Park, Soo Jung; Kim, Tae Il; Kim, Won Ho; Kim, Seung Won; Cheon, Jae Hee] Yonsei Univ, Coll Med, Inst Gastroenterol, Seoul, South Korea.
   [Lee, Hyun Jung] Seoul Natl Univ, Coll Med, Dept Internal Med, Seoul, South Korea.
   [Lee, Hyun Jung] Seoul Natl Univ, Coll Med, Liver Res Inst, Seoul, South Korea.
   [Kim, Jae Hyeon; Kim, Seung Won; Cheon, Jae Hee] Yonsei Univ, Coll Med, Brain Korea 21 PLUS Project Med Sci, Seoul, South Korea.
   [Hong, Sujeong; Hwang, Inhwa; Yu, Je-Wook] Yonsei Univ, Brain Korea 21 PLUS Project Med Sci, Dept Microbiol, Inst Immunol & Immunol Dis,Coll Med, Seoul, South Korea.
   [Kim, Seung Won; Cheon, Jae Hee] Yonsei Univ, Coll Med, Severance Biomed Sci Inst, Seoul, South Korea.
RP Kim, SW; Cheon, JH (corresponding author), Yonsei Univ, Coll Med, Dept Internal Med, Seoul, South Korea.; Kim, SW; Cheon, JH (corresponding author), Yonsei Univ, Coll Med, Inst Gastroenterol, Seoul, South Korea.; Kim, SW; Cheon, JH (corresponding author), Yonsei Univ, Coll Med, Brain Korea 21 PLUS Project Med Sci, Seoul, South Korea.; Kim, SW; Cheon, JH (corresponding author), Yonsei Univ, Coll Med, Severance Biomed Sci Inst, Seoul, South Korea.
EM swk21c@hanmail.net; GENIUSHEE@yuhs.ac
RI Cheon, Jae Hee/B-4523-2015
OI Cheon, Jae Hee/0000-0002-2282-8904; Kim, Seung Won/0000-0002-1692-1192;
   Hwang, Inhwa/0000-0001-5235-3519; Yu, Je-Wook/0000-0001-5943-4071; Kim,
   Jaehyeon/0000-0003-0064-6656; Kim, Tae Il/0000-0003-4807-890X; Kim, Won
   Ho/0000-0002-5682-9972
FU National Research Foundation of Korea (NRF) - Korea government (MSIP)
   [NRF-2014R1A1A1008096, NRF-2017R1A1A1A05001011]; faculty research grant
   of Yonsei University College of Medicine [6-2012-0135]; Korea Health
   Technology R&D Project through Korea Health Industry Development
   Institute (KHIDI); Ministry of Health & Welfare, Republic of
   KoreaMinistry of Health & Welfare, Republic of Korea [HI13C1345]
FX This research was supported by National Research Foundation of Korea
   (NRF) grants funded by the Korea government (MSIP)
   (NRF-2014R1A1A1008096, NRF-2017R1A1A1A05001011), a faculty research
   grant of Yonsei University College of Medicine (6-2012-0135), a grant of
   the Korea Health Technology R&D Project through the Korea Health
   Industry Development Institute (KHIDI), funded by the Ministry of Health
   & Welfare, Republic of Korea (grant number: HI13C1345). We also wish to
   acknowledge technical support from Yonsei Proteome Research Center
   (www.proteomix.org).
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NR 54
TC 5
Z9 5
U1 1
U2 5
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 2045-2322
J9 SCI REP-UK
JI Sci Rep
PD AUG 12
PY 2019
VL 9
AR 11716
DI 10.1038/s41598-019-48291-1
PG 13
WC Multidisciplinary Sciences
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Science & Technology - Other Topics
GA IP9QN
UT WOS:000480385200109
PM 31406212
OA gold, Green Published
DA 2022-04-25
ER

PT J
AU Kang, MR
   Kim, MS
   Oh, JE
   Kim, YR
   Song, SY
   Kim, SS
   Ahn, CH
   Yoo, NJ
   Lee, SH
AF Kang, Mi Ran
   Kim, Min Sung
   Oh, Ji Eun
   Kim, Yoo Ri
   Song, Sang Yong
   Kim, Sung Soo
   Ahn, Chang Hyeok
   Yoo, Nam Jin
   Lee, Sug Hyung
TI Frameshift mutations of autophagy-related genes ATG2B, ATG5, ATG9B and
   ATG12 in gastric and colorectal cancers with microsatellite instability
SO JOURNAL OF PATHOLOGY
LA English
DT Article
DE autophagy; ATG; MSI; mutation; gastric cancer; colorectal cancer
ID INACTIVATING MUTATIONS; PROTEIN; CARCINOMAS; BECLIN-1; DEATH; UVRAG;
   EXPRESSION; APOPTOSIS; PATHWAYS; THERAPY
AB Mounting evidence indicates that alterations of autophagy processes are directly involved in the development of many human diseases, including cancers. Autophagy-related gene (ATG) products are main players in the autophagy process. In humans there are 16 known ATG genes, of which four (ATG2B, ATG5, ATG9B and ATG12) have mononucleotide repeats with seven or more nucleotides. Frameshift mutations of genes with mononucleotide repeats are features of cancers with microsatellite instability (MSI). It is not known whether ATG genes with mononucleotide repeats are altered by frameshift mutations in gastric and colorectal carcinomas with MSI. For this, we analysed the mononecleotide repeats in ATG2B, ATG5, ATG9B and ATG12 in 32 gastric carcinomas with high MSI (MSI-H), 13 gastric carcinomas with low MSI (MSI-L), 43 colorectal carcinomas with MSI-H and 15 colorectal carcinomas with MSI-L by a single-strand conformation polymorphism (SSCP) analysis. We found ATG2B, ATG5, ATG9B and ATG12 mutations in 10, 2, 13 and 0 cancers, respectively. The mutations were detected in MSI-H cancers but not in MSI-L cancers. Gastric and colorectal cancers with MSI-H harboured one or more ATG mutations in 28.1% and 27.9%, respectively. Our data indicate that frameshift mutations in ATG genes with mononucleotide repeats are common in gastric and colorectal carcinomas with MSI-H, and suggest that these mutations may contribute to cancer development by deregulating the autophagy process. Copyright (C) 2008 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.
C1 [Kang, Mi Ran; Kim, Min Sung; Oh, Ji Eun; Kim, Yoo Ri; Yoo, Nam Jin; Lee, Sug Hyung] Catholic Univ Korea, Coll Med, Dept Pathol, Seoul 137701, South Korea.
   [Song, Sang Yong] Sungkyunkwan Univ, Sch Med, Samsung Med Ctr, Dept Pathol, Seoul, South Korea.
   [Ahn, Chang Hyeok] Catholic Univ Korea, Coll Med, Dept Internal Med, Seoul 137701, South Korea.
   [Ahn, Chang Hyeok] Catholic Univ Korea, Coll Med, Dept Gen Surg, Seoul 137701, South Korea.
RP Lee, SH (corresponding author), Catholic Univ Korea, Coll Med, Dept Pathol, 505 Bonpo Dong, Seoul 137701, South Korea.
EM suhulee@catholic.ac.kr
FU Ministry for Health, Welfare and Family Affairs, KoreaMinistry of Health
   & Welfare, Republic of Korea [A080083]
FX This study was supported by the Ministry for Health, Welfare and Family
   Affairs, Korea (Grant No. A080083).
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TC 167
Z9 179
U1 0
U2 23
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0022-3417
EI 1096-9896
J9 J PATHOL
JI J. Pathol.
PD APR
PY 2009
VL 217
IS 5
BP 702
EP 706
DI 10.1002/path.2509
PG 5
WC Oncology; Pathology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Pathology
GA 425YU
UT WOS:000264674900010
PM 19197948
DA 2022-04-25
ER

PT J
AU Zhang, RN
   Pan, T
   Xiang, Y
   Zhang, MM
   Feng, J
   Liu, SP
   Duan, T
   Chen, P
   Zhai, BT
   Chen, XY
   Wang, WG
   Chen, B
   Han, XM
   Chen, LX
   Yan, LL
   Jin, T
   Liu, Y
   Li, GH
   Huang, XX
   Zhang, WZ
   Sun, YT
   Li, QJ
   Zhang, Q
   Zhuo, J
   Xie, T
   Wu, QB
   Sui, XB
AF Zhang, Ruonan
   Pan, Ting
   Xiang, Yu
   Zhang, Mingming
   Feng, Jiao
   Liu, Shuiping
   Duan, Ting
   Chen, Peng
   Zhai, Bingtao
   Chen, Xiaying
   Wang, Wengang
   Chen, Bi
   Han, Xuemeng
   Chen, Liuxi
   Yan, Lili
   Jin, Ting
   Liu, Ying
   Li, Guohua
   Huang, Xingxing
   Zhang, Wenzheng
   Sun, Yitian
   Li, Qiujie
   Zhang, Qin
   Zhuo, Lvjia
   Xie, Tian
   Wu, Qibiao
   Sui, Xinbing
TI beta-Elemene Reverses the Resistance of p53-Deficient Colorectal Cancer
   Cells to 5-Fluorouracil by Inducing Pro-death Autophagy and Cyclin
   D3-Dependent Cycle Arrest
SO FRONTIERS IN BIOENGINEERING AND BIOTECHNOLOGY
LA English
DT Article
DE colorectal cancer; p53; beta-elemene; 5-fluorouracil; autophagy; cell
   cycle; drug resistance
ID DOWN-REGULATION; KINASE; INHIBITION; STATISTICS; EXPRESSION; TOXICITY;
   EFFICACY; GROWTH
AB Objective Colorectal cancer is a malignant tumor of the digestive system with high morbidity and mortality. 5-fluorouracil remains a widely used chemotherapeutic drug in the treatment of advanced colorectal cancer, but chemotherapy drugs are prone to develop drug resistance, p53 deletion or mutation is an important reason for the resistance of colorectal cancer cells to 5-fluorouracil. beta-elemene has been proved to have the potential of reverse chemotherapy drug resistance, but the mechanism is unknown. This study aimed to investigate the effect of beta-elemene to 5-fluorouracil in drug-resistant p53-deficient colorectal cancer cells HCT116p53(-/-), and determine the possible molecular mechanism of beta-elemene to reverse 5-fluorouracil resistance. Methods The effect of beta-elemene on HCT116p53(-/-) cell activity was detected by Cell counting Kit-8. Cell proliferation was detected by monoclonal plate. The apoptosis was detected by flow cytometry and western blot. The autophagy was detected by western blot, immunofluorescence and transmission electron microscope. Determine the role of Cyclin-related protein Cyclin D3 in beta-elemene reversing the resistance of HCT116p53(-/-) to 5-fluorouracil was detected by overexpression of Cyclin D3. The effect of beta-elemene on the tumorigenic ability of p53-deficient colorectal cancer cells was detected establishing HCT116p53(-/-) all line xenograft model. Results For p53 wildtype colorectal cancer cells, beta-elemene could augment the sensitivity of 5-fluorouracil, for p53-deficient colorectal cancer cells, beta-elemene significantly inhibited cell proliferation in a concentration-dependent manner, and reversed the resistance of HCT116p53(-/-) to 5-fluorouracil by inducing pro-death autophagy and Cyclin D3-dependent cycle arrest. Conclusion beta-elemene enhances the sensitivity of p53 wild-type cells to 5-fluorouracil, beta-elemene can reverse the resistance of HCT116p53(-/-) to 5-fluorouracil by inducing pro-death autophagy and Cyclin D3-dependent cycle arrest in p53-deficient colorectal cancer, which will provide a new method for the treatment of p53 deletion colorectal cancer patients.
C1 [Zhang, Ruonan; Pan, Ting; Xiang, Yu; Zhang, Mingming; Feng, Jiao; Liu, Shuiping; Duan, Ting; Chen, Peng; Zhai, Bingtao; Chen, Xiaying; Wang, Wengang; Chen, Bi; Han, Xuemeng; Chen, Liuxi; Yan, Lili; Jin, Ting; Li, Guohua; Huang, Xingxing; Zhang, Wenzheng; Sun, Yitian; Li, Qiujie; Zhang, Qin; Zhuo, Lvjia; Xie, Tian; Sui, Xinbing] Hangzhou Normal Univ, Coll Med, Dept Med Oncol, Holist Integrat Pharm Inst,Affiliated Hosp, Hangzhou, Peoples R China.
   [Zhang, Ruonan; Pan, Ting; Xiang, Yu; Zhang, Mingming; Feng, Jiao; Liu, Shuiping; Duan, Ting; Chen, Peng; Zhai, Bingtao; Chen, Xiaying; Wang, Wengang; Chen, Bi; Han, Xuemeng; Chen, Liuxi; Yan, Lili; Jin, Ting; Li, Guohua; Huang, Xingxing; Zhang, Wenzheng; Sun, Yitian; Li, Qiujie; Zhang, Qin; Zhuo, Lvjia; Xie, Tian; Sui, Xinbing] Hangzhou Normal Univ, Key Lab Elemene Class Anticanc Chinese Med, Zhejiang Prov & Engn Lab Dev & Applicat Tradit Ch, Hangzhou, Peoples R China.
   [Zhang, Ruonan; Chen, Bi; Wu, Qibiao; Sui, Xinbing] Macau Univ Sci & Technol, State Key Lab Qual Res Chinese Med, Fac Chinese Med, Macau, Peoples R China.
   [Liu, Ying] Zhejiang Univ, Sir Run Run Shaw Hosp, Dept Med Oncol, Hangzhou, Peoples R China.
RP Xie, T; Sui, XB (corresponding author), Hangzhou Normal Univ, Coll Med, Dept Med Oncol, Holist Integrat Pharm Inst,Affiliated Hosp, Hangzhou, Peoples R China.; Xie, T; Sui, XB (corresponding author), Hangzhou Normal Univ, Key Lab Elemene Class Anticanc Chinese Med, Zhejiang Prov & Engn Lab Dev & Applicat Tradit Ch, Hangzhou, Peoples R China.; Wu, QB; Sui, XB (corresponding author), Macau Univ Sci & Technol, State Key Lab Qual Res Chinese Med, Fac Chinese Med, Macau, Peoples R China.
EM drxiet@aliyun.com; qbwu@must.edu.mo; hzzju@zju.edu.cn
FU National Natural Science Foundation of ChinaNational Natural Science
   Foundation of China (NSFC) [81672932, 81730108, 81874380, 81973635];
   Zhejiang Provincial Natural Science Foundation of China for
   Distinguished Young Scholars [LR18H160001]; Science and Technology
   Development Fund, Macau SAR [130/2017/A3, 0099/2018/A3]; Zhejiang
   Province Science and Technology Project of TCM [2019ZZ016]
FX This work was was supported by grants from the National Natural Science
   Foundation of China (Grant Nos. 81672932, 81730108, 81874380, and
   81973635), Zhejiang Provincial Natural Science Foundation of China for
   Distinguished Young Scholars (Grant No. LR18H160001), the Science and
   Technology Development Fund, Macau SAR (File Nos. 130/2017/A3 and
   0099/2018/A3), and Zhejiang Province Science and Technology Project of
   TCM (Grant No. 2019ZZ016).
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NR 54
TC 11
Z9 11
U1 8
U2 20
PU FRONTIERS MEDIA SA
PI LAUSANNE
PA AVENUE DU TRIBUNAL FEDERAL 34, LAUSANNE, CH-1015, SWITZERLAND
SN 2296-4185
J9 FRONT BIOENG BIOTECH
JI Front. Bioeng. Biotechnol.
PD MAY 8
PY 2020
VL 8
AR 378
DI 10.3389/fbioe.2020.00378
PG 13
WC Biotechnology & Applied Microbiology; Multidisciplinary Sciences
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biotechnology & Applied Microbiology; Science & Technology - Other
   Topics
GA LS9OX
UT WOS:000536709400001
PM 32457882
OA Green Published, gold
DA 2022-04-25
ER

PT J
AU Lu, YT
   Xiao, LM
   Liu, YW
   Wang, H
   Li, H
   Zhou, Q
   Pan, J
   Lei, BX
   Huang, A
   Qi, ST
AF Lu, Yuntao
   Xiao, Limin
   Liu, Yawei
   Wang, Hai
   Li, Hong
   Zhou, Qiang
   Pan, Jun
   Lei, Bingxi
   Huang, Annie
   Qi, Songtao
TI MIR517C inhibits autophagy and the epithelial-to-mesenchymal (-like)
   transition phenotype in human glioblastoma through KPNA2-dependent
   disruption of TP53 nuclear translocation
SO AUTOPHAGY
LA English
DT Article
DE autophagy; epithelial-to-mesenchymal (-like) transition; glioblastoma;
   microRNA; TP53
ID MALIGNANT GLIOMA-CELLS; BREAST-CANCER; HEPATOCELLULAR-CARCINOMA;
   ADJUVANT TEMOZOLOMIDE; TUMOR PROGRESSION; METABOLIC STRESS; C19MC
   CLUSTER; IN-VITRO; INDUCTION; P53
AB The epithelial-to-mesenchymal (-like) transition (EMT), a crucial embryonic development program, has been linked to the regulation of glioblastoma (GBM) progression and invasion. Here, we investigated the role of MIR517C/miR-517c, which belongs to the C19MC microRNA cluster identified in our preliminary studies, in the pathogenesis of GBM. We found that MIR517C was associated with improved prognosis in patients with GBM. Furthermore, following treatment with the autophagy inducer temozolomide (TMZ) and low glucose (LG), MIR517C degraded KPNA2 (karyopherin alpha 2 [RAG cohort 1, importin alpha 1]) and subsequently disturbed the nuclear translocation of TP53 in the GBM cell line U87 in vitro. Interestingly, this microRNA could inhibit autophagy and reduce cell migration and infiltration in U87 cells harboring wild-type (WT) TP53, but not in U251 cells harboring mutant (MU) TP53. Moreover, the expression of epithelial markers (i.e., CDH13/T-cadherin and CLDN1 [claudin 1]) increased, while the expression of mesenchymal markers (i.e., CDH2/N-cadherin, SNAI1/Snail, and VIM [vimentin]) decreased, indicating that the EMT status was blocked by MIR517C in U87 cells. Compared with MIR517C overexpression, MIR517C knockdown promoted infiltration of U87 cells to the surrounding structures in nude mice in vivo. The above phenotypic changes were also observed in TP53(+/+) and TP53(-/-) HCT116 colon cancer cells. In summary, our study provided support for a link between autophagy and EMT status in WT TP53 GBM cells and provided evidence for the signaling pathway (MIR517C-KPNA2-cytoplasmic TP53) involved in attenuating autophagy and eliminating the increased migration and invasion during the EMT.
C1 [Lu, Yuntao; Xiao, Limin; Wang, Hai; Li, Hong; Zhou, Qiang; Pan, Jun; Lei, Bingxi; Qi, Songtao] Southern Med Univ, Nanfang Hosp, Dept Neurosurg, Guangzhou, Guangdong, Peoples R China.
   [Lu, Yuntao; Liu, Yawei; Qi, Songtao] Nanfang Hosp, Nanfang Neurol Res Inst, Guangzhou, Guangdong, Peoples R China.
   [Lu, Yuntao; Qi, Songtao] Nanfang Glioma Ctr, Guangzhou, Guangdong, Peoples R China.
   [Huang, Annie] Hosp Sick Children, Brain Tumor Res Ctr, Toronto, ON M5G 1X8, Canada.
RP Lu, YT (corresponding author), Southern Med Univ, Nanfang Hosp, Dept Neurosurg, Guangzhou, Guangdong, Peoples R China.
EM lllu2000yun@gmail.com; sjwk_songtao@live.cn
OI Lu, Yuntao/0000-0003-4125-304X
FU National Natural Science Foundation of ChinaNational Natural Science
   Foundation of China (NSFC) [81101921]; Natural science Foundation of
   Guangdong ProvinceNational Natural Science Foundation of Guangdong
   Province [2014A030313298]; National Key Clinical Specialist Construction
   Program of China
FX This project was supported by the National Natural Science Foundation of
   China (Grant Nos. 81101921), Natural science Foundation of Guangdong
   Province (Grant Nos. 2014A030313298) and the National Key Clinical
   Specialist Construction Program of China.
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NR 55
TC 71
Z9 76
U1 6
U2 25
PU TAYLOR & FRANCIS INC
PI PHILADELPHIA
PA 530 WALNUT STREET, STE 850, PHILADELPHIA, PA 19106 USA
SN 1554-8627
EI 1554-8635
J9 AUTOPHAGY
JI Autophagy
PD DEC
PY 2015
VL 11
IS 12
BP 2213
EP 2232
DI 10.1080/15548627.2015.1108507
PG 20
WC Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Cell Biology
GA DA4XO
UT WOS:000367806300008
PM 26553592
OA Green Published, Bronze
DA 2022-04-25
ER

PT J
AU Zhao, HB
   Yan, L
   Xu, XG
   Jiang, CM
   Shi, JL
   Zhang, YW
   Liu, L
   Lei, SZ
   Shao, DY
   Huang, QS
AF Zhao, Haobin
   Yan, Lu
   Xu, Xiaoguang
   Jiang, Chunmei
   Shi, Junling
   Zhang, Yawen
   Liu, Li
   Lei, Shuzhen
   Shao, Dongyan
   Huang, Qingsheng
TI Potential of Bacillus subtilis lipopeptides in anti-cancer I: induction
   of apoptosis and paraptosis and inhibition of autophagy in K562 cells
SO AMB EXPRESS
LA English
DT Article
DE Lipopeptide; Apoptosis; Anticancer; Paraptosis
ID CHRONIC MYELOGENOUS LEUKEMIA; BREAST-CANCER; SIGNALING PATHWAY;
   SURFACTIN; DEATH; ACTIVATION; GROWTH; SUPPRESSION; FIBROBLASTS;
   TRANSITION
AB The lipopeptide iturin from Bacillus subtilis has been found to have a potential inhibitory effect on breast cancer, alveolar adenocarcinoma, renal carcinoma, and colon adenocarcinoma. In this study, the potential of B. subtilis lipopeptides (a mixture of iturin homologues, concentration of 42.75%) to inhibit chronic myelogenous leukemia was evaluated using K562 myelogenous leukemia cells. The results showed that the lipopeptides could completely inhibit the growth of K562 at 100 mu M, with an IC50 value of 65.76 mu M. The lipopeptides inhibited the profile of K562 via three pathways: (1) induction of paraptosis indicated by the occurrence of cytoplasmic vacuoles, and swelling of the mitochondria and endoplasmic reticulum (ER) without membrane blebbing in the presence of a caspase inhibitor; (2) inhibition of autophagy progress illustrated by the upregulated expression of LCII and P62; and (3) induction of apoptosis by causing ROS burst, and induction of the intrinsic pathway indicated by the upregulated expression of cytochrome c (Cyto-c), bax, and bad, together with downregulated expression of Bcl-2. The ROS-dependent apoptosis and caspase-independent paraptosis were verified using the ROS inhibitor and caspase inhibitor, respectively. The extrinsic apoptosis pathway was not involved in the lipopeptide's effects on K562. Overall, the B. subtilis lipopeptides (consisting of a majority of iturin) exhibited promising potential in inhibiting chronic myelogenous leukemia in vitro via simultaneously causing paraptosis, apoptosis, and inhibition of autophagy.
C1 [Zhao, Haobin; Yan, Lu; Xu, Xiaoguang; Jiang, Chunmei; Shi, Junling; Zhang, Yawen; Liu, Li; Lei, Shuzhen; Shao, Dongyan; Huang, Qingsheng] Northwestern Polytech Univ, Sch Life Sci, Key Lab Space Biosci & Biotechnol, 127 Youyi West Rd, Xian 710072, Shaanxi, Peoples R China.
RP Shi, JL (corresponding author), Northwestern Polytech Univ, Sch Life Sci, Key Lab Space Biosci & Biotechnol, 127 Youyi West Rd, Xian 710072, Shaanxi, Peoples R China.
EM sjlshi2004@nwpu.edu.cn
OI Xu, Xiaoguang/0000-0001-9754-9857
FU National Key Technology RD ProgramNational Key Technology R&D Program
   [2015BAD16B02]; National Natural Science Foundation of ChinaNational
   Natural Science Foundation of China (NSFC) [31471718, 1701722]; Modern
   Agricultural Industry Technology System [CARS-30]; Key research and
   development plan of Shaanxi Province [2017ZDXL-NY-0304]
FX This research was supported by the National Key Technology R&D Program
   (2015BAD16B02), the National Natural Science Foundation of China (Grant
   Nos. 31471718, 1701722), the Modern Agricultural Industry Technology
   System (CARS-30), and Key research and development plan of Shaanxi
   Province (2017ZDXL-NY-0304).
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NR 43
TC 38
Z9 38
U1 5
U2 25
PU BIOMED CENTRAL LTD
PI LONDON
PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND
SN 2191-0855
J9 AMB EXPRESS
JI AMB Express
PD MAY 9
PY 2018
VL 8
AR 78
DI 10.1186/s13568-018-0606-3
PG 16
WC Biotechnology & Applied Microbiology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biotechnology & Applied Microbiology
GA GH0SS
UT WOS:000433112900001
PM 29777449
OA Green Published, gold
DA 2022-04-25
ER

PT J
AU Huang, YC
   Hung, WC
   Chye, SM
   Chen, WT
   Chai, CY
AF Huang, Ya-Chun
   Hung, Wen-Chun
   Chye, Soi-Moi
   Chen, Wan-Tzu
   Chai, Chee-Yin
TI para-Phenylenediamine-induced autophagy in human uroepithelial cell line
   mediated mutant p53 and activation of ERK signaling pathway
SO TOXICOLOGY IN VITRO
LA English
DT Article
DE para-Phenylenediamine; SV-HUC-1 cells; Autophagy; Mutant p53; Beclin-1
ID TUMOR-SUPPRESSOR P53; COLON-CANCER CELLS; P-PHENYLENEDIAMINE;
   PROTEIN-KINASE; DNA-DAMAGE; UP-REGULATION; MOUSE CELLS; INHIBITION;
   DEATH; BECLIN-1
AB para-Phenylenediamine (p-PD) is a major aromatic amine that is a widely used commercial oxidative-type hair dye. Some epidemiologic studies have suggested that the use of p-PD-based hair dyes might be related to increased risk of human malignant tumors including bladder cancer. However, the effects of p-PD on autophagy in human uroepithelial cells (SV-HUC-1) is still unclear. In this study, we demonstrate that p-PD can activate the extracellular signaling-regulated protein kinase 1/2 (ERK1/2) signaling pathway in SV-HUC-1 cells. In addition, we observed that autophagosomes increased in p-PD-treated SV-HUC-1 cells as shown by electron microscopy. Our results showed incremental increase of the concentrations, Beclin-1 and microtubule-associated protein light chain 3B (LC3B), which are important regulators of autophagosomes. In contrast, the MEK inhibitor (U0126) was suppressed autophagy and the effect of p-PD on ERK1/2, Beclin-1 and LC3B proteins expression, except for mutant p53. In this study, we demonstrated that inactivation of p53 induces a potent autophagy response. Finally, our results suggest that p-PD can activate the ERK1/2 signaling pathway and mutant p53, leading to the stimulation of autophagy in SV-HUC-1 cells. These results provide us with new insights for the understanding of the mechanism of p-PD-induced cell death in urothelial cells. (C) 2011 Elsevier Ltd. All rights reserved.
C1 [Chen, Wan-Tzu; Chai, Chee-Yin] Kaohsiung Med Univ Hosp, Dept Pathol, Kaohsiung 807, Taiwan.
   [Huang, Ya-Chun; Chai, Chee-Yin] Kaohsiung Med Univ, Grad Inst Med, Coll Med, Kaohsiung, Taiwan.
   [Huang, Ya-Chun; Chai, Chee-Yin] Kaohsiung Med Univ, Dept Pathol, Coll Med, Kaohsiung, Taiwan.
   [Hung, Wen-Chun; Chai, Chee-Yin] Natl Sun Yat Sen Univ, Inst Biomed Sci, Kaohsiung 80424, Taiwan.
   [Hung, Wen-Chun; Chai, Chee-Yin] Natl Sun Yat Sen Univ, Kaohsiung Med Univ Joint Res Ctr, Kaohsiung 80424, Taiwan.
RP Chai, CY (corresponding author), Kaohsiung Med Univ Hosp, Dept Pathol, 100,Tzyou 1st Rd, Kaohsiung 807, Taiwan.
EM cychai@kmu.edu.tw
OI Chai, Chee-Yin/0000-0003-0486-9742
FU National Sun Yat-Sen University-Kaohsiung Medical University Joint
   Research Center, Kaohsiung, Taiwan
FX This work was supported by a research grant from the National Sun
   Yat-Sen University-Kaohsiung Medical University Joint Research Center,
   Kaohsiung, Taiwan.
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NR 57
TC 12
Z9 13
U1 1
U2 7
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0887-2333
J9 TOXICOL IN VITRO
JI Toxicol. Vitro
PD DEC
PY 2011
VL 25
IS 8
BP 1630
EP 1637
DI 10.1016/j.tiv.2011.06.013
PG 8
WC Toxicology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Toxicology
GA 866EE
UT WOS:000298362500015
PM 21741467
DA 2022-04-25
ER

PT J
AU Ding, XF
   Shen, M
   Xu, LY
   Dong, JH
   Chen, G
AF Ding, Xiao-Fei
   Shen, Mao
   Xu, Li-Ying
   Dong, Jin-Hua
   Chen, Guang
TI 13,14-bis(cis-3,5-dimethyl-1-piperazinyl)-beta-elemene, a novel
   beta-elemene derivative, shows potent antitumor activities via
   inhibition of mTOR in human breast cancer cells
SO ONCOLOGY LETTERS
LA English
DT Article
DE 13,14-bis(cis-3,5-dimethyl-1-piperazinyl)-beta-elemene; beta-elemene;
   mTOR; autophagy; cancer
ID IN-VITRO; CARCINOMA
AB Elemene has been approved for the treatment of advanced cancer in China, however, it inhibits cell growth only at high concentrations and is an essential oil with poor water solubility and stability. The discovery of new beta-elemene derivatives is of increasing interest. We recently reported that the compound 13,14-bis(cis-3,5-dimethyl-1-piperazinyl)-beta-elemene (IIi), a novel beta-elemene derivative with a cis-2,6-dimethylpiperazine substitution, is a potent agent for inhibiting the proliferation of SGC-7901 and He La cells. In the present study, we further verified that Hi is cytotoxic to a wide spectrum of human cancer cells in culture, including those of breast, ovarian, lung, gastric, hepatocellular and colon cancer, as well as leukemia cell lines, with an average IC50 of 3.44 mu mol/l. Notably, m showed significant cytotoxicity in two multidrug-resistant (MDR) cell lines, with an average resistance factor (RF) of 1.66. Moreover, in mice with S-180 sarcoma xenografts, the intraperitoneal administration of Hi inhibited tumor growth. The immunoblotting study showed that treatment with IIi decreases phosphorylated p70S6K1 and 4EBP1 levels in the human breast cancer MCF-7 and MDA-MB-468 cells. In the MCF-7 cells, Ili also significantly increased the expression of cleaved LC3. This indicated that Hi inhibits mTOR activity and induces autophagy. The mTOR inhibitory function and the potent antitumor activity, taken together with the appreciable anti-multidrug resistance action, shows Ili to be a novel potential antitumor agent, which merits further research and development.
C1 [Ding, Xiao-Fei] Taizhou Coll, Sch Med, Taizhou 318000, Zhejiang, Peoples R China.
   [Shen, Mao; Chen, Guang] Taizhou Coll, Sch Pharmaceut & Chem Engn, Taizhou 318000, Zhejiang, Peoples R China.
   [Xu, Li-Ying; Dong, Jin-Hua] Shenyang Pharmaceut Univ, Minist Educ, Key Lab Struct Based Drug Design & Discovery, Shenyang 110016, Liaoning, Peoples R China.
RP Chen, G (corresponding author), Taizhou Coll, Sch Pharmaceut & Chem Engn, 1139 Shifu Ave, Taizhou 318000, Zhejiang, Peoples R China.
EM guang.yz.chen@gmail.com
FU National Natural Science Foundation of ChinaNational Natural Science
   Foundation of China (NSFC) [81201530]; Zhejiang Provincial Natural
   Science Foundation of ChinaNatural Science Foundation of Zhejiang
   Province [Y2110474, LY12H31001]
FX This study was supported by the National Natural Science Foundation of
   China (No. 81201530) and Zhejiang Provincial Natural Science Foundation
   of China (No. Y2110474 and LY12H31001).
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NR 19
TC 26
Z9 29
U1 1
U2 13
PU SPANDIDOS PUBL LTD
PI ATHENS
PA POB 18179, ATHENS, 116 10, GREECE
SN 1792-1074
EI 1792-1082
J9 ONCOL LETT
JI Oncol. Lett.
PD MAY
PY 2013
VL 5
IS 5
BP 1554
EP 1558
DI 10.3892/ol.2013.1213
PG 5
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA 136TE
UT WOS:000318385500022
PM 23761818
OA gold, Green Published, Green Submitted
DA 2022-04-25
ER

PT J
AU Rayner, KJ
   Moore, KJ
AF Rayner, Katey J.
   Moore, Kathryn J.
TI MicroRNA Control of High-Density Lipoprotein Metabolism and Function
SO CIRCULATION RESEARCH
LA English
DT Review
DE cholesterol; HDL; lipid metabolism; microRNAs
ID REVERSE CHOLESTEROL TRANSPORT; RAISES PLASMA HDL; LIPID-METABOLISM;
   TANGIER-DISEASE; CIRCULATING MICRORNAS; MICROBIOTA METABOLISM;
   ENDOTHELIAL-CELLS; ABCA1 EXPRESSION; COLON-CANCER; AUTOPHAGY
AB Recent discoveries of microRNAs (miRNAs) that control high-density lipoprotein abundance and function have expanded our knowledge of the mechanisms regulating this important lipoprotein subclass. miRNAs have been shown to regulate gene networks that control high-density lipoprotein biogenesis and uptake, as well as discrete steps in the reverse cholesterol transport pathway. Furthermore, high-density lipoprotein itself has been shown to transport miRNAs selectively in health and disease, offering new possibilities of how this lipoprotein may alter gene expression in distal target cells and tissues. Collectively, these discoveries offer new insights into the mechanisms governing high-density lipoprotein metabolism and function and open new avenues for the development of therapeutics for the treatment of cardiovascular disease.
C1 [Rayner, Katey J.] Univ Ottawa, Inst Heart, Ottawa, ON, Canada.
   [Moore, Kathryn J.] NYU, Leon H Charney Div Cardiol, Dept Med, Marc & Ruti Bell Vasc Biol & Dis Program,Sch Med, New York, NY 10016 USA.
RP Moore, KJ (corresponding author), NYU, Leon H Charney Div Cardiol, Dept Med, Sch Med, 522 First Ave,Smilow 705, New York, NY 10016 USA.
EM Kathryn.Moore@nyumc.org
RI Moore, Kathryn/ABE-6416-2020
OI Moore, Kathryn/0000-0003-2505-2547; Rayner, Katey/0000-0001-6230-426X
FU National Institutes of HealthUnited States Department of Health & Human
   ServicesNational Institutes of Health (NIH) - USA [R01 HL108182];
   Canadian Institutes of Health ResearchCanadian Institutes of Health
   Research (CIHR); NATIONAL HEART, LUNG, AND BLOOD INSTITUTEUnited States
   Department of Health & Human ServicesNational Institutes of Health (NIH)
   - USANIH National Heart Lung & Blood Institute (NHLBI) [R01HL108182]
   Funding Source: NIH RePORTER
FX Research on microRNAs in the Moore Laboratory is supported by the
   National Institutes of Health (R01 HL108182). K.J. Rayner is supported
   by a Canadian Institutes of Health Research Operating Grant and Salary
   Award.
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NR 103
TC 57
Z9 62
U1 0
U2 19
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA TWO COMMERCE SQ, 2001 MARKET ST, PHILADELPHIA, PA 19103 USA
SN 0009-7330
EI 1524-4571
J9 CIRC RES
JI Circ.Res.
PD JAN 3
PY 2014
VL 114
IS 1
BP 183
EP 192
DI 10.1161/CIRCRESAHA.114.300645
PG 10
WC Cardiac & Cardiovascular Systems; Hematology; Peripheral Vascular
   Disease
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Cardiovascular System & Cardiology; Hematology
GA AG7GQ
UT WOS:000335586700023
PM 24385511
OA Green Accepted, Bronze
DA 2022-04-25
ER

PT J
AU Farooqi, AA
   Naureen, H
   Zahid, R
   Youssef, L
   Attar, R
   Xu, BJ
AF Farooqi, Ammad Ahmad
   Naureen, Humaira
   Zahid, Rabbia
   Youssef, Lara
   Attar, Rukset
   Xu, Baojun
TI Cancer chemopreventive role of fisetin: Regulation of cell signaling
   pathways in different cancers
SO PHARMACOLOGICAL RESEARCH
LA English
DT Review
DE Fisetin; Cancer prevention; Cell signaling pathway; PI3K/AKT/mTOR;
   Wnt/beta-catenin; TRAIL/TRAIL-R
ID DIETARY FLAVONOID FISETIN; NATURAL-PRODUCTS; BETA-CATENIN; COLON-CANCER;
   INDUCED APOPTOSIS; PROSTATE-CANCER; MESENCHYMAL TRANSITION; DRUG
   DISCOVERY; CYCLE ARREST; LUNG-CANCER
AB It is becoming progressively more understandable that pharmaceutical targeting of drug-resistant cancers is challenging because of intra- and inter-tumor heterogeneity. Interestingly, naturally derived bioactive compounds have unique ability to modulate wide-ranging deregulated oncogenic cell signaling pathways. In this review, we have focused on the available evidence related to regulation of PI3K/AKT/mTOR, Wnt/beta-catenin, NF-kappa B and TRAIL/TRAIL-R by fisetin in different cancers. Fisetin has also been shown to inhibit the metastatic spread of cancer cells in tumor-bearing mice. We have also summarized how fisetin regulated autophagy in different cancers. In addition, this review also covers fisetin-mediated regulation of VEGF/VEGFR, EGFR, necroptosis and Hippo pathway. Fisetin has entered into clinical trials particularly in context of COVID19-associated inflammations. Furthermore, fisetin mediated effects are also being tested in clinical trials with reference to osteoarthritis and senescence. These developments will surely pave the way for full-fledge and well-designed clinical trials of fisetin in different cancers. However, we still have to comprehensively analyze and fully unlock pharmacological potential of fisetin against different oncogenic signaling cascades and non-coding RNAs. Fisetin has remarkable potential as chemopreventive agent and future studies must converge on the identification of additional regulatory roles of fisetin for inhibition and prevention of cancers.
C1 [Farooqi, Ammad Ahmad] Inst Biomed & Genet Engn IBGE, Dept Mol Oncol, Islamabad, Pakistan.
   [Naureen, Humaira] Riphah Int Univ, Fac Pharmaceut Sci, Islamabad, Pakistan.
   [Zahid, Rabbia] Univ Punjab, Inst Chem, Lahore, Pakistan.
   [Youssef, Lara] Univ Balamand UOB, Fac Med & Med Sci, Dept Biomed Sci, Al Kurah, Lebanon.
   [Attar, Rukset] Yeditepe Univ, Dept Obstet & Gynecol, Istanbul, Turkey.
   [Xu, Baojun] BNU HKBU United Int Coll, Food Sci & Technol Programme, Zhuhai, Peoples R China.
RP Farooqi, AA (corresponding author), Inst Biomed & Genet Engn IBGE, Dept Mol Oncol, Islamabad, Pakistan.; Xu, BJ (corresponding author), BNU HKBU United Int Coll, Food Sci & Technol Programme, Zhuhai, Peoples R China.
EM Faeooqiammadahmad@gmail.com; baojunxu@uic.edu.cn
RI ; Xu, Baojun/B-7971-2017
OI Youssef, Lara/0000-0003-3259-0706; Xu, Baojun/0000-0003-0739-3735
FU Beijing Normal University-Hong Kong Baptist University United
   International College [UIC202107];  [R5201911]
FX This project is jointly supported by one grant (project code: UIC202107)
   from Beijing Normal University-Hong Kong Baptist University United
   International College and one research grant from Guangdong Education
   Bureau (Project code: R5201911).
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NR 92
TC 3
Z9 3
U1 8
U2 10
PU ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD
PI LONDON
PA 24-28 OVAL RD, LONDON NW1 7DX, ENGLAND
SN 1043-6618
EI 1096-1186
J9 PHARMACOL RES
JI Pharmacol. Res.
PD OCT
PY 2021
VL 172
AR 105784
DI 10.1016/j.phrs.2021.105784
EA AUG 2021
PG 11
WC Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA UR3UW
UT WOS:000696677900005
PM 34302980
DA 2022-04-25
ER

PT J
AU Kar, R
   Singha, PK
   Venkatachalam, MA
   Saikumar, P
AF Kar, R.
   Singha, P. K.
   Venkatachalam, M. A.
   Saikumar, P.
TI A novel role for MAP1 LC3 in nonautophagic cytoplasmic vacuolation death
   of cancer cells
SO ONCOGENE
LA English
DT Article
DE cell death; cytoplasmic vacuolation; LC3; ER stress; MAPK; 15d-PGJ2
ID 15-DEOXY-DELTA(12,14)-PROSTAGLANDIN J(2); OXIDATIVE STRESS; INDUCE
   APOPTOSIS; DRUG-RESISTANCE; DNA-BINDING; AUTOPHAGY; ACTIVATION;
   MECHANISMS; PROTEASOME; INHIBITION
AB Thiol reactive cyclopentenone prostaglandin, 15-deoxy-Delta(12,14)-prostaglandin J(2) (15d-PGJ2), induced a novel, nonapoptotic and microtubule-associated protein 1 light chain 3 (MAP1 LC3) dependent but nonautophagic form of cell death in colon, breast and prostate cancer cell lines, characterized by extensive cytoplasmic vacuolation with dilatation of endoplasmic reticulum (ER). Disruption of sulfhydryl homeostasis, which resulted in ER stress, accumulation of ubiquitinated proteins and subsequent ER dilation, contributed to peroxisome proliferator-activated receptor gamma (PPAR gamma)-independent cell death by 15d-PGJ2. Absence of intracellular organelles in these vacuoles, shown by electron microscopy and unique fragmentation of lamin B, suggested this form of cell death to be different from autophagy and apoptosis. Cell death induced by 15d-PGJ2 is prevented by cycloheximide and actinomycin D, suggesting a requirement of new protein synthesis for death with cytoplasmic vacuolation. Here, we report for the. first time that upregulation and processing of autophagy marker LC3 is an important event in nonautophagic cytoplasmic vacuolation and cell death. Notably, knockdown of LC3 conferred significant protection against 15d-PGJ2-induced cytoplasmic vacuolation and cell death, suggesting a novel role of LC3 in a death process other than autophagy. Oncogene (2009) 28, 2556-2568; doi: 10.1038/onc.2009.118; published online 18 May 2009
C1 [Kar, R.; Singha, P. K.; Venkatachalam, M. A.; Saikumar, P.] Univ Texas Hlth Sci Ctr San Antonio, Dept Pathol, San Antonio, TX 78229 USA.
RP Saikumar, P (corresponding author), Univ Texas Hlth Sci Ctr San Antonio, Dept Pathol, 7703 Floyd Curl Dr, San Antonio, TX 78229 USA.
EM saikumar@uthscsa.edu
FU National Institutes of HealthUnited States Department of Health & Human
   ServicesNational Institutes of Health (NIH) - USA [DK54472, DK37139];
   Morrison Trust; NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY
   DISEASESUnited States Department of Health & Human ServicesNational
   Institutes of Health (NIH) - USANIH National Institute of Diabetes &
   Digestive & Kidney Diseases (NIDDK) [R01DK037139, R01DK054472,
   R37DK037139] Funding Source: NIH RePORTER
FX We thank Dr Tamotsu Yoshimori of Osaka University, Japan, for LC3
   antibody and GFP-LC3 construct and Drs Anthony J Valente and Robert A
   Clark of UTHSCSA, TX, for Calreticulin antibody. This work was supported
   by National Institutes of Health grant DK54472 and Morrison Trust Grant
   to PS and National Institutes of Health grant DK37139 to MAV.
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NR 43
TC 95
Z9 99
U1 0
U2 8
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0950-9232
EI 1476-5594
J9 ONCOGENE
JI Oncogene
PD JUL 16
PY 2009
VL 28
IS 28
BP 2556
EP 2568
DI 10.1038/onc.2009.118
PG 13
WC Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics &
   Heredity
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics &
   Heredity
GA 471LJ
UT WOS:000268058900002
PM 19448671
OA Bronze, Green Accepted
DA 2022-04-25
ER

PT J
AU Zang, XL
   Cheng, MY
   Zhang, XX
   Chen, XH
AF Zang, Xinlong
   Cheng, Mingyang
   Zhang, Xiaoxu
   Chen, Xuehong
TI Quercetin nanoformulations: a promising strategy for tumor therapy
SO FOOD & FUNCTION
LA English
DT Review
ID MESOPOROUS SILICA NANOPARTICLES; COLON-CANCER CELLS; BREAST-CANCER;
   MULTIDRUG-RESISTANCE; OXIDE NANOPARTICLES; ANTITUMOR-ACTIVITY; TARGETED
   DELIVERY; LUNG METASTASIS; IN-VITRO; APOPTOSIS
AB Phytochemicals as dietary constituents are being widely explored for the prevention and treatment of various diseases. Quercetin, a major constituent of various dietary products, has attracted extensive interest due to its anti-proliferative capability, reversal of multidrug resistance, autophagy promotion and tumor microenvironment modulation on different cancer types. Although quercetin has shown potent medical value, its application as an antitumor drug is limited. Problems like poor solubility, bioavailability and stability, short half-life and weak tumor-targeting biodistribution make quercetin an unreliable candidate for cancer therapy. Nanoparticle based platforms have shown a number of advantages in delivering a hydrophobic drug like quercetin to diseased tissues. Quercetin nanoparticles have demonstrated high encapsulation efficiency, stability, sustained release, prolonged circulation time, improved accumulation at tumor sites and therapeutic efficiency. Moreover, a combination of quercetin with other diagnostic or therapeutic agents in one nanocarrier has achieved enhancements in detecting or treating tumors. In this review, we have tried to summarize the pharmacological activities of quercetin with regard to tumor cells and microenvironments in vitro and in vivo. Furthermore, various nanoformulations have been highlighted for quercetin delivery for cancer treatment. These results suggest that quercetin nanoparticles may be a promising antitumor therapeutic agent.
C1 [Zang, Xinlong; Cheng, Mingyang; Zhang, Xiaoxu; Chen, Xuehong] Qingdao Univ, Sch Basic Med, Ningxia Rd 308, Qingdao, Peoples R China.
RP Zang, XL (corresponding author), Qingdao Univ, Sch Basic Med, Ningxia Rd 308, Qingdao, Peoples R China.
EM zangxinlong@126.com
OI chen, xuehong/0000-0003-0102-4023; zang, xinlong/0000-0002-9250-2782
FU National Natural Science Foundation of ChinaNational Natural Science
   Foundation of China (NSFC) [82003676]
FX This work is funded by the National Natural Science Foundation of China
   (82003676).
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NR 118
TC 4
Z9 4
U1 22
U2 40
PU ROYAL SOC CHEMISTRY
PI CAMBRIDGE
PA THOMAS GRAHAM HOUSE, SCIENCE PARK, MILTON RD, CAMBRIDGE CB4 0WF, CAMBS,
   ENGLAND
SN 2042-6496
EI 2042-650X
J9 FOOD FUNCT
JI Food Funct.
PD AUG 7
PY 2021
VL 12
IS 15
BP 6664
EP 6681
DI 10.1039/d1fo00851j
EA JUN 2021
PG 18
WC Biochemistry & Molecular Biology; Food Science & Technology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Food Science & Technology
GA TX5GO
UT WOS:000663885300001
PM 34152346
DA 2022-04-25
ER

PT J
AU Luo, SL
   Li, ZY
   Mao, LZ
   Chen, SQ
   Sun, SX
AF Luo, Shunli
   Li, Ziyin
   Mao, Lianzhi
   Chen, Siqiang
   Sun, Suxia
TI Sodium butyrate induces autophagy in colorectal cancer cells through
   LKB1/AMPK signaling
SO JOURNAL OF PHYSIOLOGY AND BIOCHEMISTRY
LA English
DT Article
DE Sodium butyrate; Autophagy; Colorectal cancer; Liver kinase B1 (LKB1);
   AMP-activated protein kinase (AMPK)
ID MEDIATED APOPTOSIS; DEPENDENT MANNER; RECENT PROGRESS; PATHWAY;
   CARCINOMA; METABOLISM; ACTIVATION; LKB1; ACETYLATION; EXPRESSION
AB Butyrate is produced by the fermentation of undigested dietary fibers and acts as the promising candidate for cancer treatment. However, the mechanism underlying sodium butyrate (NaB)-induced autophagy in colorectal cancer is not yet completely understood. The expressions of LC3-II protein and mRNA were detected by western blot and quantitative RT-PCR in colorectal cancer (CRC) cell lines HCT-116 and HT-29, respectively. Autolysosome formation was observed by transmission electron microscope. AMPK and LKB1 were inhibited by chemical inhibitor or siRNAs and confirmed by western blot. NaB elevated the protein and mRNA expressions of LC3 in a dose-dependent manner. NaB treatment increased the formation of autolysosome and expression of phosphorylated liver kinase B1 (LKB1), AMP-activated protein kinase (AMPK), and acetyl-CoA carboxylase (ACC). Treatment with compound C (an inhibitor of AMPK) and siRNA-mediated knockdown of AMPK and LKB1 significantly attenuated NaB-induced autophagy in CRC cells. Collectively, these findings indicated that LKB1 and AMPK are critical for NaB-mediated autophagy and may act as the novel targets for colorectal cancer therapy in the future.
C1 [Luo, Shunli; Li, Ziyin; Mao, Lianzhi; Sun, Suxia] Southern Med Univ, Dept Nutr & Food Hyg, Guangdong Prov Key Lab Trop Dis Res, Sch Publ Hlth, 1023 South Sha Tai Rd, Guangzhou 510515, Guangdong, Peoples R China.
   [Luo, Shunli] Hunan Univ Med, Sch Lab Med, Huaihua 418000, Peoples R China.
   [Chen, Siqiang] Guangzhou Customs Dist, 66 Huacheng Ave, Guangzhou 510623, Guangdong, Peoples R China.
RP Sun, SX (corresponding author), Southern Med Univ, Dept Nutr & Food Hyg, Guangdong Prov Key Lab Trop Dis Res, Sch Publ Hlth, 1023 South Sha Tai Rd, Guangzhou 510515, Guangdong, Peoples R China.
EM suxia.sun@yale.edu
OI Sun, Suxia/0000-0002-1159-6191; Mao, Lianzhi/0000-0003-1153-0990
FU National Natural Science Foundation of ChinaNational Natural Science
   Foundation of China (NSFC) [81773429, 81202204]; Guangdong National
   Natural Science Foundation [S2012010009467]; Project for Excellent Young
   University Teacher award
FX This study was supported by the grants from National Natural Science
   Foundation of China (No. 81773429 and 81202204), Guangdong National
   Natural Science Foundation (No. S2012010009467), Project for Excellent
   Young University Teacher awarded to Southern Medical University.
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NR 44
TC 15
Z9 17
U1 3
U2 13
PU SPRINGER
PI DORDRECHT
PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS
SN 1138-7548
EI 1877-8755
J9 J PHYSIOL BIOCHEM
JI J. Physiol. Biochem.
PD FEB
PY 2019
VL 75
IS 1
BP 53
EP 63
DI 10.1007/s13105-018-0651-z
PG 11
WC Biochemistry & Molecular Biology; Physiology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Physiology
GA HO2PB
UT WOS:000460756300006
PM 30362049
DA 2022-04-25
ER

PT J
AU Sivridis, E
   Koukourakis, MI
   Zois, CE
   Ledaki, I
   Ferguson, DJP
   Harris, AL
   Gatter, KC
   Giatromanolaki, A
AF Sivridis, Efthimios
   Koukourakis, Michael I.
   Zois, Christos E.
   Ledaki, Ioanna
   Ferguson, David J. P.
   Harris, Adrian L.
   Gatter, Kevin C.
   Giatromanolaki, Alexandra
TI LC3A-Positive Light Microscopy Detected Patterns of Autophagy and
   Prognosis in Operable Breast Carcinomas
SO AMERICAN JOURNAL OF PATHOLOGY
LA English
DT Article
ID NUTRIENT DEPRIVATION; MOLECULAR MACHINERY; TUMOR ANGIOGENESIS;
   PANCREATIC-CANCER; INDUCED APOPTOSIS; ATG9 TRAFFICKING; MAMMARY-GLAND;
   HYPOXIA; BECLIN-1; PROTEIN
AB Autophagy is a self-degradation mechanism by which cells recycle their own cytoplasmic constituents and dispose of excess or defective organelles after starvation and oxygen deprivation. An antibody to the microtubule-associated protein 1 light chain 3 (LC3A), recognizing both the soluble (LC3A-I) and the membrane-bound form (LC3A-II) of the protein, was used to detect autophagic activity in 102 breast carcinomas. Three distinct patterns were recognized: (1) diffuse cytoplasmic, (2) cytoplasmic/juxta-nuclear, and (3) "stone-like" pattern - dense, rounded, amorphous structures, 5 mu m on average, typically enclosed within cytoplasmic vacuoles. The diffuse cytoplasmic pattern showed a direct association with estrogen and progesterone receptor expression. The juxta-nuclear pattern indicated a similar association with hormone receptors, an inverse association with tumor size, and a favorable prognosis. By contrast, an increased number of stonelike structures, probably representing an excessive autophagic response, was related to high-grade tumors and a less favorable outcome. Interestingly, 60 additional epithelial tumors of nonbreast origin disclosed identical autophagic patterns, and so did MDA231 breast cancer xenografts and HCT116 colon tumor spheroids (also analyzed by electron microscopy). Moreover, MCF-7 human breast cancer cell lines confirmed induction of LC3A by anoxia and Thapsigargin. It is concluded that autophagy can be readily recognized in breast carcinomas by light microscopy, after immunohistochemical staining with LC3A, but the significance of the various patterns expressed would need further evaluation. (Am J Pathol 2010, 176:2477-2489; DOI: 10.2353/ajpath.2010.090049)
C1 [Sivridis, Efthimios; Giatromanolaki, Alexandra] Democritus Univ Thrace, Dept Pathol, Alexandroupolis 68100, Greece.
   [Koukourakis, Michael I.; Zois, Christos E.] Democritus Univ Thrace, Dept Radiotherapy Oncol, Alexandroupolis 68100, Greece.
   Univ Gen Hosp Alexandroupolis, Alexandroupolis, Greece.
   [Ledaki, Ioanna; Ferguson, David J. P.; Harris, Adrian L.; Gatter, Kevin C.] Univ Oxford, John Radcliffe Hosp, Canc Res UK, Weatherall Inst Mol Med,Mol Oncol Labs, Oxford OX3 9DU, England.
   Univ Oxford, John Radcliffe Hosp, Dept Clin Lab Sci, Oxford OX3 9DU, England.
RP Giatromanolaki, A (corresponding author), Democritus Univ Thrace, Dept Pathol, Alexandroupolis 68100, Greece.
EM agiatrom@med.duth.gr
RI Harris, Adrian/ABA-3343-2020
OI Harris, Adrian/0000-0003-1376-8409; Ferguson, David/0000-0001-5045-819X
FU Tumor and Angiogenesis Research Group; Cancer Research, UKCancer
   Research UK; Oxford NIHR
FX Supported by the Tumor and Angiogenesis Research Group, the Cancer
   Research, UK, and the Oxford NIHR Biomedical Research Center Programme.
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NR 65
TC 97
Z9 100
U1 0
U2 5
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA STE 800, 230 PARK AVE, NEW YORK, NY 10169 USA
SN 0002-9440
EI 1525-2191
J9 AM J PATHOL
JI Am. J. Pathol.
PD MAY
PY 2010
VL 176
IS 5
BP 2477
EP 2489
DI 10.2353/ajpath.2010.090049
PG 13
WC Pathology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pathology
GA 627XV
UT WOS:000280078600042
PM 20382705
OA Green Published, Bronze
DA 2022-04-25
ER

PT J
AU Figueroa-Gonzalez, G
   Garcia-Castillo, V
   Coronel-Hernandez, J
   Lopez-Urrutia, E
   Leon-Cabrera, S
   Arias-Romero, LE
   Terrazas, LI
   Rodriguez-Sosa, M
   Campos-Parra, AD
   Zuniga-Calzada, E
   Lopez-Camarillo, C
   Morales-Gonzalez, F
   Jacobo-Herrera, NJ
   Perez-Plasencia, C
AF Figueroa-Gonzalez, Gabriela
   Garcia-Castillo, Veronica
   Coronel-Hernandez, Jossimar
   Lopez-Urrutia, Eduardo
   Leon-Cabrera, Sonia
   Arias-Romero, Luis E.
   Terrazas, L. I.
   Rodriguez-Sosa, Miriam
   Delia Campos-Parra, Alma
   Zuniga-Calzada, Eduardo
   Lopez-Camarillo, Cesar
   Morales-Gonzalez, Fermin
   Jacobo-Herrera, Nadia J.
   Perez-Plasencia, Carlos
TI Anti-inflammatory and Antitumor Activity of a Triple Therapy for a
   Colitis-Related Colorectal Cancer
SO JOURNAL OF CANCER
LA English
DT Article
DE Colorectal Cancer; Chronic Inflammation; Glycolysis; mTOR; Autophagy
ID LACTATE-DEHYDROGENASE; LDH-A; METFORMIN; DOXORUBICIN; INFLAMMATION;
   INHIBITION; RESISTANCE; RECEPTOR; GROWTH
AB Colorectal cancer (CRC) is an important health issue worldwide, accounting for the third place of cancer incidence. Chronic inflammation, as seen in Crohn's disease and ulcerative colitis, is the most important risk factor for developing CRC, as it favours neoplastic transformation by enhancing epithelial cell turnover in the colonic mucosa. Treatments for CRC need to be improved; currently they are not specific and have several secondary effects in patients. The main objective of this work was to evaluate a new therapeutic strategy against a colitis-related colorectal cancer in vivo and in vitro by targeting mTOR-signaling and lactate dehydrogenase A. Together, these mechanisms directly affect tumor energetics. In this study we evaluated a better and more efficient triple therapy against a chronic inflammation-associated CRC in vivo and in vitro. After the development of tumors, mice were treated intraperitoneally during a forty-day period with single drugs or different combinations of Metformin, Sodium Oxamate and Doxorubicin.
   Targeted inhibition of the mTOR pathway, lactate dehydrogenase A and the concurrent use of Doxorubicin (called in this work as triple therapy), leaded to a notable reduction in the number and size of tumors in mice, and, a significant pro-inflammatory cytokines reduction Besides, we showed that treated cells were induced to early autophagy, and apoptosis cell death.
   Our results represent a novel and robust therapeutic strategy for overcoming CRC by means of targeting central molecular pathways in cancer by the combination of Metformin, Oxamate, and Doxorubicin leading to a rapid tumor growth inhibition and a dramatic colorectal crypt restoration. Besides, drug combination resulted in a notable reduction of anti-inflammatory cytokines.
C1 [Figueroa-Gonzalez, Gabriela; Garcia-Castillo, Veronica; Coronel-Hernandez, Jossimar; Lopez-Urrutia, Eduardo; Leon-Cabrera, Sonia; Arias-Romero, Luis E.; Terrazas, L. I.; Rodriguez-Sosa, Miriam; Perez-Plasencia, Carlos] Univ Nacl Autonoma Mexico, Unidad Biomed, FES Iztacala, Av Los Barrios, Tlalnepantla 54090, Estado De Mexic, Mexico.
   [Figueroa-Gonzalez, Gabriela; Delia Campos-Parra, Alma; Perez-Plasencia, Carlos] Inst Nacl Cancerol, Lab Genom, Direcc Invest, Av San Fernando 22,Secc 16, Mexico City 14080, DF, Mexico.
   [Leon-Cabrera, Sonia] Univ Nacl Autonoma Mexico, Carrera Med Cirujano, FES Iztacala, Av Los Barrios, Tlalnepantla 54090, Estado De Mexic, Mexico.
   [Zuniga-Calzada, Eduardo] Inst Nacl Seguridad Social Estado Mexico & Munici, Dept Anat Patol, Ave Trabajo S-N, Ecatepec De Morelos 55000, Estado De Mexic, Mexico.
   [Lopez-Camarillo, Cesar] UACM, Programa Ciencias Genom, Mexico City, DF, Mexico.
   [Morales-Gonzalez, Fermin] Inst Jalisciense Cancerol, Direcc Med, Coronel Calderon 715, Guadalajara 44280, Jalisco, Mexico.
   [Jacobo-Herrera, Nadia J.] Inst Nacl Ciencias Med & Nutr Salvador Zubiran, Bioquim, Vasco de Quiroga 15,Secc 16, Mexico City 14000, DF, Mexico.
RP Perez-Plasencia, C (corresponding author), Univ Nacl Autonoma Mexico, Unidad Biomed, FES Iztacala, Av Los Barrios, Tlalnepantla 54090, Estado De Mexic, Mexico.; Perez-Plasencia, C (corresponding author), Inst Nacl Cancerol, Lab Genom, Direcc Invest, Av San Fernando 22,Secc 16, Mexico City 14080, DF, Mexico.; Jacobo-Herrera, NJ (corresponding author), Inst Nacl Ciencias Med & Nutr Salvador Zubiran, Bioquim, Vasco de Quiroga 15,Secc 16, Mexico City 14000, DF, Mexico.
EM nadia.jacobo@gmail.com; carlos.pplas@gmail.com
RI Terrazas, Luis I/AAV-8858-2020; Lopez-Urrutia, Eduardo/N-7360-2019;
   Jacobo-Herrera, Nadia/AGG-8009-2022; Figueroa, Gabriela/ABD-1060-2021;
   Perez-Plasencia, Carlos/P-2372-2019; Leon-Cabrera, Sonia/L-6596-2019;
   Lopez-Camarillo, Cesar/I-1946-2019
OI Lopez-Urrutia, Eduardo/0000-0002-5307-2003; Jacobo-Herrera,
   Nadia/0000-0002-1026-3774; Figueroa, Gabriela/0000-0001-8169-4478;
   Perez-Plasencia, Carlos/0000-0002-8593-8211; Leon-Cabrera,
   Sonia/0000-0002-1661-5013; Lopez-Camarillo, Cesar/0000-0002-9417-2609;
   Arias-Romero, Luis E./0000-0001-5676-2483; Campos-Parra, Alma
   D./0000-0003-1750-5171; Coronel-Hernandez, Jossimar/0000-0001-6543-5310;
   GARCIA, VERONICA/0000-0002-8726-1224; Terrazas, Luis
   I./0000-0003-1635-9467
FU Direccion General de Asuntos del Personal Academico
FX G. F-G. Is grateful to Direccion General de Asuntos del Personal
   Academico for a postdoctoral scholarship.
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NR 40
TC 13
Z9 13
U1 0
U2 11
PU IVYSPRING INT PUBL
PI LAKE HAVEN
PA PO BOX 4546, LAKE HAVEN, NSW 2263, AUSTRALIA
SN 1837-9664
J9 J CANCER
JI J. Cancer
PY 2016
VL 7
IS 12
BP 1632
EP 1644
DI 10.7150/jca.13123
PG 13
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA EJ2YB
UT WOS:000393076400007
PM 27698900
OA Green Published, Green Submitted, gold
DA 2022-04-25
ER

PT J
AU Mazouffre, C
   Geyl, S
   Perraud, A
   Blondy, S
   Jauberteau, MO
   Mathonnet, M
   Verdier, M
AF Mazouffre, Clement
   Geyl, Sophie
   Perraud, Aurelie
   Blondy, Sabrina
   Jauberteau, Marie-Odile
   Mathonnet, Muriel
   Verdier, Mireille
TI Dual inhibition of BDNF/TrkB and autophagy: a promising therapeutic
   approach for colorectal cancer
SO JOURNAL OF CELLULAR AND MOLECULAR MEDICINE
LA English
DT Article
DE colorectal cancer; neurotrophins; autophagy; therapy
ID KINASE-B; RECEPTOR; ACTIVATION; CONTRIBUTES; CHLOROQUINE; EXPRESSION;
   RESISTANCE; RELEVANCE; APOPTOSIS; PATHWAY
AB Colorectal cancer (CRC) is the most common digestive cancer in the Western world. Despite effective therapies, resistance and/or recurrence frequently occur. The present study investigated the impact of two survival pathwaysneurotrophic factors (TrkB/BDNF) and autophagyon cell fate and tumour evolution. In vitro studies were performed on two CRC cell lines, SW480 (primary tumour) and SW620 (lymph node invasion), which were also used for subcutaneous xenografts on a nude mouse model. In addition, the presence of neurotrophic factors (NTs) and autophagy markers were assessed in tissue samples representative of different stages. On the basis of our previous study (which demonstrated that TrkB overexpression is associated with prosurvival signaling in CRC cells), we pharmacologically inhibited NTs pathways with K252a. As expected, an inactivation of the PI3K/AKT pathway was observed and CRC cells initiated autophagy. Conversely, blocking the autophagic flux with chloroquine or with ATG5-siRNA overactivated TrkB/BDNF signaling. In vitro, dual inhibition improved the effectiveness of single treatment by significantly reducing metabolic activity and enhancing apoptotic cell death. These findings were accentuated in vivo, in which dual inhibition induced a spectacular reduction in tumour volume following long-term treatment (21 days for K252a and 12 days for CQ). Finally, significant amounts of phospho-TrkB and LC3II were found in the patients' tissues, highlighting their relevance in CRC tumour biology. Taken together, our results show that targeting NTs and autophagy pathways potentially constitutes a new therapeutic approach for CRC.
C1 [Mazouffre, Clement; Geyl, Sophie; Perraud, Aurelie; Blondy, Sabrina; Jauberteau, Marie-Odile; Mathonnet, Muriel; Verdier, Mireille] Univ Limoges, Fac Med & Pharm, Homeostasie Cellulaire & Pathol, Lab EA 3842, Limoges, France.
   [Perraud, Aurelie; Mathonnet, Muriel] CHU Limoges, Serv Chirurg Digest Gen & Endocrinienne, Limoges, France.
RP Verdier, M (corresponding author), Univ Limoges, Fac Med & Pharm, Homeostasie Cellulaire & Pathol, Lab EA 3842, Limoges, France.
EM mireille.verdier@unilim.fr
RI Mathonnet, Muriel/ABD-3021-2020
OI Mathonnet, Muriel/0000-0002-9127-3068; Jauberteau,
   Marie-Odile/0000-0002-8811-8948; VERDIER, Mireille/0000-0002-8162-4856;
   Perraud, Aurelie/0000-0001-7882-0613
FU Conseil Regional du LimousinRegion Nouvelle-Aquitaine; Agence Regionale
   de Sante Limousin (ARS); La Ligue Contre le Cancer (Comite du Limousin);
   Le Comite d'Orientation de la Recherche sur le Cancer (CORC) en Limousin
FX C.M. received a fellowship from the Conseil Regional du Limousin and
   S.G. received a fellowship from the Agence Regionale de Sante Limousin
   (ARS). Additional financial support was provided by La Ligue Contre le
   Cancer (Comite du Limousin) and by Le Comite d'Orientation de la
   Recherche sur le Cancer (CORC) en Limousin. The funding institutions had
   no role in study design, data collection and analysis, decision to
   publish, or preparation of the manuscript. Autors are grateful to the
   Anatomopathology department from the Limoges' Hospital for histological
   and immunohistochemical support, and to Michelle Nouailles for
   patients'informations. C.M., S.G., A.P. and S.B. performed the research;
   M.O.J., M.M. and M.V. designed the research study; M.M. and M.V.
   analysed the data; C.M., S.G., A.P. and M.V. wrote the paper.
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NR 52
TC 14
Z9 14
U1 0
U2 5
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1582-1838
EI 1582-4934
J9 J CELL MOL MED
JI J. Cell. Mol. Med.
PD OCT
PY 2017
VL 21
IS 10
BP 2610
EP 2622
DI 10.1111/jcmm.13181
PG 13
WC Cell Biology; Medicine, Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Cell Biology; Research & Experimental Medicine
GA FI3OV
UT WOS:000411875400033
PM 28597984
OA Green Published, gold
DA 2022-04-25
ER

PT J
AU Chiacchiera, F
   Matrone, A
   Ferrari, E
   Ingravallo, G
   Lo Sasso, G
   Murzilli, S
   Petruzzelli, M
   Salvatore, L
   Moschetta, A
   Simone, C
AF Chiacchiera, F.
   Matrone, A.
   Ferrari, E.
   Ingravallo, G.
   Lo Sasso, G.
   Murzilli, S.
   Petruzzelli, M.
   Salvatore, L.
   Moschetta, A.
   Simone, C.
TI p38 alpha blockade inhibits colorectal cancer growth in vivo by inducing
   a switch from HIF1 alpha- to FoxO-dependent transcription
SO CELL DEATH AND DIFFERENTIATION
LA English
DT Article
DE p38 alpha; autophagy; FoxO; HIF1 alpha; colorectal cancer cell
   metabolism
ID ACTIVATED PROTEIN-KINASE; AUTOPHAGIC CELL-DEATH; MAP KINASE; P38;
   HYPOXIA; PHOSPHORYLATION; PATHWAYS; CARCINOGENESIS; PROLIFERATION;
   METABOLISM
AB Colorectal cancer cell (CRC) fate is governed by an intricate network of signaling pathways, some of which are the direct target of DNA mutations, whereas others are functionally deregulated. As a consequence, cells acquire the ability to grow under nutrients and oxygen shortage conditions. We earlier reported that p38 alpha activity is necessary for proliferation and survival of CRCs in a cell type-specific manner and regardless of their phenotype and genotype. Here, we show that p38 alpha sustains the expression of HIF1 alpha target genes encoding for glycolytic rate-limiting enzymes, and that its inhibition causes a drastic decrease in ATP intracellular levels in CRCs. Prolonged inactivation of p38 alpha triggers AMPK-dependent nuclear localization of FoxO3A and subsequent activation of its target genes, leading to autophagy, cell cycle arrest and cell death. In vivo, pharmacological blockade of p38 alpha inhibits CRC growth in xenografted nude mice and azoxymethane-treated Apc(Min) mice, achieving both a cytostatic and cytotoxic effect, associated with high nuclear expression of FoxO3A and increased expression of its target genes p21 and PTEN. Hence, inhibition of p38 alpha affects the aerobic glycolytic metabolism specific of cancer cells and might be taken advantage of as a therapeutic strategy targeted against CRCs. Cell Death and Differentiation (2009) 16, 1203-1214; doi: 10.1038/cdd.2009.36; published online 3 April 2009
C1 [Chiacchiera, F.; Matrone, A.; Ferrari, E.; Simone, C.] Ist Ric Farmacol Mario Negri, Consorzio Mario Negri Sud, Dept Translat Pharmacol, Lab Signal Dependent Transcript, I-66030 Santa Maria Imbaro, Ch, Italy.
   [Ingravallo, G.] Univ Bari, Dept Pathol Anat, I-70124 Bari, Italy.
   [Lo Sasso, G.; Murzilli, S.; Petruzzelli, M.; Salvatore, L.; Moschetta, A.] Ist Ric Farmacol Mario Negri, Consorzio Mario Negri Sud, Dept Translat Pharmacol, Lab Lipid Metab & Canc, I-66030 Santa Maria Imbaro, Ch, Italy.
   [Petruzzelli, M.; Moschetta, A.] Univ Bari, Clin Med Murri, Dept Internal & Publ Med, I-70124 Bari, Italy.
RP Simone, C (corresponding author), Ist Ric Farmacol Mario Negri, Consorzio Mario Negri Sud, Dept Translat Pharmacol, Lab Signal Dependent Transcript, Via Nazl 8A, I-66030 Santa Maria Imbaro, Ch, Italy.
EM simone@negrisud.it
RI Ingravallo, Giuseppe/Q-1477-2016; Simone, Cristiano/K-3452-2018;
   Chiacchiera, Fulvio/K-6740-2016; INGRAVALLO, Giuseppe/N-2466-2019;
   Moschetta, Antonio/K-6211-2016; Moschetta, Antonio/AAC-5295-2022;
   Chiacchiera, Fulvio/ABD-6137-2020
OI Ingravallo, Giuseppe/0000-0002-4792-3545; Simone,
   Cristiano/0000-0002-2628-7658; Chiacchiera, Fulvio/0000-0003-3830-2090;
   INGRAVALLO, Giuseppe/0000-0002-4792-3545; Moschetta,
   Antonio/0000-0003-2123-6074
FU FIRC (Italian Foundation for Cancer Research)Fondazione AIRC per la
   ricerca sul cancro; AIRC (Italian Association for Cancer
   Research)Fondazione AIRC per la ricerca sul cancro; Fondazione Negri Sud
   ONLUS
FX We thank Dr. Francesco Paolo Jori for his helpful discussion during the
   preparation of the manuscript and editorial assistance and Dr. Nicola
   Martelli for technical assistance. Dr. Chiacchiera and Dr. Matrone are
   supported by FIRC (Italian Foundation for Cancer Research) and AIRC
   (Italian Association for Cancer Research) fellowships, respectively.;
   This work was partially supported by a 'My First Grant' (to CS) and a
   'Start-Up Grant' (to AM) from the Italian Association for Cancer
   Research and by a grant from 'Fondazione Negri Sud ONLUS' (to CS). CS is
   grateful to his wife Viviana for continuous encouragement and support.
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NR 44
TC 97
Z9 100
U1 0
U2 2
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 1350-9047
EI 1476-5403
J9 CELL DEATH DIFFER
JI Cell Death Differ.
PD SEP
PY 2009
VL 16
IS 9
BP 1203
EP 1214
DI 10.1038/cdd.2009.36
PG 12
WC Biochemistry & Molecular Biology; Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Cell Biology
GA 484NY
UT WOS:000269054200003
PM 19343039
OA Green Published, Bronze
DA 2022-04-25
ER

PT J
AU Tatebayashi, D
   Himori, K
   Yamada, R
   Ashida, Y
   Miyazaki, M
   Yamada, T
AF Tatebayashi, Daisuke
   Himori, Koichi
   Yamada, Ryotaro
   Ashida, Yuki
   Miyazaki, Mitsunori
   Yamada, Takashi
TI High-intensity eccentric training ameliorates muscle wasting in colon 26
   tumor-bearing mice
SO PLOS ONE
LA English
DT Article
ID HUMAN SKELETAL-MUSCLE; MYOSIN HEAVY-CHAIN; PARENTERAL-NUTRITION; CANCER;
   ATROPHY; CACHEXIA; ACTIVATION; EXPRESSION; AUTOPHAGY; EXERCISE
AB Eccentric (ECC) contractions are used to maintain skeletal muscle mass and strength in healthy subjects and patients. Here we investigated the effects of ECC training induced by electrical stimulation (ES) on muscle wasting in colon 26 (C-26) tumor-bearing mice. Mice were divided into four groups: control (CNT), CNT + ECC, C-26, and C-26 + ECC. Cancer cachexia was induced by a subcutaneous injection of C-26 cells and developed for four weeks. In experiment 1, muscle protein synthesis rate and mammalian target of rapamycin complex (mTORC) 1 signaling were investigated six hours after one bout of ECC-ES (2 s contraction given every 6 s, 20 degrees/s, 4 sets of 5 contractions). In experiment 2, ECC-ES training, a total of 14 sessions, was performed every other day starting one day after C-26 injection. Compared to the CNT mice, the gastrocnemius muscle weight was significantly decreased in the tumor-bearing mice. This change was accompanied by a reduction in protein synthesis rate and a marked increase in the expression levels of genes including regulated in development and DNA damage responses (REDD) 1, forkhead box protein 01 (FoxO1), muscle-specific E3 ubiquitin ligases atrogin-1, and muscle ring finger 1 (MuRF-1) mRNA. ECC-ES increased the protein synthesis rate and the phosphorylation levels of p70S6K (Thr389) and rpS6 (Ser240/244), markers for mTORC1 signaling, and reversed an upregulation of MuRF-1 mRNA in muscles from C-26 mice. Our findings suggest that ECC-ES training reduces skeletal muscle atrophy in C-26 tumor-bearing mice through activation of mTORC1 signaling and the inhibition of ubiquitin-proteasome pathway. Thus, ECC-ES training might be used to effectively ameliorate muscle wasting in patients with cancer cachexia.
C1 [Tatebayashi, Daisuke; Himori, Koichi; Yamada, Ryotaro; Ashida, Yuki; Yamada, Takashi] Sapporo Med Univ, Grad Sch Hlth Sci, Sapporo, Hokkaido, Japan.
   [Miyazaki, Mitsunori] Hlth Sci Univ Hokkaido, Sch Rehabil Sci, Tobetsu, Japan.
RP Yamada, T (corresponding author), Sapporo Med Univ, Grad Sch Hlth Sci, Sapporo, Hokkaido, Japan.
EM takashi.yamada1976@sapmed.ac.jp
RI Yamada, Takashi/U-8443-2019; Yamada, Takashi/AAZ-6212-2021; Miyazaki,
   Mitsunori/AAM-8598-2021
OI Yamada, Takashi/0000-0003-1797-3880; Yamada,
   Takashi/0000-0003-1797-3880; Miyazaki, Mitsunori/0000-0001-7824-2091
FU Japan Society for the Promotion of ScienceMinistry of Education,
   Culture, Sports, Science and Technology, Japan (MEXT)Japan Society for
   the Promotion of Science [50583176]
FX This study was supported by grants from the Japan Society for the
   Promotion of Science (No. 50583176).
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NR 43
TC 6
Z9 9
U1 0
U2 8
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 1160 BATTERY STREET, STE 100, SAN FRANCISCO, CA 94111 USA
SN 1932-6203
J9 PLOS ONE
JI PLoS One
PD JUN 12
PY 2018
VL 13
IS 6
AR e0199050
DI 10.1371/journal.pone.0199050
PG 15
WC Multidisciplinary Sciences
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Science & Technology - Other Topics
GA GJ1PQ
UT WOS:000435030900047
PM 29894511
OA Green Submitted, gold, Green Published
DA 2022-04-25
ER

PT J
AU Le, DDT
   Jung, S
   Quynh, NTN
   Sandag, Z
   Lee, BS
   Kim, S
   Lee, H
   Lee, H
   Lee, MS
AF Dan-Diem Thi Le
   Jung, Samil
   Nguyen Thi Ngoc Quynh
   Sandag, Zolzaya
   Lee, Beom Suk
   Kim, Subeen
   Lee, Hyegyeong
   Lee, Hyojeong
   Lee, Myeong-Sok
TI Inhibitory role of AMP-activated protein kinase in necroptosis of HCT116
   colon cancer cells with p53 null mutation under nutrient starvation
SO INTERNATIONAL JOURNAL OF ONCOLOGY
LA English
DT Article
DE necroptosis; p53; AMP-activated protein kinase
ID PERMEABILITY TRANSITION; PROGRAMMED NECROSIS; INTRACELLULAR ATP;
   TARGETING AMPK; NECROTIC DEATH; COMPOUND C; APOPTOSIS; TOLERANCE;
   AUTOPHAGY; SURVIVAL
AB Simultaneous induction of other types of programmed cell death, alongside apoptosis, in cancer cells may be considered an attractive strategy for the development of more effective anticancer therapies. The present study aimed to investigate the role of AMP-activated protein kinase (AMPK) in nutrient/serum starvation-induced necroptosis, which is a programmed form of necrosis, in the presence or absence of p53. The present study detected higher cell proliferation and lower cell death rates in the HCT116 human colon cancer cell line containing a p53 null mutation (HCT116 p53(-/-)) compared with in HCT116 cells harboring wild-type p53 (HCT116 p53(+/+)), as determined using a cell viability assay. Notably, western blot analysis revealed a relatively lower level of necroptosis in HCT116 p53(-/-) cells compared with in HCT116 p53(+/+) cells. Investigating the mechanism, it was revealed that necroptosis may be induced in HCT116 p53(+/+) cells by significantly increasing reactive oxygen species (ROS) and decreasing mitochondrial membrane potential (MMP), whereas little alterations were detected in HCT116 p53(-/-) cells. Unexpectedly, a much lower level of ATP was detected in HCT116 p53(-/-) cells compared with in HCT116 p53(+/+) cells. Accordingly, AMPK phosphorylation on the Thr172 residue was markedly increased in HCT116 p53(-/-) cells. Furthermore, western blot analysis and ROS measurements indicated that AMPK inhibition, using dorsomorphin dihydrochloride, accelerated necroptosis by increasing ROS generation in HCT116 p53(-/-) cells. However, AMPK activation by AICAR did not suppress necroptosis in HCT116 p53(+/+) cells. In conclusion, these data strongly suggested that AMPK activation may be enhanced in HCT116 p53(-/-) cells under serum-depleted conditions via a drop in cellular ATP levels. In addition, activated AMPK may be at least partially responsible for the inhibition of necroptosis in HCT116 p53(-/-) cells, but not in HCT116 p53(+/+)cells.
C1 [Dan-Diem Thi Le; Jung, Samil; Nguyen Thi Ngoc Quynh; Sandag, Zolzaya; Lee, Beom Suk; Kim, Subeen; Lee, Hyegyeong; Lee, Hyojeong; Lee, Myeong-Sok] Sookmyung Womens Univ, Dept Biol Sci, 100 Cheongpa Ro 47 Gil, Seoul 04310, South Korea.
RP Lee, MS (corresponding author), Sookmyung Womens Univ, Dept Biol Sci, 100 Cheongpa Ro 47 Gil, Seoul 04310, South Korea.
EM mslee@sookmyung.ac.kr
FU Sookmyung Women's University
FX The present study was supported by Sookmyung Women's University (2015).
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NR 68
TC 7
Z9 7
U1 5
U2 21
PU SPANDIDOS PUBL LTD
PI ATHENS
PA POB 18179, ATHENS, 116 10, GREECE
SN 1019-6439
EI 1791-2423
J9 INT J ONCOL
JI Int. J. Oncol.
PD FEB
PY 2019
VL 54
IS 2
BP 702
EP 712
DI 10.3892/ijo.2018.4634
PG 11
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA HG4DG
UT WOS:000454923900024
PM 30431068
OA Bronze
DA 2022-04-25
ER

PT J
AU Kumari, N
   Bansal, S
AF Kumari, Neha
   Bansal, Saurabh
TI Arginine depriving enzymes: applications as emerging therapeutics in
   cancer treatment
SO CANCER CHEMOTHERAPY AND PHARMACOLOGY
LA English
DT Review
DE Auxotrophic cancer; Argininosuccinate synthetase; Therapeutic enzyme;
   Deprivation therapy; Arginase; Arginine deiminase; Arginine
   decarboxylase
ID RECOMBINANT HUMAN ARGINASE; CELL-CYCLE ARREST; ADI-PEG 20; HUMAN
   HEPATOCELLULAR-CARCINOMA; IN-VIVO PROLIFERATION; NITRIC-OXIDE SYNTHASE;
   LACTIC-ACID BACTERIA; ARGININOSUCCINATE SYNTHETASE; TUMOR-CELLS;
   INHIBITS PROLIFERATION
AB Cancer is the second leading cause of death globally. Chemotherapy and radiation therapy and other medications are employed to treat various types of cancer. However, each treatment has its own set of side effects, owing to its low specificity. As a result, there is an urgent need for newer therapeutics that do not disrupt healthy cells' normal functioning. Depriving nutrient or non/semi-essential amino acids to which cancerous cells are auxotrophic remains one such promising anticancer strategy. l-Arginine (Arg) is a semi-essential vital amino acid involved in versatile metabolic processes, signaling pathways, and cancer cell proliferation. Hence, the administration of Arg depriving enzymes (ADE) such as arginase, arginine decarboxylase (ADC), and arginine deiminase (ADI) could be effective in cancer therapy. The Arg auxotrophic cancerous cells like hepatocellular carcinoma, human colon cancer, leukemia, and breast cancer cells are sensitive to ADE treatment due to low expression of crucial enzymes argininosuccinate synthetase (ASS), argininosuccinate lyase (ASL), and ornithine transcarbamylase (OCT). These therapeutic enzyme treatments induce cell death through inducing autophagy, apoptosis, generation of oxidative species, i.e., oxidative stress, and arresting the progression and expansion of cancerous cells at certain cell cycle checkpoints. The enzymes are undergoing clinical trials and could be successfully exploited as potential anticancer agents in the future.
C1 [Kumari, Neha; Bansal, Saurabh] Jaypee Univ Informat Technol Waknaghat, Dept Biotechnol & Bioinformat, Solan 173234, Himachal Prades, India.
RP Bansal, S (corresponding author), Jaypee Univ Informat Technol Waknaghat, Dept Biotechnol & Bioinformat, Solan 173234, Himachal Prades, India.
EM saurab.bansal02@gmail.com
RI Bansal, Saurabh/S-9094-2016
OI Bansal, Saurabh/0000-0002-0574-4063
FU Jaypee University of Information Technology Waknaghat, Solan, Himachal
   Pradesh, India
FX The authors acknowledge the Jaypee University of Information Technology
   Waknaghat, Solan, Himachal Pradesh, India, for providing infrastructure
   and financial support for carrying out the present work.
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NR 195
TC 3
Z9 3
U1 3
U2 9
PU SPRINGER
PI NEW YORK
PA ONE NEW YORK PLAZA, SUITE 4600, NEW YORK, NY, UNITED STATES
SN 0344-5704
EI 1432-0843
J9 CANCER CHEMOTH PHARM
JI Cancer Chemother. Pharmacol.
PD OCT
PY 2021
VL 88
IS 4
BP 565
EP 594
DI 10.1007/s00280-021-04335-w
EA JUL 2021
PG 30
WC Oncology; Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Pharmacology & Pharmacy
GA UC7LE
UT WOS:000679012300001
PM 34309734
DA 2022-04-25
ER

PT J
AU De Angelis, ML
   Francescangeli, F
   La Torre, F
   Zeuner, A
AF De Angelis, Maria Laura
   Francescangeli, Federica
   La Torre, Filippo
   Zeuner, Ann
TI Stem Cell Plasticity and Dormancy in the Development of Cancer Therapy
   Resistance
SO FRONTIERS IN ONCOLOGY
LA English
DT Review
DE cancer stem cells; chemoresistance; dormancy; quiescence; plasticity;
   drug resistance; target therapies
ID DISSEMINATED TUMOR-CELLS; BREAST-CANCER; COLON-CANCER; TARGETED THERAPY;
   OXIDATIVE-PHOSPHORYLATION; EARLY DISSEMINATION; DRUG-RESISTANCE;
   OVARIAN-CANCER; METASTASIS; INHIBITION
AB Cancer treatment with either standard chemotherapy or targeted agents often results in the emergence of drug-refractory cell populations, ultimately leading to therapy failure. The biological features of drug resistant cells are largely overlapping with those of cancer stem cells and include heterogeneity, plasticity, self-renewal ability, and tumor-initiating capacity. Moreover, drug resistance is usually characterized by a suppression of proliferation that can manifest as quiescence, dormancy, senescence, or proliferative slowdown. Alterations in key cellular pathways such as autophagy, unfolded protein response or redox signaling, as well as metabolic adaptations also contribute to the establishment of drug resistance, thus representing attractive therapeutic targets. Moreover, a complex interplay of drug resistant cells with the micro/macroenvironment and with the immune system plays a key role in dictating and maintaining the resistant phenotype. Recent studies have challenged traditional views of cancer drug resistance providing innovative perspectives, establishing new connections between drug resistant cells and their environment and indicating unexpected therapeutic strategies. In this review we discuss recent advancements in understanding the mechanisms underlying drug resistance and we report novel targeting agents able to overcome the drug resistant status, with particular focus on strategies directed against dormant cells. Research on drug resistant cancer cells will take us one step forward toward the development of novel treatment approaches iand the improvement of relapse-free survival in solid and hematological cancer patients.
C1 [De Angelis, Maria Laura; Francescangeli, Federica; Zeuner, Ann] Ist Super Sanita, Dept Oncol & Mol Med, Rome, Italy.
   [La Torre, Filippo] Sapienza Univ Rome, Policlin Umberto I, Dept Surg Sci, Rome, Italy.
RP Zeuner, A (corresponding author), Ist Super Sanita, Dept Oncol & Mol Med, Rome, Italy.
EM ann.zeuner@iss.it
RI La Torre, Filippo/AAI-7284-2020; Francescangeli, Federica/K-6500-2016;
   De Angelis, Maria Laura/Y-4004-2019; Zeuner, Ann/K-8607-2016; Zeuner,
   Ann/A-8529-2010
OI La Torre, Filippo/0000-0002-0787-8794; Francescangeli,
   Federica/0000-0002-1086-5265; De Angelis, Maria
   Laura/0000-0003-4220-8822; Zeuner, Ann/0000-0002-8295-3715
FU ERA-NET TRANSCAN grant [TRS-2015-00000096]; Italian Association for
   Cancer Research (AIRC) Investigator GrantFondazione AIRC per la ricerca
   sul cancro [20744]; Awards Sapienza University of Rome grant
   [C26H15ZKWL]
FX This work was supported by an ERA-NET TRANSCAN grant TRS-2015-00000096
   to AZ, by Italian Association for Cancer Research (AIRC) Investigator
   Grant 20744 to AZ, and by Awards Sapienza University of Rome grant
   C26H15ZKWL to FL.
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NR 183
TC 77
Z9 77
U1 12
U2 21
PU FRONTIERS MEDIA SA
PI LAUSANNE
PA AVENUE DU TRIBUNAL FEDERAL 34, LAUSANNE, CH-1015, SWITZERLAND
SN 2234-943X
J9 FRONT ONCOL
JI Front. Oncol.
PD JUL 10
PY 2019
VL 9
AR 626
DI 10.3389/fonc.2019.00626
PG 14
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA IH8AE
UT WOS:000474725600004
PM 31355143
OA Green Published, gold
HC Y
HP N
DA 2022-04-25
ER

PT J
AU Scherr, AL
   Jassowicz, A
   Pato, A
   Elssner, C
   Ismail, L
   Schmitt, N
   Hoffmeister, P
   Neukirch, L
   Gdynia, G
   Goeppert, B
   Schulze-Bergkamen, H
   Jager, D
   Kohler, BC
AF Scherr, Anna-Lena
   Jassowicz, Adam
   Pato, Anna
   Elssner, Christin
   Ismail, Lars
   Schmitt, Nathalie
   Hoffmeister, Paula
   Neukirch, Lasse
   Gdynia, Georg
   Goeppert, Benjamin
   Schulze-Bergkamen, Henning
   Jaeger, Dirk
   Koehler, Bruno Christian
TI Knockdown of Atg7 Induces Nuclear-LC3 Dependent Apoptosis and Augments
   Chemotherapy in Colorectal Cancer Cells
SO INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
LA English
DT Article
DE Atg7; LC3; autophagy; apoptosis; colorectal cancer
ID CHAIN EXPRESSION; AUTOPHAGY; INHIBITION; PROTEINS; DISEASE; RESISTANCE;
   INITIATION; DEATH
AB Autophagy is a catabolic process that enables cells to degrade obsolete content and refuel energy depots. In colorectal cancer (CRC) autophagy has been shown to promote tumorigenesis through energy delivery in the condition of uncontrolled proliferation. With this study, we aimed at evaluating whether autophagy sustains CRC cell viability and if it impacts therapy resistance. Initially, a colorectal cancer tissue micro array, containing mucosa (n = 10), adenoma (n = 18) and adenocarcinoma (n = 49) spots, was stained for expression of essential autophagy proteins LC3b, Atg7, p62 and Beclin-1. Subsequently, central autophagy proteins were downregulated in CRC cells using siRNA technology. Viability assays, flow cytometry and immunoblotting were performed and three-dimensional cell culture was utilized to study autophagy in a tissue mimicking environment. In our study we found an upregulation of Atg7 in CRC. Furthermore, we identified Atg7 as crucial factor within the autophagy network for CRC cell viability. Its disruption induced cell death via triggering apoptosis and in combination with conventional chemotherapy it exerted synergistic effects in inducing CRC cell death. Cell death was strictly dependent on nuclear LC3b, since simultaneous knockdown of Atg7 and LC3b completely restored viability. This study unravels a novel cell death preventing function of Atg7 in interaction with LC3b, thereby unmasking a promising therapeutic target in CRC.
C1 [Scherr, Anna-Lena; Jassowicz, Adam; Pato, Anna; Elssner, Christin; Ismail, Lars; Schmitt, Nathalie; Hoffmeister, Paula; Jaeger, Dirk; Koehler, Bruno Christian] Univ Hosp Heidelberg, Natl Ctr Tumor Dis, D-69120 Heidelberg, Germany.
   [Neukirch, Lasse] Natl Ctr Tumor Dis, Clin Cooperat Unit Appl Tumor Immun, D-69120 Heidelberg, Germany.
   [Neukirch, Lasse] German Canc Res Ctr, D-69120 Heidelberg, Germany.
   [Gdynia, Georg; Goeppert, Benjamin] Univ Hosp Heidelberg, Inst Pathol, D-69120 Heidelberg, Germany.
   [Schulze-Bergkamen, Henning] Marien Hosp, Dept Internal Med 2, D-4648 Wesel, Germany.
RP Kohler, BC (corresponding author), Univ Hosp Heidelberg, Natl Ctr Tumor Dis, D-69120 Heidelberg, Germany.
EM anna-lena.scherr@nct-heidelberg.de; adam@jassowicz.com;
   patoannaterezia@gmail.com; Christin.Elssner@gmx.de;
   lars.ismail1986@googlemail.com; nathalie.schmitt@nct-heidelberg.de;
   paula.hoffmeister@googlemail.com; lasse.neukirch@nct-heidelberg.de;
   Georg.Gdynia@med.uni-heidelberg.de;
   Benjamin.Goeppert@med.uni-heidelberg.de;
   Henning.Schulze-Bergkamen@prohomine.de; dirk.jaeger@nct-heidelberg.de;
   bruno.koehler@nct-heidelberg.de
RI Goeppert, Benjamin/AAC-2303-2022
OI Pato, Anna/0000-0003-1238-3662; Neukirch, Lasse/0000-0002-2055-4743
FU German Research Foundation (DFG)German Research Foundation (DFG)
   [KO5205/1-1]; German Cancer Aid (DKH)Deutsche Krebshilfe [70113593];
   Brigitte and Dr. KonstanzeWegener foundation; Medical Faculty of the
   University Heidelberg
FX This study was supported by a stipend of the Medical Faculty of the
   University Heidelberg to ALS (Rahel-Goitein-Strauss Program) and by
   research grants of the Brigitte and Dr. KonstanzeWegener foundation, the
   German Research Foundation (DFG, grant No. KO5205/1-1) and the German
   Cancer Aid (DKH, grant No. 70113593) to BCK.
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NR 49
TC 5
Z9 5
U1 1
U2 5
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 1422-0067
J9 INT J MOL SCI
JI Int. J. Mol. Sci.
PD FEB
PY 2020
VL 21
IS 3
AR 1099
DI 10.3390/ijms21031099
PG 15
WC Biochemistry & Molecular Biology; Chemistry, Multidisciplinary
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Chemistry
GA KY4PQ
UT WOS:000522551607026
PM 32046105
OA gold, Green Published
DA 2022-04-25
ER

PT J
AU Caicedo-Lopez, LH
   Cuellar-Nunez, ML
   Luzardo-Ocampo, I
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AF Caicedo-Lopez, Laura H.
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   Campos-Vega, Rocio
   Loarca-Pina, Guadalupe
TI Colonic metabolites from digested Moringa oleifera leaves induced HT-29
   cell death via apoptosis, necrosis, and autophagy
SO INTERNATIONAL JOURNAL OF FOOD SCIENCES AND NUTRITION
LA English
DT Article
DE Moringa oleifera; apoptosis; autophagy; colorectal cancer; colonic
   metabolites; short-chain fatty acids
AB Colorectal cancer is an important concern in modern society. Risk factors such as the diet indicate the need to find healthy food products displaying additional health benefits. This study aimed to characterise and evaluate the impact of the colonic metabolites from the fermented non-digestible fraction of Moringa oleifera (MO) leaves (FNFM) on cell death mechanisms from HT-29 cells. MO leaves were digested in vitro, and the 12 h-colonic extract was obtained. FNFM mainly contained morin and chlorogenic acids (41.97 and 25.33 mu g/g sample). Butyric acid was ranked as the most important metabolite of FNFM. The FNFM exerted antiproliferative effect against HT-29 colorectal cancer cells (half lethal concentration, LC50: 5.9 mL/100 mL). Compared to untreated control, LC50 increased H2O2 production (149.43%); induced apoptosis (119.02%), autophagy (75.60%), and necrosis (87.72%). These results suggested that digested MO colonic metabolites exert antiproliferative effect against HT-29 cells, providing additional health benefits associated with MO consumption.
C1 [Caicedo-Lopez, Laura H.; Luzardo-Ocampo, Ivan; Campos-Vega, Rocio; Loarca-Pina, Guadalupe] Univ Autonoma Queretaro, Sch Chem, Res & Grad Program Food Sci, Queretaro, Mexico.
   [Caicedo-Lopez, Laura H.] Univ Autonoma Queretaro, Sch Engn, Biosyst Engn Grp, Queretaro, Mexico.
   [Cuellar-Nunez, M. Liceth] Univ Autonoma Queretaro, Fac Med, Queretaro, Mexico.
RP Loarca-Pina, G (corresponding author), Univ Autonoma Queretaro, Sch Chem, Res & Grad Program Food Sci, Queretaro, Mexico.
EM loarca@uaq.mx
RI Luzardo-Ocampo, Ivan/R-4350-2019; Campos-Vega, Rocio/L-3151-2016
OI Luzardo-Ocampo, Ivan/0000-0002-8033-3520; CAICEDO LOPEZ, LAURA
   HELENA/0000-0001-5184-0112; Campos-Vega, Rocio/0000-0003-4054-1250;
   Loarca-Pina, Guadalupe/0000-0002-8416-9617
FU Consejo Nacional de Ciencia y Tecnologia (CONACyT-Mexico)Consejo
   Nacional de Ciencia y Tecnologia (CONACyT) [582098, 384201, 278375];
   Universidad Autonoma de Queretaro [231214]
FX This work was supported by the Consejo Nacional de Ciencia y Tecnologia
   (CONACyT-Mexico) under Grant [grant number: 582098, 384201, and 278375];
   Universidad Autonoma de Queretaro under Grant [grant number 231214].
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NR 49
TC 2
Z9 3
U1 0
U2 3
PU TAYLOR & FRANCIS LTD
PI ABINGDON
PA 2-4 PARK SQUARE, MILTON PARK, ABINGDON OR14 4RN, OXON, ENGLAND
SN 0963-7486
EI 1465-3478
J9 INT J FOOD SCI NUTR
JI Int. J. Food Sci. Nutr.
PD MAY 19
PY 2021
VL 72
IS 4
BP 485
EP 498
DI 10.1080/09637486.2020.1849039
EA NOV 2020
PG 14
WC Food Science & Technology; Nutrition & Dietetics
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Food Science & Technology; Nutrition & Dietetics
GA SB4IT
UT WOS:000597406800001
PM 33302731
DA 2022-04-25
ER

PT J
AU Min, H
   Xu, M
   Chen, ZR
   Zhou, JD
   Huang, M
   Zheng, K
   Zou, XP
AF Min, Han
   Xu, Min
   Chen, Zhi-rong
   Zhou, Jun-dong
   Huang, Min
   Zheng, Kai
   Zou, Xiao-ping
TI Bortezomib induces protective autophagy through AMP-activated protein
   kinase activation in cultured pancreatic and colorectal cancer cells
SO CANCER CHEMOTHERAPY AND PHARMACOLOGY
LA English
DT Article
DE Bortezomib; Autophagy; AMPK; Apoptosis-resistance and
   chemo-sensitization
ID SIGNALING PATHWAY; STEM-CELLS; ALK KINASE; NEUROBLASTOMA; DEATH;
   MUTATIONS; RECEPTOR; ENERGY; GROWTH; PHOSPHORYLATION
AB Bortezomib, a selective and potent inhibitor of the proteasome, has demonstrated broad anti-tumor activities in many malignancies. In the current study, we aimed to understand the potential resistance factor of bortezomib in cultured pancreatic and colorectal cancer cells.
   We observed that bortezomib-induced protective autophagy in cultured PANC-1 pancreatic cancer cells and HT-29 colorectal cancer cells. Inhibition of autophagy by 3-methyladenine (3-MA) and chloroquine enhanced bortezomib-induced apoptosis and cytotoxicity in both PANC-1 and HT-29 cells. Activation of AMP-activated protein kinase (AMPK) was required for bortezomib-induced autophagy induction in PANC-1 and HT-29 cells, and AMPK inhibition by its inhibitor compound C (CC) or RNAi-depletion suppressed bortezomib-induced autophagy, while dramatically enhancing cancer cell apoptosis/cytotoxicity. Meanwhile, significant AMPK activation and autophagy induction were observed after bortezomib stimulation in primary cultured pancreatic cancer cells derived from a patient's tumor tissue. Both CC and 3-MA facilitated bortezomib-induced cytotoxicity in primary cultured pancreatic cancer cells.
   In conclusion, our data here suggest that bortezomib induces protective autophagy in pancreatic and colorectal cancer cells through activating AMPK-Ulk1 signalings. AMPK or autophagy inhibitors could be developed as an adjunct or chemo-sensitizer for bortezomib.
C1 [Min, Han; Zou, Xiao-ping] Nanjing Med Univ, Dept Gastroenterol, Drum Tower Clin Med Coll, Nanjing 210008, Peoples R China.
   [Min, Han; Chen, Zhi-rong] Nanjing Med Univ, Affiliated Suzhou Hosp, Dept Gastroenterol, Suzhou 215001, Peoples R China.
   [Xu, Min] Wuxi Peoples Hosp, Dept GI Med, Wuxi 214000, Jiangsu, Peoples R China.
   [Zhou, Jun-dong; Huang, Min; Zheng, Kai] Nanjing Med Univ, Suzhou Hosp, Tumor Lab, Suzhou 215001, Peoples R China.
RP Zou, XP (corresponding author), Nanjing Med Univ, Dept Gastroenterol, Drum Tower Clin Med Coll, Zhongshan Rd 321, Nanjing 210008, Peoples R China.
EM minhanmd1981@163.com; szchenzhirong@163.com; zouxiaoping795@hotmail.com
FU National Natural Science FoundationNational Natural Science Foundation
   of China (NSFC)
FX This research was supported by grants from the National Natural Science
   Foundation (to Jun-dong Zhou).
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NR 50
TC 41
Z9 41
U1 2
U2 25
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0344-5704
EI 1432-0843
J9 CANCER CHEMOTH PHARM
JI Cancer Chemother. Pharmacol.
PD JUL
PY 2014
VL 74
IS 1
BP 167
EP 176
DI 10.1007/s00280-014-2451-7
PG 10
WC Oncology; Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Pharmacology & Pharmacy
GA AK9PT
UT WOS:000338759700016
PM 24842158
DA 2022-04-25
ER

PT J
AU Tirodkar, TS
   Lu, P
   Bai, AP
   Scheffel, MJ
   Gencer, S
   Garrett-Mayer, E
   Bielawska, A
   Ogretmen, B
   Voelkel-Johnson, C
AF Tirodkar, Tejas S.
   Lu, Ping
   Bai, Aiping
   Scheffel, Matthew J.
   Gencer, Salih
   Garrett-Mayer, Elizabeth
   Bielawska, Alicja
   Ogretmen, Besim
   Voelkel-Johnson, Christina
TI Expression of Ceramide Synthase 6 Transcriptionally Activates Acid
   Ceramidase in a c-Jun N-terminal Kinase (JNK)-dependent Manner
SO JOURNAL OF BIOLOGICAL CHEMISTRY
LA English
DT Article
ID COLON-CANCER CELLS; SPHINGOLIPID METABOLISM; INDUCED APOPTOSIS;
   CARCINOMA-CELLS; TUMOR-CELLS; INDUCTION; STRESS; AUTOPHAGY; LIVER;
   SUPPRESSION
AB A family of six ceramide synthases with distinct but overlapping substrate specificities is responsible for generation of ceramides with acyl chains ranging from similar to 14-26 carbons. Ceramide synthase 6 (CerS6) preferentially generates C-14- and C-16-ceramides, and we have previously shown that down-regulation of this enzyme decreases apoptotic susceptibility. In this study, we further evaluated how increased CerS6 expression impacts sphingolipid composition and metabolism. Overexpression of CerS6 in HT29 colon cancer cells resulted in increased apoptotic susceptibility and preferential generation of C-16-ceramide, which occurred at the expense of very long chain, saturated ceramides. These changes were also reflected in sphingomyelin composition. HT-CerS6 cells had increased intracellular levels of sphingosine, which is generated by ceramidases upon hydrolysis of ceramide. qRT-PCR analysis revealed that only expression of acid ceramidase (ASAH1) was increased. The increase in acid ceramidase was confirmed by expression and activity analyses. Pharmacological inhibition of JNK (SP600125) or curcumin reduced transcriptional up-regulation of acid ceramidase. Using an acid ceramidase promoter driven luciferase reporter plasmid, we demonstrated that CerS1 has no effect on transcriptional activation of acid ceramidase and that CerS2 slightly but significantly decreased the luciferase signal. Similar to CerS6, overexpression of CerS3-5 resulted in an similar to 2-fold increase in luciferase reporter gene activity. Exogenous ceramide failed to induce reporter activity, while a CerS inhibitor and a catalytically inactive mutant of CerS6 failed to reduce it. Taken together, these results suggest that increased expression of CerS6 can mediate transcriptional activation of acid ceramidase in a JNK-dependent manner that is independent of CerS6 activity.
C1 [Tirodkar, Tejas S.; Lu, Ping; Scheffel, Matthew J.; Voelkel-Johnson, Christina] Med Univ S Carolina, Dept Microbiol & Immunol, Charleston, SC 29425 USA.
   [Bai, Aiping; Gencer, Salih; Bielawska, Alicja; Ogretmen, Besim] Med Univ S Carolina, Dept Biochem & Mol Biol, Charleston, SC 29425 USA.
   [Garrett-Mayer, Elizabeth] Med Univ S Carolina, Dept Publ Hlth, Charleston, SC 29425 USA.
   [Gencer, Salih] Dept Mol Biol & Genet, TR-34662 Istanbul, Turkey.
RP Voelkel-Johnson, C (corresponding author), Med Univ S Carolina, Dept Microbiol & Immunol, 173 Ashley Ave, Charleston, SC 29425 USA.
EM johnsocv@musc.edu
RI Regan, Clinton/E-6250-2012; Gencer, Salih/AAL-5502-2020; Gencer,
   Salih/B-6436-2012
OI Garrett-Mayer, Elizabeth/0000-0003-4709-0333
FU MUSC; Lipidomics and Flow Cytometry Shared Resources, Hollings Cancer
   Center, MUSC [P30 CA138313]; National Institutes of HealthUnited States
   Department of Health & Human ServicesNational Institutes of Health (NIH)
   - USA [P01 CA154778];  [CA88032];  [CA173687];  [DE016572]; NATIONAL
   CANCER INSTITUTEUnited States Department of Health & Human
   ServicesNational Institutes of Health (NIH) - USANIH National Cancer
   Institute (NCI) [R01CA173687, P30CA138313, P01CA154778] Funding Source:
   NIH RePORTER; NATIONAL INSTITUTE OF DENTAL & CRANIOFACIAL RESEARCHUnited
   States Department of Health & Human ServicesNational Institutes of
   Health (NIH) - USANIH National Institute of Dental & Craniofacial
   Research (NIDCR) [R01DE016572] Funding Source: NIH RePORTER
FX This project was supported by MUSC intramural funds (to C. V. J.) and in
   part by the Lipidomics and Flow Cytometry Shared Resources, Hollings
   Cancer Center, MUSC (P30 CA138313).; Supported by CA88032, CA173687, and
   DE016572.; Supported by National Institutes of Health Grant P01
   CA154778.
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NR 50
TC 25
Z9 25
U1 1
U2 9
PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3996 USA
EI 1083-351X
J9 J BIOL CHEM
JI J. Biol. Chem.
PD MAY 22
PY 2015
VL 290
IS 21
BP 13157
EP 13167
DI 10.1074/jbc.M114.631325
PG 11
WC Biochemistry & Molecular Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology
GA CI7WL
UT WOS:000354975700018
PM 25839235
OA Green Published, hybrid
DA 2022-04-25
ER

PT J
AU Liu, WM
   Huang, P
   Kar, N
   Burgett, M
   Muller-Greven, G
   Nowacki, AS
   Distelhorst, CW
   Lathia, JD
   Rich, JN
   Kappes, JC
   Gladson, CL
AF Liu, Wei Michael
   Huang, Ping
   Kar, Niladri
   Burgett, Monica
   Muller-Greven, Gaelle
   Nowacki, Amy S.
   Distelhorst, Clark W.
   Lathia, Justin D.
   Rich, Jeremy N.
   Kappes, John C.
   Gladson, Candece L.
TI Lyn Facilitates Glioblastoma Cell Survival under Conditions of Nutrient
   Deprivation by Promoting Autophagy
SO PLOS ONE
LA English
DT Article
ID SRC FAMILY KINASES; CHRONIC LYMPHOCYTIC-LEUKEMIA; COLON-CARCINOMA CELLS;
   MYELOGENOUS LEUKEMIA; TYROSINE KINASE; MONITORING AUTOPHAGY;
   PROSTATE-CANCER; RESISTANT CELLS; TUMOR-GROWTH; DNA-DAMAGE
AB Members of the Src family kinases (SFK) can modulate diverse cellular processes, including division, death and survival, but their role in autophagy has been minimally explored. Here, we investigated the roles of Lyn, a SFK, in promoting the survival of human glioblastoma tumor (GBM) cells in vitro and in vivo using lentiviral vector-mediated expression of constitutively-active Lyn (CA-Lyn) or dominant-negative Lyn (DN-Lyn). Expression of either CA-Lyn or DN-Lyn had no effect on the survival of U87 GBM cells grown under nutrient-rich conditions. In contrast, under nutrient-deprived conditions (absence of supplementation with L-glutamine, which is essential for growth of GBM cells, and FBS) CA-Lyn expression enhanced survival and promoted autophagy as well as inhibiting cell death and promoting proliferation. Expression of DN-Lyn promoted cell death. In the nutrient-deprived GBM cells, CA-Lyn expression enhanced AMPK activity and reduced the levels of pS6 kinase whereas DN-Lyn enhanced the levels of pS6 kinase. Similar results were obtained in vitro using another cultured GBM cell line and primary glioma stem cells. On propagation of the transduced GBM cells in the brains of nude mice, the CA-Lyn xenografts formed larger tumors than control cells and autophagosomes were detectable in the tumor cells. The DN-Lyn xenografts formed smaller tumors and contained more apoptotic cells. Our findings suggest that on nutrient deprivation in vitro Lyn acts to enhance the survival of GBM cells by promoting autophagy and proliferation as well as inhibiting cell death, and Lyn promotes the same effects in vivo in xenograft tumors. As the levels of Lyn protein or its activity are elevated in several cancers these findings may be of broad relevance to cancer biology.
C1 [Liu, Wei Michael; Huang, Ping; Kar, Niladri; Burgett, Monica; Muller-Greven, Gaelle; Gladson, Candece L.] Cleveland Clin, Lerner Res Inst, Dept Canc Biol, Cleveland, OH 44106 USA.
   [Nowacki, Amy S.] Cleveland Clin, Dept Quantitat Hlth Sci, Cleveland, OH 44106 USA.
   [Lathia, Justin D.; Rich, Jeremy N.] Cleveland Clin, Lerner Res Inst, Dept Stem Cell Biol & Regenerat Med, Cleveland, OH 44106 USA.
   [Burgett, Monica; Muller-Greven, Gaelle] Kent State Univ, Sch Biomed Sci, Kent, OH 44242 USA.
   [Distelhorst, Clark W.] Case Western Reserve Univ, Dept Med, Cleveland, OH 44106 USA.
   [Kappes, John C.] Univ Alabama Birmingham, Dept Med, Birmingham, AL 35294 USA.
RP Gladson, CL (corresponding author), Cleveland Clin, Lerner Res Inst, Dept Canc Biol, Cleveland, OH 44106 USA.
EM gladsoc@ccf.org
RI Rich, Jeremy/AAM-1445-2021
FU NIH NCIUnited States Department of Health & Human ServicesNational
   Institutes of Health (NIH) - USANIH National Cancer Institute (NCI)
   [CA043703, CA109748, CA127620, CA152883]; University of Alabama at
   Birmingham (UAB) Center for AIDS Research Virology and Sequencing Cores
   [P30-AI-27767]; Genetically Defined Microbe and Expression Core of the
   UAB Mucosal HIV and Immunobiology Center [R24 DK-64400]; NATIONAL CANCER
   INSTITUTEUnited States Department of Health & Human ServicesNational
   Institutes of Health (NIH) - USANIH National Cancer Institute (NCI)
   [R01CA152883, R01CA127620, R01CA175120, R01CA085804, R01CA109748,
   P30CA043703] Funding Source: NIH RePORTER; NATIONAL INSTITUTE OF ALLERGY
   AND INFECTIOUS DISEASESUnited States Department of Health & Human
   ServicesNational Institutes of Health (NIH) - USANIH National Institute
   of Allergy & Infectious Diseases (NIAID) [P30AI027767] Funding Source:
   NIH RePORTER; NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY
   DISEASESUnited States Department of Health & Human ServicesNational
   Institutes of Health (NIH) - USANIH National Institute of Diabetes &
   Digestive & Kidney Diseases (NIDDK) [R24DK064400] Funding Source: NIH
   RePORTER
FX This work was supported by NIH NCI grants CA043703 (CWD), CA109748,
   CA127620 and CA152883(CLG), the University of Alabama at Birmingham
   (UAB) Center for AIDS Research Virology and Sequencing Cores
   (P30-AI-27767) and the Genetically Defined Microbe and Expression Core
   of the UAB Mucosal HIV and Immunobiology Center (R24 DK-64400) (JCK).
   The funders had no role in study design, data collection and analysis,
   decision to publish, or preparation of the manuscript.
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NR 53
TC 18
Z9 18
U1 0
U2 11
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 1160 BATTERY STREET, STE 100, SAN FRANCISCO, CA 94111 USA
SN 1932-6203
J9 PLOS ONE
JI PLoS One
PD AUG 2
PY 2013
VL 8
IS 8
AR e70804
DI 10.1371/journal.pone.0070804
PG 13
WC Multidisciplinary Sciences
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Science & Technology - Other Topics
GA 219XU
UT WOS:000324545800050
PM 23936469
OA gold, Green Submitted, Green Published
DA 2022-04-25
ER

PT J
AU Shi, Y
   Xu, SF
   Ngoi, NYL
   Hui, YJ
   Ye, Z
AF Shi, Yin
   Xu, Shengfeng
   Ngoi, Natalie Y. L.
   Hui, Yuanjian
   Ye, Zu
TI Rag GTPases suppress PRL-3 degradation and predict poor clinical
   diagnosis of cancer patients with low PRL-3 mRNA expression
SO BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
LA English
DT Article
DE Rag GTPases; PRL-3; Protein stability
ID MTORC1
AB Ras-related GTP binding (Rag) GTPases are required to activate mechanistic target of rapamycin complex 1 (mTORC1), which plays a central role in cell growth and metabolism and is considered as one of the most important oncogenic pathways. Therefore, Rag GTPases have been speculated to play a pro-cancer role via mTOR induction. However, aside from stimulation of mTOR signaling, firm links connecting Rag GTPase activity and their downstream effectors with cancer progression, remain largely unreported. In this study, we reported a novel link between RagB/C and a known oncoprotein phosphatase of regenerating liver-3 (PRL-3) by screening 22 pairs of tumors and their adjacent normal tissues from gastric, liver and lung cancers, and validating our findings in cancer cell lines with ectopic RagB/C expression. RagB/C was found to enhance PRL-3 stability by modulating two major cellular protein degradation pathways: lysosomal-autophagy and ubiquitin-proteasome system (UPS). Functionally, we identified the correlation between RagB/C expression with poor clinical outcomes in breast or colon cancer patients who also showed low PRL-3 mRNA expression from data retrieved from TCGA datasets, highlighting the potential relevance of Rag GTPase and PRL-3 mRNA in combination as a prognostic clinical biomarker. (c) 2021 Published by Elsevier Inc.
C1 [Shi, Yin] Zhejiang Univ, Inst Immunol, Sch Med, Hangzhou, Peoples R China.
   [Shi, Yin; Ye, Zu] Natl Univ Singapore, Yong Loo Lin Sch Med, Dept Physiol, Singapore, Singapore.
   [Xu, Shengfeng] Univ Texas MD Anderson Canc Ctr, Dept Genet, Houston, TX 77030 USA.
   [Ngoi, Natalie Y. L.] Univ Texas MD Anderson Canc Ctr, Div Canc Med, Dept Invest Canc Therapeut, Houston, TX 77030 USA.
   [Ngoi, Natalie Y. L.] Natl Univ Canc Inst, Dept Hematol Oncol, Singapore, Singapore.
   [Hui, Yuanjian] Hubei Univ Med, Taihe Hosp, Dept Gen Surg, Shiyan, Hubei, Peoples R China.
   [Ye, Zu] ASTAR, Inst Mol & Cell Biol, Singapore, Singapore.
   [Ye, Zu] Univ Texas MD Anderson Canc Ctr, Dept Mol & Cellular Oncol, Houston, TX 77030 USA.
RP Shi, Y (corresponding author), Zhejiang Univ, Inst Immunol, Sch Med, Hangzhou, Peoples R China.; Ye, Z (corresponding author), Univ Texas MD Anderson Canc Ctr, Dept Mol & Cellular Oncol, Houston, TX 77030 USA.
EM yinshi@zju.edu.cn; zye4@mdanderson.org
OI Xu, Shengfeng/0000-0002-5774-7549
FU National Natural Sci-ence Foundation of ChinaNational Natural Science
   Foundation of China (NSFC) [31801161]
FX This work was supported by grants from National Natural Sci-ence
   Foundation of China (No. 31801161) to Y.S.
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NR 24
TC 0
Z9 0
U1 0
U2 4
PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 0006-291X
EI 1090-2104
J9 BIOCHEM BIOPH RES CO
JI Biochem. Biophys. Res. Commun.
PD OCT 22
PY 2021
VL 576
BP 108
EP 116
DI 10.1016/j.bbrc.2021.08.090
EA SEP 2021
PG 9
WC Biochemistry & Molecular Biology; Biophysics
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Biophysics
GA UO5EZ
UT WOS:000694718600003
PM 34482023
DA 2022-04-25
ER

PT J
AU Dai, RC
   Liu, MF
   Nabil, WNN
   Xi, ZC
   Xu, HX
AF Dai, Rongchen
   Liu, Mengfan
   Nabil, Wan Najbah Nik
   Xi, Zhichao
   Xu, Hongxi
TI Mycomedicine: A Unique Class of Natural Products with Potent Anti-tumour
   Bioactivities
SO MOLECULES
LA English
DT Review
DE mycomedicine; medicinal fungi; anti-cancer; polysaccharides;
   triterpenoids
ID CELL-CYCLE ARREST; GANODERMA-LUCIDUM POLYSACCHARIDE;
   HEPATOCELLULAR-CARCINOMA GROWTH; AGARICUS-BLAZEI MURILL; COLON-CANCER
   CELLS; GRIFOLA-FRONDOSA; IN-VITRO; ANTICANCER PROPERTIES;
   BIOLOGICAL-ACTIVITIES; MOLECULAR-MECHANISMS
AB Mycomedicine is a unique class of natural medicine that has been widely used in Asian countries for thousands of years. Modern mycomedicine consists of fruiting bodies, spores, or other tissues of medicinal fungi, as well as bioactive components extracted from them, including polysaccharides and, triterpenoids, etc. Since the discovery of the famous fungal extract, penicillin, by Alexander Fleming in the late 19th century, researchers have realised the significant antibiotic and other medicinal values of fungal extracts. As medicinal fungi and fungal metabolites can induce apoptosis or autophagy, enhance the immune response, and reduce metastatic potential, several types of mushrooms, such as Ganoderma lucidum and Grifola frondosa, have been extensively investigated, and anti-cancer drugs have been developed from their extracts. Although some studies have highlighted the anti-cancer properties of a single, specific mushroom, only limited reviews have summarised diverse medicinal fungi as mycomedicine. In this review, we not only list the structures and functions of pharmaceutically active components isolated from mycomedicine, but also summarise the mechanisms underlying the potent bioactivities of several representative mushrooms in the Kingdom Fungi against various types of tumour.
C1 [Dai, Rongchen; Liu, Mengfan; Nabil, Wan Najbah Nik; Xi, Zhichao] Shanghai Univ Tradit Chinese Med, Sch Pharm, Shanghai 201203, Peoples R China.
   [Nabil, Wan Najbah Nik] Minist Hlth, Pharmaceut Serv Program, Petaling Jaya 46200, Selangor, Malaysia.
   [Xu, Hongxi] Shanghai Univ Tradit Chinese Med, Shuguang Hosp, Shanghai 201203, Peoples R China.
RP Xi, ZC (corresponding author), Shanghai Univ Tradit Chinese Med, Sch Pharm, Shanghai 201203, Peoples R China.; Xu, HX (corresponding author), Shanghai Univ Tradit Chinese Med, Shuguang Hosp, Shanghai 201203, Peoples R China.
EM ycy220823@gmail.com; mengfanliush@163.com; najbah@yahoo.com;
   xizhichao@shutcm.edu.cn; hxxu@shutcm.edu.cn
RI Dai, Rongchen/AAO-4747-2021; Xi, Zhichao/AAD-5842-2020; Liu,
   Mengfan/AAO-4758-2021; Rongchen, DAI/AAQ-8585-2021
OI Xi, Zhichao/0000-0001-7366-9045; Liu, Mengfan/0000-0002-5402-5102; Xu,
   Hongxi/0000-0001-6238-4511; Nik Nabil, Wan Najbah/0000-0001-6400-8691
FU National Natural Science Foundation ofChinaNational Natural Science
   Foundation of China (NSFC) [.81803571, 81973438]; NSFC-Joint Foundation
   of Yunnan Province [U1902213]; Key-Area Research and Development Program
   of Guangdong Province [2020B1111110003]
FX This researchwas funded by National Natural Science Foundation ofChina
   (GrantNo.81803571, 81973438); NSFC-Joint Foundation of Yunnan Province
   (Grant No. U1902213); Key-Area Research and Development Program of
   Guangdong Province (Grant No. 2020B1111110003).
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NR 126
TC 1
Z9 1
U1 15
U2 24
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 1420-3049
J9 MOLECULES
JI Molecules
PD FEB
PY 2021
VL 26
IS 4
AR 1113
DI 10.3390/molecules26041113
PG 22
WC Biochemistry & Molecular Biology; Chemistry, Multidisciplinary
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Chemistry
GA QP9JH
UT WOS:000624144700001
PM 33669877
OA Green Published, gold
DA 2022-04-25
ER

PT J
AU Wang, H
   Wang, YA
   Qian, L
   Wang, X
   Gu, HL
   Dong, XQ
   Huang, SQ
   Jin, M
   Ge, HL
   Xu, CF
   Zhang, YY
AF Wang, Hui
   Wang, Yanan
   Qian, Liu
   Wang, Xue
   Gu, Hailiang
   Dong, Xiaoqiang
   Huang, Shiqian
   Jin, Min
   Ge, Hailiang
   Xu, Congfeng
   Zhang, Yanyun
TI RNF216 contributes to proliferation and migration of colorectal cancer
   via suppressing BECN1-dependent autophagy
SO ONCOTARGET
LA English
DT Article
DE RNF216; BECN1; autophagy; colorectal cancer
ID BECLIN 1; DEGRADATION; TRIAD3A; GROWTH; SWITCH; CELLS
AB Originally identified as an E3 ligase regulating toll-like receptor (TLR) signaling, ring finger protein 216 (RNF216) also plays an essential role in autophagy, which is fundamental to cellular homeostasis. Autophagy dysfunction leads to an array of pathological events, including tumor formation. In this study, we found that RNF216 was upregulated in human colorectal cancer (CRC) tissues and cell lines, and was associated with progression of CRC. RNF216 promoted CRC cell proliferation and migration in vitro and in vivo, largely by enhancing proteasomal degradation of BECN1, a key autophagy regulator and tumor suppressor. RNF216 restricted CRC cell autophagy through BECN1 inhibition under nutritional starvation conditions. RNF216 knockdown increased the autophagy, limiting CRC cell proliferation and migration. Moreover, BECN1 knockdown or autophagy inhibition restored proliferation and migration of RNF216-knockdown CRC cells. Collectively, our results suggested that RNF216 promoted CRC cell proliferation and migration by negatively regulating BECN1-dependent autophagy. This makes RNF216 as a potential biomarker and novel therapeutic target for inhibiting CRC development and progression.
C1 [Wang, Hui; Wang, Yanan; Qian, Liu; Wang, Xue; Huang, Shiqian; Jin, Min; Ge, Hailiang; Xu, Congfeng; Zhang, Yanyun] Shanghai Jiao Tong Univ, Sch Med, Shanghai Inst Immunol, Inst Med Sci,SJTUSM, Shanghai, Peoples R China.
   [Wang, Hui; Wang, Yanan; Qian, Liu; Wang, Xue; Huang, Shiqian; Jin, Min; Ge, Hailiang; Xu, Congfeng; Zhang, Yanyun] Chinese Acad Sci, Shanghai Inst Biol Sci, Inst Hlth Sci, Key Lab Stem Cell Biol, Shanghai, Peoples R China.
   [Wang, Hui; Wang, Yanan; Qian, Liu; Wang, Xue; Huang, Shiqian; Jin, Min; Ge, Hailiang; Xu, Congfeng; Zhang, Yanyun] SJTUSM, Shanghai, Peoples R China.
   [Gu, Hailiang; Dong, Xiaoqiang] Soochow Univ, Affiliated Hosp 1, Dept Gen Surg, Suzhou, Peoples R China.
RP Ge, HL; Xu, CF; Zhang, YY (corresponding author), Shanghai Jiao Tong Univ, Sch Med, Shanghai Inst Immunol, Inst Med Sci,SJTUSM, Shanghai, Peoples R China.; Ge, HL; Xu, CF; Zhang, YY (corresponding author), Chinese Acad Sci, Shanghai Inst Biol Sci, Inst Hlth Sci, Key Lab Stem Cell Biol, Shanghai, Peoples R China.; Ge, HL; Xu, CF; Zhang, YY (corresponding author), SJTUSM, Shanghai, Peoples R China.
EM ghl@shsmu.edu.cn; cxu@shsmu.edu.cn; yyzhang@sibs.ac.cn
RI Xu, Congfeng/E-4806-2013
OI Xu, Congfeng/0000-0002-8009-4865
FU Ministry of Science and Technology of ChinaMinistry of Science and
   Technology, China [2015CB943303, 2014CB943303]; National Natural Science
   Foundation of ChinaNational Natural Science Foundation of China (NSFC)
   [81502607, 81502506, 31570905, 31300708, 81471217]; Program of Science
   and Technology Commission of Shanghai MunicipalityScience & Technology
   Commission of Shanghai Municipality (STCSM) [15JC1402900, 13ZR1423200,
   14ZR1446300]
FX This study was supported by the Ministry of Science and Technology of
   China (2015CB943303, 2014CB943303), National Natural Science Foundation
   of China (81502607, 81502506, 31570905, 31300708 and 81471217), the
   Program of Science and Technology Commission of Shanghai Municipality
   (15JC1402900, 13ZR1423200 and 14ZR1446300).
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NR 35
TC 23
Z9 26
U1 3
U2 6
PU IMPACT JOURNALS LLC
PI ORCHARD PARK
PA 6666 E QUAKER ST, STE 1, ORCHARD PARK, NY 14127 USA
EI 1949-2553
J9 ONCOTARGET
JI Oncotarget
PD AUG 9
PY 2016
VL 7
IS 32
BP 51174
EP 51183
DI 10.18632/oncotarget.9433
PG 10
WC Oncology; Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Cell Biology
GA DY9CC
UT WOS:000385429100034
PM 27203674
OA gold, Green Published, Green Submitted
DA 2022-04-25
ER

PT J
AU Bahreyni-Toossi, MT
   Dolat, E
   Khanbabaei, H
   Zafari, N
   Azimian, H
AF Bahreyni-Toossi, Mohammad-Taghi
   Dolat, Elham
   Khanbabaei, Hashem
   Zafari, Navid
   Azimian, Hosein
TI microRNAs: Potential glioblastoma radiosensitizer by targeting
   radiation-related molecular pathways
SO MUTATION RESEARCH-FUNDAMENTAL AND MOLECULAR MECHANISMS OF MUTAGENESIS
LA English
DT Review
DE Radiosensitivity; Radiation therapy; Ionizing radiation; Glioblastoma;
   Cancer; microRNA
ID GLIOMA STEM-CELLS; BREAST-CANCER CELLS; ROS PRODUCTION; TUMOR-GROWTH;
   ENHANCES RADIOSENSITIVITY; AUTOPHAGY INHIBITION; COLON-CANCER; U87MG
   CELLS; DNA-REPAIR; EXPRESSION
AB Glioblastoma (GBM) is the most lethal type of primary brain tumor. Currently, even with optimal and multimodal cancer therapies, the survival rate of GBM patients remains poor. One reason for inadequate response of GBM tumors to radiotherapy is radioresistance (RR). Thus, there is a critical need for new insights about GBM treatment to increase the chance of treatment. microRNAs (miRNAs) are important regulatory molecules that can effectively control GBM radiosensitivity (RS) by affecting radiation-related signal transduction pathways such as apoptosis, proliferation, DNA repair and cell cycle regulation. miRNAs provide new clinical perspectives for developing effective GBM treatments. A growing body of literature has demonstrated that GBM RS can be modified by modulating the expression of miRNAs such as miR-7, miR-10b, miR-124, miR-128, miR-320, miR-21, miR-203, and miR-153. This paper highlights the miRNAs and the underlying molecular mechanisms that are involved in the RS of GBM. Besides highlighting the role of miRNAs in different signaling pathways, we explain the mechanisms that affect RS of GBM for modulating radiation response at the clinical level.
C1 [Bahreyni-Toossi, Mohammad-Taghi; Azimian, Hosein] Mashhad Univ Med Sci, Med Phys Res Ctr, Buali Sq,Ferdousi Sq,POB 9196773117, Mashhad, Razavi Khorasan, Iran.
   [Dolat, Elham; Zafari, Navid] Mashhad Univ Med Sci, Fac Med, Dept Med Phys, Mashhad, Razavi Khorasan, Iran.
   [Khanbabaei, Hashem] Ahvaz Jundishapur Univ Med Sci, Fac Med, Med Phys Dept, Ahvaz, Iran.
RP Azimian, H (corresponding author), Mashhad Univ Med Sci, Med Phys Res Ctr, Buali Sq,Ferdousi Sq,POB 9196773117, Mashhad, Razavi Khorasan, Iran.; Zafari, N (corresponding author), Mashhad Univ Med Sci, Fac Med, Dept Med Phys, Mashhad, Razavi Khorasan, Iran.
EM ZafariGN941@mums.ac.ir; AzimianH@mums.ac.ir
RI Azimian, Hosein/N-4866-2018
OI Azimian, Hosein/0000-0003-2951-8228; Dolat, Elham/0000-0002-3207-0850
FU Iran National Science Foundation (INSF)Iran National Science Foundation
   (INSF)
FX The authors would like to thank the Iran National Science Foundation
   (INSF) for financial support of this work.
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NR 106
TC 13
Z9 14
U1 2
U2 5
PU ELSEVIER
PI AMSTERDAM
PA RADARWEG 29, 1043 NX AMSTERDAM, NETHERLANDS
SN 0027-5107
EI 1873-135X
J9 MUTAT RES-FUND MOL M
JI Mutat. Res.-Fundam. Mol. Mech. Mutagen.
PD NOV
PY 2019
VL 816
AR 111679
DI 10.1016/j.mrfmmm.2019.111679
PG 9
WC Biotechnology & Applied Microbiology; Genetics & Heredity; Toxicology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biotechnology & Applied Microbiology; Genetics & Heredity; Toxicology
GA JS7YO
UT WOS:000500519700008
PM 31715522
DA 2022-04-25
ER

PT J
AU Koustas, E
   Sarantis, P
   Kyriakopoulou, G
   Papavassiliou, AG
   Karamouzis, MV
AF Koustas, Evangelos
   Sarantis, Panagiotis
   Kyriakopoulou, Georgia
   Papavassiliou, Athanasios G.
   Karamouzis, Michalis, V
TI The Interplay of Autophagy and Tumor Microenvironment in Colorectal
   Cancer-Ways of Enhancing Immunotherapy Action
SO CANCERS
LA English
DT Review
DE Autophagy; colorectal cancer; immunotherapy; tumor stroma; tumor
   microenvironment
ID MISMATCH-REPAIR DEFICIENCY; REGULATORY T-CELLS; MICROSATELLITE
   INSTABILITY; SUPPRESSOR-CELLS; PROTEIN BECLIN-1; PD-L2 EXPRESSION;
   STROMAL CELLS; MYELOID CELLS; NEUTROPHILS; ACTIVATION
AB Autophagy as a primary homeostatic and catabolic process is responsible for the degradation and recycling of proteins and cellular components. The mechanism of autophagy has a crucial role in several cellular functions and its dysregulation is associated with tumorigenesis, tumor-stroma interactions, and resistance to cancer therapy. A growing body of evidence suggests that autophagy is also a key regulator of the tumor microenvironment and cellular immune response in different types of cancer, including colorectal cancer (CRC). Furthermore, autophagy is responsible for initiating the immune response especially when it precedes cell death. However, the role of autophagy in CRC and the tumor microenvironment remains controversial. In this review, we identify the role of autophagy in tumor microenvironment regulation and the specific mechanism by which autophagy is implicated in immune responses during CRC tumorigenesis and the context of anticancer therapy.
C1 [Koustas, Evangelos; Sarantis, Panagiotis; Kyriakopoulou, Georgia; Papavassiliou, Athanasios G.; Karamouzis, Michalis, V] Natl & Kapodistrian Univ Athens, Med Sch, Dept Biol Chem, Mol Oncol Unit, Athens 11527, Greece.
   [Karamouzis, Michalis, V] Natl & Kapodistrian Univ Athens, Med Sch, Laiko Gen Hosp, Dept Internal Med 1, Athens 11527, Greece.
RP Karamouzis, MV (corresponding author), Natl & Kapodistrian Univ Athens, Med Sch, Dept Biol Chem, Mol Oncol Unit, Athens 11527, Greece.; Karamouzis, MV (corresponding author), Natl & Kapodistrian Univ Athens, Med Sch, Laiko Gen Hosp, Dept Internal Med 1, Athens 11527, Greece.
EM vang.koustas@gmail.com; psarantis@bioacademy.gr;
   gpkyriakopoulou@yahoo.com; papavas@med.uoa.gr; mkaramouz@med.uoa.gr
RI Sarantis, Panagiotis/AAF-4774-2021; Koustas, Evangelos/ABE-9336-2020;
   Karamouzis, Michalis/AAD-2860-2020
OI Sarantis, Panagiotis/0000-0001-5848-7905; Papavassiliou,
   Athanasios/0000-0001-5803-4527; Karamouzis, Michalis/0000-0003-1369-8201
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NR 159
TC 23
Z9 23
U1 1
U2 3
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 2072-6694
J9 CANCERS
JI Cancers
PD APR
PY 2019
VL 11
IS 4
AR 533
DI 10.3390/cancers11040533
PG 22
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA HY0BE
UT WOS:000467773400101
PM 31013961
OA Green Published, gold, Green Submitted
DA 2022-04-25
ER

PT J
AU Gullulu, O
   Hehlgans, S
   Rodel, C
   Fokas, E
   Rodel, F
AF Guelluelue, Oemer
   Hehlgans, Stephanie
   Roedel, Claus
   Fokas, Emmanouil
   Roedel, Franz
TI Tumor Suppressor Protein p53 and Inhibitor of Apoptosis Proteins in
   Colorectal Cancer-A Promising Signaling Network for Therapeutic
   Interventions
SO CANCERS
LA English
DT Review
DE cIAP1; 2; colorectal carcinoma; inhibitor of apoptosis protein family;
   Survivin; TP53; XIAP; BRUCE; LIVIN
AB Simple Summary
   Tumor suppressor 53 (p53) is a multifunctional protein that regulates cell cycle, DNA repair, apoptosis and metabolic pathways. In colorectal cancer (CRC), mutations of the gene occur in 60% of patients and are associated with a more aggressive tumor phenotype and resistance to anti-cancer therapy. In addition, inhibitor of apoptosis (IAP) proteins are distinguished biomarkers overexpressed in CRC that impact on a diverse set of signaling pathways associated with the regulation of apoptosis/autophagy, cell migration, cell cycle and DNA damage response. As these mechanisms are further firmly controlled by p53, a transcriptional and post-translational regulation of IAPs by p53 is expected to occur in cancer cells. Here, we aim to review the molecular regulatory mechanisms between IAPs and p53 and discuss the therapeutic potential of targeting their interrelationship by multimodal treatment options.
   Despite recent advances in the treatment of colorectal cancer (CRC), patient's individual response and clinical follow-up vary considerably with tumor intrinsic factors to contribute to an enhanced malignancy and therapy resistance. Among these markers, upregulation of members of the inhibitor of apoptosis protein (IAP) family effects on tumorigenesis and radiation- and chemo-resistance by multiple pathways, covering a hampered induction of apoptosis/autophagy, regulation of cell cycle progression and DNA damage response. These mechanisms are tightly controlled by the tumor suppressor p53 and thus transcriptional and post-translational regulation of IAPs by p53 is expected to occur in malignant cells. By this, cellular IAP1/2, X-linked IAP, Survivin, BRUCE and LIVIN expression/activity, as well as their intracellular localization is controlled by p53 in a direct or indirect manner via modulating a multitude of mechanisms. These cover, among others, transcriptional repression and the signal transducer and activator of transcription (STAT)3 pathway. In addition, p53 mutations contribute to deregulated IAP expression and resistance to therapy. This review aims at highlighting the mechanistic and clinical importance of IAP regulation by p53 in CRC and describing potential therapeutic strategies based on this interrelationship.
C1 [Guelluelue, Oemer; Hehlgans, Stephanie; Roedel, Claus; Fokas, Emmanouil; Roedel, Franz] Univ Hosp Frankfurt, Dept Radiotherapy & Oncol, Theodor Stern Kai 7, D-60590 Frankfurt, Germany.
   [Roedel, Claus; Fokas, Emmanouil; Roedel, Franz] Goethe Univ Frankfurt, Frankfurt Canc Inst FCI, Theodor Stern Kai 7, D-60590 Frankfurt, Germany.
   [Roedel, Claus; Fokas, Emmanouil; Roedel, Franz] German Canc Res Ctr, Neuenheimer Feld 280, D-69120 Heidelberg, Germany.
   [Roedel, Claus; Fokas, Emmanouil; Roedel, Franz] German Canc Consortium DKTK, Partner Site, D-60590 Frankfurt, Germany.
RP Rodel, F (corresponding author), Univ Hosp Frankfurt, Dept Radiotherapy & Oncol, Theodor Stern Kai 7, D-60590 Frankfurt, Germany.; Rodel, F (corresponding author), Goethe Univ Frankfurt, Frankfurt Canc Inst FCI, Theodor Stern Kai 7, D-60590 Frankfurt, Germany.; Rodel, F (corresponding author), German Canc Res Ctr, Neuenheimer Feld 280, D-69120 Heidelberg, Germany.; Rodel, F (corresponding author), German Canc Consortium DKTK, Partner Site, D-60590 Frankfurt, Germany.
EM oemer.guelluelue@kgu.de; stephanie.hehlgans@kgu.de; claus.roedel@kgu.de;
   emmanouil.fokas@kgu.de; franz.roedel@kgu.de
OI Rodel, Franz/0000-0001-6057-1022; Gullulu, Omer/0000-0003-0218-7721
FU German Research Foundation (DFG) (Graduate school GRK 1657)German
   Research Foundation (DFG); German Federal Ministry of Education and
   Research (BMBF)Federal Ministry of Education & Research (BMBF)
   [GREWISalpha: 02NUK050D]
FX This research was funded by the German Research Foundation (DFG)
   (Graduate school GRK 1657, projects 2B) and the German Federal Ministry
   of Education and Research (BMBF), grant number GREWISalpha: 02NUK050D.
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NR 185
TC 5
Z9 5
U1 5
U2 8
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 2072-6694
J9 CANCERS
JI Cancers
PD FEB
PY 2021
VL 13
IS 4
AR 624
DI 10.3390/cancers13040624
PG 22
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA QO7UC
UT WOS:000623344100001
PM 33557398
OA Green Published
DA 2022-04-25
ER

PT J
AU Wu, J
   Wu, JJ
   Yang, LJ
   Wei, LX
   Zou, DJ
AF Wu, Jie
   Wu, Jun-jie
   Yang, Lin-jun
   Wei, Li-xin
   Zou, Da-jin
TI Rosiglitazone protects against palmitate-induced pancreatic beta-cell
   death by activation of autophagy via 5 '-AMP-activated protein kinase
   modulation
SO ENDOCRINE
LA English
DT Article
DE Rosiglitazone; Autophagy; Palmitate; AMPK
ID ENDOPLASMIC-RETICULUM STRESS; COLON-CANCER CELL; MOLECULAR-MECHANISMS;
   INSULIN-RESISTANCE; INDUCED APOPTOSIS; RECEPTOR-GAMMA; MASS;
   LIPOTOXICITY; INHIBITION; TOXICITY
AB Promoting beta-cell survival is crucial for the prevention of beta-cell failure in diabetes. Thiazolidinediones, a widely used drug to improve insulin sensitivity in clinical practice, is found to have a protective effect on islet beta-cell. To date, the mechanism underlying the protective role of thiazolidinedione on beta-cell survival remain largely unknown. Activation of autophagy was detected by transmission electron microscopy, western blot, and GFP-LC3 transfection. Cell viability was examined by WST-8. Cell apoptosis was demonstrated by DAPI and Annexin V/PI staining. Colony formation assay was used to detect long-term cell viability. We demonstrated that rosiglitazone-treated beta-cells were more resistant to palmitate-induced apoptosis. The conversion of LC3-I to LC3-II and accumulated autophagosomes were found to be upregulated in rosiglitazone-treated cells. Inhibition of autophagy augmented palmitate-induced apoptosis with rosiglitazone treatment, suggesting that autophagy plays an important role in the survival function of rosiglitazone on beta-cells. Furthermore, we showed that rosiglitazone could induce AMP-activated protein kinase (AMPK) phosphorylation and reduce p70S6 kinase phosphorylation. Inhibition of AMPK impaired autophagy activation and enhanced palmitate-induced apoptosis during rosiglitazone treatment. These findings reveal that rosiglitazone-induced autophagy contributes to its protective function on beta-cells during palmitate treatment.
C1 [Wu, Jie; Zou, Da-jin] Second Mil Med Univ, Chang Hai Hosp, Dept Endocrinol, Shanghai 200438, Peoples R China.
   [Wu, Jie] Tongji Univ, Tong Ji Hosp, Dept Endocrinol, Shanghai, Peoples R China.
   [Wu, Jie] Fudan Univ, Sch Life Sci, Key Lab Contemporary Anthropol, Natl Minist Educ, Shanghai 200433, Peoples R China.
   [Yang, Lin-jun] Second Mil Med Univ, Chang Hai Hosp, Dept Oncol, Shanghai 200438, Peoples R China.
   [Wei, Li-xin] Second Mil Med Univ, Eastern Hepatobiliary Surg Hosp, Dept Tumor Immunol, Shanghai 200438, Peoples R China.
   [Wei, Li-xin] Second Mil Med Univ, Eastern Hepatobiliary Surg Hosp, Gene Therapy Ctr, Shanghai 200438, Peoples R China.
RP Zou, DJ (corresponding author), Second Mil Med Univ, Chang Hai Hosp, Dept Endocrinol, 168 Changhai Rd, Shanghai 200438, Peoples R China.
EM jielin1080@gmail.com; zwjd22@medmail.com.cn
FU Special Funds for National Natural Science Foundation of ChinaNational
   Natural Science Foundation of China (NSFC) [81070619]; Commission of
   Science and Technology of Shanghai MunicipalityScience & Technology
   Commission of Shanghai Municipality (STCSM) [08411967100]
FX This project was supported by the Special Funds for National Natural
   Science Foundation of China (Grant No. 81070619), the Commission of
   Science and Technology of Shanghai Municipality (No. 08411967100).
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NR 48
TC 47
Z9 52
U1 1
U2 19
PU HUMANA PRESS INC
PI TOTOWA
PA 999 RIVERVIEW DRIVE SUITE 208, TOTOWA, NJ 07512 USA
SN 1355-008X
J9 ENDOCRINE
JI Endocrine
PD AUG
PY 2013
VL 44
IS 1
BP 87
EP 98
DI 10.1007/s12020-012-9826-5
PG 12
WC Endocrinology & Metabolism
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Endocrinology & Metabolism
GA 192KP
UT WOS:000322483500014
PM 23109223
DA 2022-04-25
ER

PT J
AU Yoshioka, A
   Miyata, H
   Doki, Y
   Yamasaki, M
   Sohma, I
   Gotoh, K
   Takiguchi, S
   Fujiwara, Y
   Uchiyama, Y
   Monden, M
AF Yoshioka, Akiko
   Miyata, Hiroshi
   Doki, Yuichiro
   Yamasaki, Makoto
   Sohma, Itsuro
   Gotoh, Kunihito
   Takiguchi, Shuji
   Fujiwara, Yoshiyuki
   Uchiyama, Yasuo
   Monden, Morito
TI LC3, an autophagosome marker, is highly expressed in gastrointestinal
   cancers
SO INTERNATIONAL JOURNAL OF ONCOLOGY
LA English
DT Article
DE light chain 3; autophagy; cancer development; gastrointestinal cancer;
   esophageal cancer
ID MONITORING AUTOPHAGY; RAT HEPATOCYTES; CELL-SURVIVAL; DEATH; YEAST;
   TUMORIGENESIS; INHIBITION; DISSECTION; RADIATION; PATHWAYS
AB Autophagy is a bulk protein and organelle degradation process essential for cell maintenance and viability. Microtubule-associated protein I light chain 3 (LC3), the mammalian homologue of yeast Atg8, is involved in autophagosome formation during autophagy. The aim of this study was to investigate LC3 expression in gastrointestinal cancers to elucidate the role of autophagy in human cancer development. We evaluated LC3 expression by immunohistochemistry in 163 gastrointestinal cancers including 106 esophageal, 38 gastric and 19 colorectal cancers. Seventy precancerous intraepithelial neoplasias were found in esophageal cancer specimens. LC3 expression was compared with Ki-67 staining and expression of carbonic anhydrase (CA) IX, a hypoxic marker. LC3 was expressed in the cytoplasm of cancer cells, but not in noncancerous epithelial cells. A high expression of LC3 was observed in 53% of esophageal, 58% of gastric and 63% of colorectal cancers. LC3 immunoreactive score gradually increased during early esophageal carcinogenesis in low- and high-grade intraepithelial neoplasia and T1 carcinoma, while it did not change in later cancer progression (T2-T4 carcinomas). In early esophageal carcinogenesis, LC3 expression correlated with Ki-67 labeling index (p=0.0001), but showed no significant association with CAIX expression. In esophageal cancers, LC3 expression did not correlate with various clinicopathological factors, including survival. LC3 is upregulated in various gastrointestinal cancers and partly associated with Ki-67 index. Our results suggest that LC3 expression is advantageous to cancer development especially in early-phase carcinogenesis.
C1 [Yoshioka, Akiko; Miyata, Hiroshi; Doki, Yuichiro; Yamasaki, Makoto; Sohma, Itsuro; Gotoh, Kunihito; Takiguchi, Shuji; Fujiwara, Yoshiyuki; Monden, Morito] Osaka Univ, Dept Surg Gastroenterol, Grad Sch Med, Suita, Osaka 5650871, Japan.
   [Gotoh, Kunihito; Uchiyama, Yasuo] Osaka Univ, Dept Cell Biol & Neurosci, Grad Sch Med, Suita, Osaka 5650871, Japan.
RP Miyata, H (corresponding author), Osaka Univ, Dept Surg Gastroenterol, Grad Sch Med, 2-2 Yamadaoka, Suita, Osaka 5650871, Japan.
EM hmiyata@surg2.med.osaka-u.ac.jp
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NR 43
TC 163
Z9 167
U1 0
U2 17
PU PROFESSOR D A SPANDIDOS
PI ATHENS
PA 1, S MERKOURI ST, EDITORIAL OFFICE,, ATHENS 116 35, GREECE
SN 1019-6439
J9 INT J ONCOL
JI Int. J. Oncol.
PD SEP
PY 2008
VL 33
IS 3
BP 461
EP 468
DI 10.3892/ijo_00000028
PG 8
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA 352TE
UT WOS:000259519500005
PM 18695874
OA Bronze
DA 2022-04-25
ER

PT J
AU Kreis, NN
   Louwen, F
   Yuan, J
AF Kreis, Nina-Naomi
   Louwen, Frank
   Yuan, Juping
TI The Multifaceted p21 (Cip1/Waf1/CDKN1A) in Cell Differentiation,
   Migration and Cancer Therapy
SO CANCERS
LA English
DT Review
DE p21; CDKN1A; differentiation; migration; metastasis; anti-cancer therapy
ID DEPENDENT KINASE INHIBITOR; NUCLEOTIDE EXCISION-REPAIR;
   EPITHELIAL-MESENCHYMAL TRANSITION; CYTOPLASMIC P21(WAF1/CIP1)
   EXPRESSION; SMALL-MOLECULE INHIBITORS; HUMAN COLON-CANCER;
   BREAST-CANCER; CDK INHIBITORS; DNA-REPLICATION; GENE-EXPRESSION
AB Loss of cell cycle control is characteristic of tumorigenesis. The protein p21 is the founding member of cyclin-dependent kinase inhibitors and an important versatile cell cycle protein. p21 is transcriptionally controlled by p53 and p53-independent pathways. Its expression is increased in response to various intra- and extracellular stimuli to arrest the cell cycle ensuring genomic stability. Apart from its roles in cell cycle regulation including mitosis, p21 is involved in differentiation, cell migration, cytoskeletal dynamics, apoptosis, transcription, DNA repair, reprogramming of induced pluripotent stem cells, autophagy and the onset of senescence. p21 acts either as a tumor suppressor or as an oncogene depending largely on the cellular context, its subcellular localization and posttranslational modifications. In the present review, we briefly mention the general functions of p21 and summarize its roles in differentiation, migration and invasion in detail. Finally, regarding its dual role as tumor suppressor and oncogene, we highlight the potential, difficulties and risks of using p21 as a biomarker as well as a therapeutic target.
C1 [Kreis, Nina-Naomi; Louwen, Frank; Yuan, Juping] Goethe Univ Frankfurt, Univ Hosp, Dept Gynecol & Obstet, Theodor Stern Kai 7, D-60590 Frankfurt, Germany.
RP Kreis, NN (corresponding author), Goethe Univ Frankfurt, Univ Hosp, Dept Gynecol & Obstet, Theodor Stern Kai 7, D-60590 Frankfurt, Germany.
EM Nina-Naomi.Kreis@kgu.de
RI Kreis, Nina-Naomi/AAF-5407-2019
OI Kreis, Nina-Naomi/0000-0003-4304-0160; Yuan, Juping/0000-0003-0694-0565
FU Deutsche Forschungsgemeinschaft (DFG, German Research Foundation)German
   Research Foundation (DFG) [390921723]
FX This research was funded by the Deutsche Forschungsgemeinschaft (DFG,
   German Research Foundation)-project number 390921723.
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NR 222
TC 74
Z9 79
U1 5
U2 8
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 2072-6694
J9 CANCERS
JI Cancers
PD SEP
PY 2019
VL 11
IS 9
AR 1220
DI 10.3390/cancers11091220
PG 23
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA JD1EW
UT WOS:000489719000005
PM 31438587
OA Green Published, gold
DA 2022-04-25
ER

PT J
AU Vidhyapriya, P
   Divya, D
   Bala, M
   Sakthivel, N
AF Vidhyapriya, P.
   Divya, D.
   Bala, Manimaran
   Sakthivel, N.
TI Photoactivated [Mn(CO)(3)Br(mu-bpcpd)](2) induces apoptosis in cancer
   cells via intrinsic pathway
SO JOURNAL OF PHOTOCHEMISTRY AND PHOTOBIOLOGY B-BIOLOGY
LA English
DT Article
DE Carbon Monoxide Releasing Molecule; Apoptosis; Targeted Therapy;
   Photoactivation
ID MONOXIDE-RELEASING MOLECULE; CARBON-MONOXIDE; CORM-3
   RU(CO)(3)CL(GLYCINATE); TRICARBONYL COMPLEXES; MITOCHONDRIAL PATHWAY;
   CYTOTOXICITY; MANGANESE(I); RESPIRATION; GENERATION; AUTOPHAGY
AB Carbon monoxide releasing molecules (CORMs) are organometallic/organic compounds that release carbon monoxide (CO) spontaneously or upon activation. PhotoCORMs are capable of releasing CO on light based activation. This group of molecules is used in photodynamic therapy due to their ability to release CO in a controlled manner. In the present investigation, the release of CO from [Mn(CO)(3)Br(mu-bpcpd)](2) (MnCORM) upon irradiation at lambda(max) 365 nm was assessed spectrophotometrically using myoglobin assay and confirmed by liquid FT-IR spectroscopic analysis. Further, the cytotoxic potential of MnCORM on normal cells (HEK 293) and cancer cell lines such as lung (A549), cervical (HeLa), breast (MDA MB-231) and colon (HCT-15) was evaluated. The IC50 values of MnCORM were found to be 21.37 +/- 1.72, 24.12 +/- 1.03, 21.89 +/- 0.59 and 13.69 +/- 0.91 mu M on cervical (HeLa), lung (A549), colon (HCT-15) and breast (MDA MB-231) cancer cells respectively. An inquest into the nature of cell death was confirmed based on the nuclear and cytological examinations, flow cytometric analyses and protein expression studies. The AO/EB dual staining and cytological evaluation of the treated cells revealed that the cell death might be due to apoptosis. The flow cytometric analysis of propidium iodide (PI) stained cells showed a significant amount of sub-G1 hypodiploid cells due to MnCORM treatment. The MnCORM-induced apoptosis was mediated through the generation of reactive oxygen species (ROS), specifically superoxide radicals leading to loss of mitochondrial membrane potential. The intrinsic pathway of apoptosis was elucidated based on the expression studies of pro-apoptotic and apoptotic proteins such as bcl-2, bax, cyt c, cleaved caspase-3, cleaved caspase-9 and cleaved PARP. Due to its innate potential to release CO upon photo activation and its ability to induce apoptosis via intrinsic pathway, the MnCORM molecule could be exploited for controlled release and photodynamic cancer therapy.
C1 [Vidhyapriya, P.; Sakthivel, N.] Pondicherry Univ, Dept Biotechnol, Pondicherry 605014, India.
   [Divya, D.; Bala, Manimaran] Pondicherry Univ, Dept Chem, Pondicherry 605014, India.
RP Sakthivel, N (corresponding author), Pondicherry Univ, Sch Life Sci, Dept Biotechnol, Pondicherry 605014, India.
EM manimaran.che@pondiuni.edu.in; puns2005@gmail.com
OI D, Divya/0000-0002-8127-2678
FU DBTDepartment of Biotechnology (DBT) India; CSIRCouncil of Scientific &
   Industrial Research (CSIR) - India
FX The authors thank DBT for providing Junior Research Fellowship to P.
   Vidhyapriya and are also thankful to CSIR for financial support. The
   authors acknowledge the facilities provided through Central Instrument
   Facility (CIF) of Pondicherry University and DST-FIST and UGC-SAP
   Programmes coordinated by Prof. N. Sakthivel.
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NR 65
TC 9
Z9 9
U1 4
U2 42
PU ELSEVIER SCIENCE SA
PI LAUSANNE
PA PO BOX 564, 1001 LAUSANNE, SWITZERLAND
SN 1011-1344
J9 J PHOTOCH PHOTOBIO B
JI J. Photochem. Photobiol. B-Biol.
PD NOV
PY 2018
VL 188
BP 28
EP 41
DI 10.1016/j.jphotobiol.2018.08.021
PG 14
WC Biochemistry & Molecular Biology; Biophysics
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Biophysics
GA GZ2TN
UT WOS:000449241400005
PM 30195977
DA 2022-04-25
ER

PT J
AU Wang, YZ
   Lina, L
   Xu, L
   Yang, Z
   Qian, Z
   Zhou, J
   Suoni, L
AF Wang, Yuzhen
   Lina, Li
   Xu, Li
   Yang, Zhai
   Qian, Zhang
   Zhou, Jing
   Suoni, Li
TI Arctigenin enhances the sensitivity of cisplatin resistant colorectal
   cancer cell by activating autophagy
SO BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
LA English
DT Article
DE Arctigenin; Cisplatin; Colorectal cancer; Autophagy; SW480; SW620
ID MULTIDRUG-RESISTANCE; PREVENTION
AB Arctigenin is the active content of arctium lappa that present anti-cancer abilities in various carcinomas. However, its role and underlying mechanism in drug-resistant colorectal cancer cells has not been addressed. The present study used SW480 and SW620 to established cisplatin-resistant colorectal cancer cell lines, and explored the impact of arctigenin on these cells. Arctigenin at 100 mu M significantly inhibited cell proliferation of cisplatin treated R-SW480 and R-SW620 cells as compared with cells treated with cisplatin alone. Arctigenin elevates cell apoptosis, up-regulated pro-apoptotic protein cleaved-caspase-3 and caspase-9 expression level in cisplatin treated R-SW480 and R-SW620 cells. Additionally, arctigenin triggered autophagy and promoted LC3-II and p65 expression, while inhibited LC3-lexpression. Arctigenin impeded the IC50 of not only cisplatin but also oxaliplatin, doxorubicin and Paclitaxel of R-SW480 and R-SW620 cells. More importantly, the mRNA expression of multi drug resistance 1 (MDR1) and protein expression of pgp were significantly inhibited by arctigenin administration. Taken together, arctigenin has the potential in sensitize colorectal cancer cells by activating autophagy, which induced cell apoptosis and inhibited cell growth. Our study revealed that arctigenin has the potential for colorectal cancer treatment and may be useful in adjuvant chemotherapy. (C) 2019 Elsevier Inc. All rights reserved.
C1 [Wang, Yuzhen; Lina, Li; Xu, Li; Yang, Zhai; Qian, Zhang; Zhou, Jing; Suoni, Li] Shaanxi Prov Tumor Hosp, Dept Internal Med, 309 Yanta West Rd, Xian 710061, Shaanxi, Peoples R China.
RP Wang, YZ (corresponding author), Shaanxi Prov Tumor Hosp, Dept Internal Med, 309 Yanta West Rd, Xian 710061, Shaanxi, Peoples R China.
EM wangyzhos@163.com
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NR 28
TC 16
Z9 17
U1 0
U2 17
PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 0006-291X
EI 1090-2104
J9 BIOCHEM BIOPH RES CO
JI Biochem. Biophys. Res. Commun.
PD NOV 26
PY 2019
VL 520
IS 1
BP 20
EP 26
DI 10.1016/j.bbrc.2019.09.086
PG 7
WC Biochemistry & Molecular Biology; Biophysics
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Biophysics
GA KB3OU
UT WOS:000506410000004
PM 31564411
DA 2022-04-25
ER

PT J
AU Lai, YY
   Lim, DN
   Tan, PH
   Leung, TKC
   Yip, GWC
   Bay, BH
AF Lai, Yiyang
   Lim, Daina
   Tan, Puay-Hoon
   Leung, Thomas King-Chor
   Yip, George Wai-Cheong
   Bay, Boon-Huat
TI Silencing the Metallothionein-2A Gene Induces Entosis in Adherent MCF-7
   Breast Cancer Cells
SO ANATOMICAL RECORD-ADVANCES IN INTEGRATIVE ANATOMY AND EVOLUTIONARY
   BIOLOGY
LA English
DT Article
DE metallothionein-2A; breast cancer; entosis; cell-in-cell; electron
   microscopy
ID CANNIBALISM; EXPRESSION; CARCINOMA; CYTOLOGY; DEATH
AB The presence of a live cell cohabiting within another cell has fascinated scientists for many decades. Far from being a spurious event, many have attempted to uncover the molecular mechanism underlying this phenomenon. In this study, we observed anchorage-dependent MCF-7 cells internalizing neighboring epithelial cells (entosis) after siRNA-mediated silencing of the Metallothionein-2A (MT-2A) gene. MTs belong to a family of low-molecular weight proteins, which bind metal ions endogenously and its over-expression has been reported in a variety of cancers that include breast, prostate, and colon. We provide microscopic evidence at light and ultrastructural levels of the occurrence of entosis after altering MT expression in a subpopulation of MCF-7 breast cancer cells by silencing the MT-2A gene. Our results demonstrate that adheren junctions may play important roles in the formation of cell-in-cell cytostructure after MT-2A. gene downregulation and the entotic process does not appear to involve genes associated with autophagy. Interiorized cells often underwent lysosomal degradation within the cytoplasmic body of the engulfing cell. It would appear that a subset of breast cancer cells could die via entosis after MT-2A gene silencing. Anat Rec, 293:1685-1691, 2010. (C) 2010 Wiley-Liss, Inc.
C1 [Lai, Yiyang; Lim, Daina; Yip, George Wai-Cheong; Bay, Boon-Huat] Natl Univ Singapore, Yong Loo Lin Sch Med, Dept Anat, Singapore 117597, Singapore.
   [Tan, Puay-Hoon] Singapore Gen Hosp, Dept Pathol, Singapore 169608, Singapore.
   [Leung, Thomas King-Chor] Natl Univ Singapore, Inst Mol & Cell Biol, GSK IMCB Grp, Singapore 117548, Singapore.
RP Bay, BH (corresponding author), Natl Univ Singapore, Yong Loo Lin Sch Med, Dept Anat, 4 Med Dr,Blk MD 10, Singapore 117597, Singapore.
EM antbaybh@nus.edu.sg
FU Singapore National Medical Research CouncilNational Medical Research
   Council, Singapore [NMRC/1019/2005, NMRC/1081/2006]; National University
   of SingaporeNational University of Singapore
FX Grant sponsor: Singapore National Medical Research Council; Grant
   numbers: NMRC/1019/2005; NMRC/1081/2006.; The authors would like to
   thank Song-Lin Bay, Yajun Wu and Yee-Gek Chan for skilful technical
   assistance. Yiyang Lai is a recipient of a Research Scholarship from the
   National University of Singapore.
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NR 23
TC 19
Z9 19
U1 0
U2 14
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1932-8486
EI 1932-8494
J9 ANAT REC
JI Anat. Rec.
PD OCT
PY 2010
VL 293
IS 10
BP 1685
EP 1691
DI 10.1002/ar.21215
PG 7
WC Anatomy & Morphology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Anatomy & Morphology
GA 668LX
UT WOS:000283272600006
PM 20652934
DA 2022-04-25
ER

PT J
AU Xu, HY
   Jiang, BH
   Meng, L
   Ren, TT
   Zeng, Y
   Wu, J
   Qu, LK
   Shou, CC
AF Xu, Huiyu
   Jiang, Beihai
   Meng, Lin
   Ren, Tingting
   Zeng, Yan
   Wu, Jian
   Qu, Like
   Shou, Chengchao
TI N-alpha-Acetyltransferase 10 protein inhibits apoptosis through
   RelA/p65-regulated MCL1 expression
SO CARCINOGENESIS
LA English
DT Article
ID FACTOR-KAPPA-B; DOWN-REGULATION; POOR-PROGNOSIS; KB ACTIVATION;
   CANCER-CELLS; TARGET
AB N-alpha-Acetyltransferase 10 protein (Naa10p/ARD1), the catalytic subunit of N-acetyltransferase A, catalyzes both N-alpha-acetylation and epsilon-acetylation, as well as autoacetylation. Naa10p is involved in controlling cell proliferation, apoptosis, autophagy and neuronal development. Our group and others had reported prognostic value of Naa10p expression in various types of cancer. Despite the efforts to elucidate the biological function of Naa10p, it remains controversial regarding its roles in tumor development. Herein, we report that depletion of Naa10p inhibited the growth of xenograft tumors in nude mice. Microarray analysis identified MCL1 gene as one of targets downstream of Naa10p. Naa10p positively regulated MCL1 expression, as exogenous Naa10p promoted MCL1 expression, whereas Naa10p silencing decreased MCL1 expression. Ablation of Naa10p sensitized cancer cells to stimuli-induced apoptosis, and the anti-apoptotic function of Naa10p was, at least in part, mediated by MCL1. Mechanistically, we found a physical interaction between Naa10p and RelA/p65. Transcriptional activation of the MCL1 gene required the recruitment of Naa10p RelA/p65 complex to the p65-binding site of MCL1 promoter region. We also demonstrated a positive correlation between MCL1 and Naa10p messenger RNA levels in both colon cancer and lung cancer tissues. These results indicate that Naa10p inhibits apoptosis through Naa10p RelA/p65-dependent MCL1 transcriptional activation.
C1 [Xu, Huiyu; Jiang, Beihai; Meng, Lin; Ren, Tingting; Zeng, Yan; Wu, Jian; Qu, Like; Shou, Chengchao] Peking Univ, Canc Hosp & Inst, Dept Biochem & Mol Biol, Key Lab Carcinogenesis & Translat Res,Minist Educ, Beijing 100142, Peoples R China.
RP Shou, CC (corresponding author), Peking Univ, Canc Hosp & Inst, Dept Biochem & Mol Biol, Key Lab Carcinogenesis & Translat Res,Minist Educ, Beijing 100142, Peoples R China.
EM qulike@bjcancer.org; scc@bjcancer.org
FU National 973 Program of ChinaNational Basic Research Program of China
   [2009CB521805]; National 863 Program of ChinaNational High Technology
   Research and Development Program of China [2006AA02A402-B07]; National
   Nature Science Foundation of ChinaNational Natural Science Foundation of
   China (NSFC) [81071658]
FX National 973 Program of China (2009CB521805), National 863 Program of
   China (2006AA02A402-B07) and National Nature Science Foundation of China
   (81071658).
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NR 40
TC 32
Z9 38
U1 1
U2 8
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 0143-3334
EI 1460-2180
J9 CARCINOGENESIS
JI Carcinogenesis
PD NOV
PY 2012
VL 33
IS 6
BP 1193
EP 1202
DI 10.1093/carcin/bgs144
PG 10
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA 970MW
UT WOS:000306135800010
PM 22496479
OA Bronze, Green Submitted
DA 2022-04-25
ER

PT J
AU Alotaibi, M
   Sharma, K
   Saleh, T
   Povirk, LF
   Hendrickson, EA
   Gewirtz, DA
AF Alotaibi, Moureq
   Sharma, Khushboo
   Saleh, Tareq
   Povirk, Lawrence F.
   Hendrickson, Eric A.
   Gewirtz, David A.
TI Radiosensitization by PARP Inhibition in DNA Repair Proficient and
   Deficient Tumor Cells: Proliferative Recovery in Senescent Cells
SO RADIATION RESEARCH
LA English
DT Article
ID DOUBLE-STRAND BREAKS; POLY(ADP-RIBOSE) POLYMERASE INHIBITOR;
   PROSTATE-CANCER RECURRENCE; DEPENDENT PROTEIN-KINASE; ACCELERATED
   SENESCENCE; LUNG-CANCER; CYTOTOXIC AUTOPHAGY; DAMAGE-RESPONSE;
   SINGLE-STRAND; HOMOLOGOUS RECOMBINATION
AB Radiotherapy continues to be a primary modality in the treatment of cancer. In addition to promoting apoptosis, radiation-induced DNA damage can promote autophagy and senescence, both of which can theoretically function to prolong tumor survival. In this work, we tested the hypothesis that autophagy and/or senescence could be permissive for DNA repair, thereby facilitating tumor cell recovery from radiation-induced growth arrest and/or cell death. In addition, studies were designed to elucidate the involvement of autophagy and senescence in radiosensitization by PARP inhibitors and the re-emergence of a proliferating tumor cell population. In the context of this work, the relationship between radiation-induced autophagy and senescence was also determined. Studies were performed using DNA repair-proficient HCT116 colon carcinoma cells and a repair-deficient ligase IV-/- isogenic cell line. Exposure to radiation promoted a parallel induction of autophagy and senescence that was strongly correlated with the extent of persistent H2AX phosphorylation in both cell lines, however, inhibition of autophagy failed to suppress senescence, indicating that the two responses were dissociable. Exposure to radiation resulted in a transient arrest in the HCT116 cells while arrest was prolonged in the ligase IV-/- cells, however, both cell lines ultimately recovered proliferative function, which may reflect maintenance of DNA repair capacity. The PARP inhibitors, olaparib and niraparib, increased the extent of persistent DNA damage induced by radiation exposure as well as the extent of both autophagy and senescence. Neither cell line underwent significant apoptosis by radiation exposure alone or in the presence of the PARP inhibitors. Inhibition of autophagy failed to attenuate radiosensitization, indicating that autophagy was not involved in the action of the PARP inhibitors. As with radiation alone, despite sensitization by PARP inhibition, proliferative recovery was evident within a period of 10-20 days. While inhibition of DNA repair via PARP inhibition may initially sensitize tumor cells to radiation via the promotion of senescence, this strategy does not appear to interfere with proliferative recovery, which could ultimately contribute to disease recurrence. (C) 2016 by Radiation Research Society
C1 [Alotaibi, Moureq; Sharma, Khushboo; Saleh, Tareq; Povirk, Lawrence F.; Gewirtz, David A.] Virginia Commonwealth Univ, Sch Med, Dept Pharmacol & Toxicol, Med Coll Virginia Campus, Richmond, VA 23298 USA.
   [Gewirtz, David A.] Virginia Commonwealth Univ, Massey Canc Ctr, 401 Coll St, Richmond, VA 23298 USA.
   [Alotaibi, Moureq] King Saud Univ, Coll Pharm, Dept Pharmacol & Toxicol, Riyadh 11451, Saudi Arabia.
   [Hendrickson, Eric A.] Univ Minnesota, Dept Biochem Mol Biol & Biophys, Minneapolis, MN 55455 USA.
RP Gewirtz, DA (corresponding author), Virginia Commonwealth Univ, Massey Canc Ctr, 401 Coll St, Richmond, VA 23298 USA.
EM david.gewirtz@vcuhealth.org
RI Saleh, Tareq/AGY-9225-2022
OI Saleh, Tareq/0000-0002-2878-1107
FU National Cancer InstituteUnited States Department of Health & Human
   ServicesNational Institutes of Health (NIH) - USANIH National Cancer
   Institute (NCI) [CA40615, CA166264, CA154461, CA190492]; National
   Institutes of General Medical SciencesUnited States Department of Health
   & Human ServicesNational Institutes of Health (NIH) - USANIH National
   Institute of General Medical Sciences (NIGMS) [GM088351]; Office of the
   Assistant Secretary of Defense for Health Affairs through the Breast
   Cancer Research Program [W81XWH-14-1-0088]; Massey Center Support Grant
   [P30 CA016059]; NATIONAL CANCER INSTITUTEUnited States Department of
   Health & Human ServicesNational Institutes of Health (NIH) - USANIH
   National Cancer Institute (NCI) [R01CA190492, R01CA040615, R01CA154461,
   P30CA016059, R01CA166264] Funding Source: NIH RePORTER; NATIONAL
   INSTITUTE OF GENERAL MEDICAL SCIENCESUnited States Department of Health
   & Human ServicesNational Institutes of Health (NIH) - USANIH National
   Institute of General Medical Sciences (NIGMS) [R01GM088351] Funding
   Source: NIH RePORTER
FX This work was supported by the National Cancer Institute [grant nos.
   CA40615 (LFP), CA166264 ( LFP), CA154461 (EAH) and CA190492 (EAH)], the
   National Institutes of General Medical Sciences [grant no. GM088351
   (EAH)] and the Office of the Assistant Secretary of Defense for Health
   Affairs through the Breast Cancer Research Program [grant no.
   W81XWH-14-1-0088 (DAG)], and Massey Center Support Grant P30 CA016059.
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NR 93
TC 48
Z9 50
U1 1
U2 13
PU RADIATION RESEARCH SOC
PI LAWRENCE
PA 810 E TENTH STREET, LAWRENCE, KS 66044 USA
SN 0033-7587
EI 1938-5404
J9 RADIAT RES
JI Radiat. Res.
PD MAR
PY 2016
VL 185
IS 3
BP 229
EP 245
DI 10.1667/RR14202.1
PG 17
WC Biology; Biophysics; Radiology, Nuclear Medicine & Medical Imaging
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Life Sciences & Biomedicine - Other Topics; Biophysics; Radiology,
   Nuclear Medicine & Medical Imaging
GA DN0KY
UT WOS:000376754000003
PM 26934368
OA Green Accepted
DA 2022-04-25
ER

PT J
AU Jiang, Q
AF Jiang, Qing
TI Natural forms of vitamin E and metabolitesregulation of cancer cell
   death and underlying mechanisms
SO IUBMB LIFE
LA English
DT Review
DE sphingolipids; cancer prevention; apoptosis; autophagy; ceramides;
   tocopherols; tocotrienols; long-chain carboxychromanol; inflammation;
   food; colon cancer; prostate cancer; breast cancer; biology; medicine
ID NF-KAPPA-B; E DELTA-TOCOTRIENOL; LONG-CHAIN CARBOXYCHROMANOLS; STEM-LIKE
   CELLS; GAMMA-TOCOPHEROL; PROSTATE-CANCER; INDUCED APOPTOSIS;
   ALPHA-TOCOPHEROL; INDUCE APOPTOSIS; MOUSE MODEL
AB The disappointing results from large clinical studies of -tocopherol (T), the major form of vitamin E in tissues, for prevention of chronic diseases including cancer have cast doubt on not only T but also other forms of vitamin E regarding their role in preventing carcinogenesis. However, basic research has shown that specific forms of vitamin E such as -tocopherol (T), -tocopherol (T), -tocotrienol (TE) and -tocotrienol (TE) can inhibit the growth and induce death of many types of cancer cells, and are capable of suppressing cancer development in preclinical cancer models. For these activities, these vitamin E forms are much stronger than T. Further, recent research revealed novel anti-inflammatory and anticancer effects of vitamin E metabolites including 13-carboxychromanols. This review focuses on anti-proliferation and induction of death in cancer cells by vitamin E forms and metabolites, and discuss mechanisms underlying these anticancer activities. The existing in vitro and in vivo evidence indicates that T, T, tocotrienols and 13-carboxychromanols have anti-cancer activities via modulating key signaling or mediators that regulate cell death and tumor progression, such as eicosanoids, NF-B, STAT3, PI3K, and sphingolipid metabolism. These results provide useful scientific rationales and mechanistic understanding for further translation of basic discoveries to the clinic with respect to potential use of these vitamin E forms and metabolites for cancer prevention and therapy. (c) 2018 IUBMB Life, 71(4):495-506, 2019
C1 [Jiang, Qing] Purdue Univ, Dept Nutr Sci, 700 W State St,Stone Hall G1A, W Lafayette, IN 47907 USA.
RP Jiang, Q (corresponding author), Purdue Univ, Dept Nutr Sci, 700 W State St,Stone Hall G1A, W Lafayette, IN 47907 USA.
EM qjiang@purdue.edu
OI Jiang, Qing/0000-0002-0579-8280
FU National Institutes of HealthUnited States Department of Health & Human
   ServicesNational Institutes of Health (NIH) - USA [R01ES023349]; 
   [P30CA023168]; NATIONAL CANCER INSTITUTEUnited States Department of
   Health & Human ServicesNational Institutes of Health (NIH) - USANIH
   National Cancer Institute (NCI) [P30CA023168] Funding Source: NIH
   RePORTER
FX The sole author is responsible for all aspects of the paper. This work
   was in part supported by a grant R01ES023349 (QJ) from National
   Institutes of Health and a pilot grant from Purdue University Center for
   Cancer Research, P30CA023168.
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NR 120
TC 27
Z9 28
U1 0
U2 12
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1521-6543
EI 1521-6551
J9 IUBMB LIFE
JI IUBMB Life
PD APR
PY 2019
VL 71
IS 4
SI SI
BP 495
EP 506
DI 10.1002/iub.1978
PG 12
WC Biochemistry & Molecular Biology; Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Cell Biology
GA HP4TU
UT WOS:000461669800010
PM 30548200
OA Bronze
DA 2022-04-25
ER

PT J
AU Zhang, CR
   Jiang, J
   Wang, LQ
   Zheng, LY
   Xu, JK
   Qi, XL
   Huang, HY
   Lu, JP
   Li, KN
   Wang, H
AF Zhang, Chunrui
   Jiang, Jing
   Wang, Liqiang
   Zheng, Liyu
   Xu, Jiankai
   Qi, Xiaolin
   Huang, Huiying
   Lu, Jianping
   Li, Kongning
   Wang, Hong
TI Identification of Autophagy-Associated Biomarkers and Corresponding
   Regulatory Factors in the Progression of Colorectal Cancer
SO FRONTIERS IN GENETICS
LA English
DT Article
DE autophagy; colorectal cancer; regulatory network; RNA-binding proteins;
   biomarkers
ID CELL-DEATH; EXPRESSION; RESOURCE; GENES; SUSCEPTIBILITY; RECURRENCE;
   PROGNOSIS; SURVIVAL
AB Autophagy is a self-degradation process that maintains homeostasis against stress in cells. Autophagy dysfunction plays a central role in the development of tumors, such as colorectal cancer (CRC). In this study, autophagy-related differentially expressed genes, their downstream functions, and upstream regulatory factors including RNA-binding proteins (RBP) involved in programmed cell death in the CRC were investigated. Transcription factors (TFs) and miRNAs have been shown to mainly regulate autophagy genes. Interestingly, we found that some of the RBP in the CRC, such as DDX17, SETDB1, and POLR3A, play an important regulatory role in maintaining autophagy at a basal level during growth by acting as TFs that regulate autophagy. Promoter methylations showed negative regulations on differentially expressed autophagy gene (DEAG), while copy number variations revealed a positive role in them. A proportional hazards regression analysis indicated that using autophagy-related prognostic signature can divide patients into high-risk and low-risk groups. Autophagy associated FDA-approved drugs were studied by a prognostic network. This would contribute to the identifications of new potential molecular therapeutic targets for CRC.
C1 [Zhang, Chunrui; Wang, Liqiang; Zheng, Liyu; Xu, Jiankai; Huang, Huiying; Lu, Jianping; Li, Kongning] Harbin Med Univ, Coll Bioinformat Sci & Technol, Harbin, Peoples R China.
   [Zhang, Chunrui] Chinese Acad Sci, Inst Genet & Dev Biol, Beijing, Peoples R China.
   [Jiang, Jing] Harbin Med Univ, Affiliated Hosp 2, Obstet & Gynecol Dept, Harbin, Peoples R China.
   [Qi, Xiaolin; Li, Kongning; Wang, Hong] Hainan Med Univ, Minist Educ, Key Lab Trop Translat Med, Haikou, Hainan, Peoples R China.
   [Qi, Xiaolin; Li, Kongning; Wang, Hong] Hainan Med Univ, Coll Biomed Informat & Engn, Haikou, Hainan, Peoples R China.
RP Lu, JP; Li, KN (corresponding author), Harbin Med Univ, Coll Bioinformat Sci & Technol, Harbin, Peoples R China.; Li, KN; Wang, H (corresponding author), Hainan Med Univ, Minist Educ, Key Lab Trop Translat Med, Haikou, Hainan, Peoples R China.; Li, KN; Wang, H (corresponding author), Hainan Med Univ, Coll Biomed Informat & Engn, Haikou, Hainan, Peoples R China.
EM lujianping1992@163.com; likongning@hainmc.edu.cn; wanghong@hainmc.edu.cn
RI Li, Kongning/L-6188-2015
OI Li, Kongning/0000-0002-4928-6922; ZHANG, CHUNRUI/0000-0002-8170-5509
FU National Natural Science Foundation of ChinaNational Natural Science
   Foundation of China (NSFC) [31501075, 31301094, 31900493]; Natural
   Science Foundation of Heilongjiang ProvinceNatural Science Foundation of
   Heilongjiang Province [B201302]; Postdoctoral Foundation of Heilongjiang
   Province [LBH-Z18167]
FX This work was supported by the National Natural Science Foundation of
   China (31501075, 31301094, and 31900493), the Natural Science Foundation
   of Heilongjiang Province (B201302), and the Postdoctoral Foundation of
   Heilongjiang Province (LBH-Z18167).
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NR 41
TC 2
Z9 2
U1 3
U2 4
PU FRONTIERS MEDIA SA
PI LAUSANNE
PA AVENUE DU TRIBUNAL FEDERAL 34, LAUSANNE, CH-1015, SWITZERLAND
EI 1664-8021
J9 FRONT GENET
JI Front. Genet.
PD MAR 18
PY 2020
VL 11
AR 245
DI 10.3389/fgene.2020.00245
PG 11
WC Genetics & Heredity
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Genetics & Heredity
GA KZ7YN
UT WOS:000523475900001
PM 32265986
OA Green Published, gold
DA 2022-04-25
ER

PT J
AU Lin, WS
   Leland, JV
   Ho, CT
   Pan, MH
AF Lin, Wei-Sheng
   Leland, Jane Valorie
   Ho, Chi-Tang
   Pan, Min-Hsiung
TI Occurrence, Bioavailability, Anti-inflammatory, and Anticancer Effects
   of Pterostilbene
SO JOURNAL OF AGRICULTURAL AND FOOD CHEMISTRY
LA English
DT Review
DE pterostilbene; bioavailability; chemoprevention; anti-inflammation;
   anticancer
ID SIGNAL-TRANSDUCTION PATHWAYS; CANCER STEM-CELLS; IN-VITRO; COLON
   CARCINOGENESIS; RESVERATROL METABOLITES; MOLECULAR-MECHANISMS;
   TRANS-RESVERATROL; CYCLE ARREST; KAPPA-B; APOPTOSIS
AB Supplementation with natural compounds found in fruits and vegetables has long been associated with a reduced risk of several types of cancer. Pterostilbene is a natural stilbenoid and a dimethylated analogue of resveratrol which is found primarily in blueberries. Pterostilbene exhibits a range of pharmacological properties, particularly anti-inflammatory and anticancer effects. Due to two methoxy groups in its skeleton, pterostilbene is more lipophilic than resveratrol and thus possesses higher intestinal permeability and cellular uptake and enhanced stability. Moreover, pterostilbene exhibits less toxicity and fewer adverse effects, providing it with superior potential in cancer chemoprevention and chemotherapy applications. Numerous research studies have demonstrated that pterostilbene possesses detoxification activities, mediating the anti-inflammation response, regulating the cell cycle, augmenting apoptosis, enhancing autophagy, and inhibiting tumor angiogenesis, invasion, and metastasis by modulating signal transduction pathways which block multiple stages of carcinogenesis. In this review, we illustrate that pterostilbene is a natural compound having bioavailability. The extensive metabolism of pterostilbene will be discussed. We also summarize recent research on pterostilbene's anti-inflammatory and anticancer properties in the multistage carcinogenesis process and related molecular mechanism and conclude that it should contribute to improved cancer management.
C1 [Lin, Wei-Sheng; Pan, Min-Hsiung] Natl Taiwan Univ, Inst Food Sci & Technol, Taipei 10617, Taiwan.
   [Leland, Jane Valorie] Leland Global Enterprises LLC, Wilmette, IL 60091 USA.
   [Pan, Min-Hsiung] China Med Univ, China Med Univ Hosp, Dept Med Res, Taichung 40402, Taiwan.
   [Pan, Min-Hsiung] Asia Univ, Dept Hlth & Nutr Biotechnol, Taichung 41354, Taiwan.
   [Ho, Chi-Tang] Rutgers State Univ, Dept Food Sci, New Brunswick, NJ 08901 USA.
RP Pan, MH (corresponding author), Natl Taiwan Univ, Inst Food Sci & Technol, Taipei 10617, Taiwan.; Pan, MH (corresponding author), China Med Univ, China Med Univ Hosp, Dept Med Res, Taichung 40402, Taiwan.; Pan, MH (corresponding author), Asia Univ, Dept Hlth & Nutr Biotechnol, Taichung 41354, Taiwan.; Ho, CT (corresponding author), Rutgers State Univ, Dept Food Sci, New Brunswick, NJ 08901 USA.
EM ho@aesop.rutgers.edu; mhpan@ntu.edu.tw
RI Pan, Min-Hsiung/AAT-8865-2021
OI Pan, Min-Hsiung/0000-0002-5188-7030; Ho, Chi-Tang/0000-0001-8273-2085
FU Ministry of Science and Technology [108-2321-B-002-020,
   108-2320-B-002-016-MY3]
FX This study was supported by the Ministry of Science and Technology
   (Grants 108-2321-B-002-020 and 108-2320-B-002-016-MY3).
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NR 138
TC 24
Z9 25
U1 12
U2 38
PU AMER CHEMICAL SOC
PI WASHINGTON
PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA
SN 0021-8561
EI 1520-5118
J9 J AGR FOOD CHEM
JI J. Agric. Food Chem.
PD NOV 18
PY 2020
VL 68
IS 46
BP 12788
EP 12799
DI 10.1021/acs.jafc.9b07860
PG 12
WC Agriculture, Multidisciplinary; Chemistry, Applied; Food Science &
   Technology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Agriculture; Chemistry; Food Science & Technology
GA OW5JM
UT WOS:000592922700005
PM 32064876
DA 2022-04-25
ER

PT J
AU Ghafouri-Fard, S
   Abak, A
   Anamag, FT
   Shoorei, H
   Fattahi, F
   Javadinia, SA
   Basiri, A
   Taheri, M
AF Ghafouri-Fard, Soudeh
   Abak, Atefe
   Tondro Anamag, Farhad
   Shoorei, Hamed
   Fattahi, Faranak
   Javadinia, Seyed Alireza
   Basiri, Abbas
   Taheri, Mohammad
TI 5-Fluorouracil: A Narrative Review on the Role of Regulatory Mechanisms
   in Driving Resistance to This Chemotherapeutic Agent
SO FRONTIERS IN ONCOLOGY
LA English
DT Review
DE lncRNA; miRNA; fluorouracil; expression; biomarker
ID HEPATOCELLULAR-CARCINOMA CELLS; HUMAN COLORECTAL-CANCER; HISTONE
   DEACETYLASE; MULTIDRUG-RESISTANCE; 5-FU RESISTANCE; DOWN-REGULATION;
   PROLIFERATION; AUTOPHAGY; COMBINATION; SENSITIVITY
AB 5-fluorouracil (5-FU) is among the mostly administrated chemotherapeutic agents for a wide variety of neoplasms. Non-coding RNAs have a central impact on the determination of the response of patients to 5-FU. These transcripts via modulation of cancer-related pathways, cell apoptosis, autophagy, epithelial-mesenchymal transition, and other aspects of cell behavior can affect cell response to 5-FU. Modulation of expression levels of microRNAs or long non-coding RNAs may be a suitable approach to sensitize tumor cells to 5-FU treatment via modulating multiple biological signaling pathways such as Hippo/YAP, Wnt/beta-catenin, Hedgehog, NF-kB, and Notch cascades. Moreover, there is an increasing interest in targeting these transcripts in various kinds of cancers that are treated by 5-FU. In the present article, we provide a review of the function of non-coding transcripts in the modulation of response of neoplastic cells to 5-FU.
C1 [Ghafouri-Fard, Soudeh] Shahid Beheshti Univ Med Sci, Res Inst Dent Sci, Sch Dent, Dent Res Ctr, Tehran, Iran.
   [Abak, Atefe] Tabriz Univ Med Sci, Dept Med Genet, Fac Med, Tabriz, Iran.
   [Tondro Anamag, Farhad] Tabriz Univ Med Sci, Fac Med, Tabriz, Iran.
   [Shoorei, Hamed] Birjand Univ Med Sci, Dept Anat Sci, Fac Med, Birjand, Iran.
   [Fattahi, Faranak] Univ Calif San Francisco, Eli & Edythe Broad Ctr Regenerat Med & Stem Cell, San Francisco, CA 94143 USA.
   [Fattahi, Faranak] Univ Calif San Francisco, Dept Biochem & Biophys, San Francisco, CA 94143 USA.
   [Javadinia, Seyed Alireza] Sabzevar Univ Med Sci, Cellular & Mol Res Ctr, Sabzevar, Iran.
   [Basiri, Abbas; Taheri, Mohammad] Shahid Beheshti Univ Med Sci, Urol & Nephrol Res Ctr, Tehran, Iran.
RP Taheri, M (corresponding author), Shahid Beheshti Univ Med Sci, Urol & Nephrol Res Ctr, Tehran, Iran.
EM mohammad.taheri@sbmu.ac.ir
RI Shoorei, Hamed/J-5929-2019; Basiri, Abbas/AAW-3718-2021
OI Shoorei, Hamed/0000-0002-7762-5362; 
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NR 187
TC 5
Z9 5
U1 7
U2 8
PU FRONTIERS MEDIA SA
PI LAUSANNE
PA AVENUE DU TRIBUNAL FEDERAL 34, LAUSANNE, CH-1015, SWITZERLAND
SN 2234-943X
J9 FRONT ONCOL
JI Front. Oncol.
PD APR 19
PY 2021
VL 11
AR 658636
DI 10.3389/fonc.2021.658636
PG 21
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA RW1WW
UT WOS:000646315300001
PM 33954114
OA gold, Green Published
DA 2022-04-25
ER

PT J
AU Lemke, D
   Pledl, HW
   Zorn, M
   Jugold, M
   Green, E
   Blaes, J
   Low, S
   Hertenstein, A
   Ott, M
   Sahm, F
   Steffen, AC
   Weiler, M
   Winkler, F
   Platten, M
   Dong, Z
   Wick, W
AF Lemke, Dieter
   Pledl, Hans-Werner
   Zorn, Markus
   Jugold, Manfred
   Green, Ed
   Blaes, Jonas
   Loew, Sarah
   Hertenstein, Anne
   Ott, Martina
   Sahm, Felix
   Steffen, Ann-Catherine
   Weiler, Markus
   Winkler, Frank
   Platten, Michael
   Dong, Zhen
   Wick, Wolfgang
TI Slowing down glioblastoma progression in mice by running or the
   anti-malarial drug dihydroartemisinin? Induction of oxidative stress in
   murine glioblastoma therapy
SO ONCOTARGET
LA English
DT Article
DE dihydroartemisinin; glioblastoma; physical exercises (PE); therapy;
   physical exercise
ID TUMOR-BEARING RATS; CELLS IN-VITRO; GLIOMA-CELLS; PHYSICAL-ACTIVITY;
   BREAST-CANCER; STEM-CELLS; RECURRENT GLIOBLASTOMA; EXERCISE PROGRAM;
   TEMOZOLOMIDE; AUTOPHAGY
AB Influencing cancer metabolism by lifestyle changes is an attractive strategy as - if effective - exercise-induced problems may be less severe than those induced by classical anti-cancer therapies. Pursuing this idea, clinical trials evaluated the benefit of e.g. different diets such as the ketogenic diet, intermittent caloric restriction and physical exercise (PE) in the primary and secondary prevention of different cancer types. PE proved to be beneficial in the context of breast and colon cancer.
   Glioblastoma has a dismal prognosis, with an average overall survival of about one year despite maximal safe resection, concomitant radiochemotherapy with temozolomide followed by adjuvant temozolomide therapy. Here, we focused on the influence of PE as an isolated and adjuvant treatment in murine GB therapy.
   PE did not reduce toxic side effects of chemotherapy in mice administered in a dose escalating scheme as shown before for starvation. Although regular treadmill training on its own had no obvious beneficial effects, its combination with temozolomide was beneficial in the treatment of glioblastoma-bearing mice. As PE might partly act through the induction of reactive oxygen species, dihydroartemisinin - an approved anti-malarial drug which induces oxidative stress in glioma cells - was further evaluated in vitro and in vivo. Dihydroartemisinin showed anti-glioma activity by promoting autophagy, reduced the clonogenic survival and proliferation capacity of glioma cells, and prolonged the survival of tumor bearing mice. Using the reactive oxygen species scavenger n-acetyl-cysteine these effects were in part reversible, suggesting that dihydroartemisinin partly acts through the generation of reactive oxygen species.
C1 [Lemke, Dieter; Pledl, Hans-Werner; Green, Ed; Blaes, Jonas; Loew, Sarah; Hertenstein, Anne; Ott, Martina; Sahm, Felix; Steffen, Ann-Catherine; Weiler, Markus; Winkler, Frank; Platten, Michael; Wick, Wolfgang] German Canc Res Ctr, German Canc Consortium DKTK, Heidelberg, Germany.
   [Lemke, Dieter; Pledl, Hans-Werner; Blaes, Jonas; Loew, Sarah; Hertenstein, Anne; Steffen, Ann-Catherine; Weiler, Markus; Winkler, Frank; Wick, Wolfgang] German Canc Res Ctr, Clin Cooperat Unit Neurooncol, Heidelberg, Germany.
   [Lemke, Dieter; Pledl, Hans-Werner; Loew, Sarah; Hertenstein, Anne; Weiler, Markus; Winkler, Frank; Platten, Michael; Wick, Wolfgang] Heidelberg Univ, German Canc Res Ctr DKFZ, Neurol Clin, Heidelberg, Germany.
   [Lemke, Dieter; Pledl, Hans-Werner; Loew, Sarah; Hertenstein, Anne; Weiler, Markus; Winkler, Frank; Platten, Michael; Wick, Wolfgang] Heidelberg Univ, German Canc Res Ctr DKFZ, Natl Ctr Tumor Dis, Heidelberg, Germany.
   [Zorn, Markus] German Canc Res Ctr, Cent Lab Heidelberg Univ Hosp, Heidelberg, Germany.
   [Jugold, Manfred] German Canc Res Ctr, Core Facil Small Anim Imaging Ctr, Heidelberg, Germany.
   [Green, Ed; Ott, Martina; Platten, Michael] German Canc Res Ctr, Clin Cooperat Unit Neuroimmunol & Brain Tumor Imm, Heidelberg, Germany.
   [Sahm, Felix] Heidelberg Univ, Inst Pathol, Dept Neuropathol, German Canc Res Ctr DKFZ, Heidelberg, Germany.
   [Sahm, Felix] German Canc Res Ctr, Clin Cooperat Unit Neuropathol, Heidelberg, Germany.
   [Dong, Zhen] Huazhong Univ Sci & Technol, Tongji Med Coll, Tongji Hosp, Dept Neurosurg, Wuhan, Peoples R China.
RP Wick, W (corresponding author), German Canc Res Ctr, German Canc Consortium DKTK, Heidelberg, Germany.; Wick, W (corresponding author), German Canc Res Ctr, Clin Cooperat Unit Neurooncol, Heidelberg, Germany.; Wick, W (corresponding author), Heidelberg Univ, German Canc Res Ctr DKFZ, Neurol Clin, Heidelberg, Germany.; Wick, W (corresponding author), Heidelberg Univ, German Canc Res Ctr DKFZ, Natl Ctr Tumor Dis, Heidelberg, Germany.; Dong, Z (corresponding author), Huazhong Univ Sci & Technol, Tongji Med Coll, Tongji Hosp, Dept Neurosurg, Wuhan, Peoples R China.
EM dongz@tjh.tjmu.edu.cn; wolfgang.wick@med.uni-heidelberg.de
RI Platten, Michael/F-2902-2013; Sahm, Felix/W-8050-2019; Wick,
   Wolfgang/AAA-2545-2020; Dong, Zhen/K-8432-2015
OI Platten, Michael/0000-0002-4746-887X; Sahm, Felix/0000-0001-5441-1962;
   Wick, Wolfgang/0000-0002-6171-634X; Dong, Zhen/0000-0002-8801-9966;
   Winkler, Frank/0000-0003-4892-6104
FU German Research FoundationGerman Research Foundation (DFG) [SFB938 TPK]
FX Supported by German Research Foundation (SFB938 TPK) to M.P. and W.W.
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NR 56
TC 16
Z9 17
U1 1
U2 11
PU IMPACT JOURNALS LLC
PI ORCHARD PARK
PA 6666 E QUAKER ST, STE 1, ORCHARD PARK, NY 14127 USA
SN 1949-2553
J9 ONCOTARGET
JI Oncotarget
PD AUG 30
PY 2016
VL 7
IS 35
BP 56713
EP 56725
DI 10.18632/oncotarget.10723
PG 13
WC Oncology; Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Cell Biology
GA EA8TL
UT WOS:000386911600062
PM 27447560
OA gold, Green Published, Green Submitted
DA 2022-04-25
ER

PT J
AU Christodoulou, EG
   Yang, H
   Lademann, F
   Pilarsky, C
   Beyer, A
   Schroeder, M
AF Christodoulou, Eleni G.
   Yang, Hai
   Lademann, Franziska
   Pilarsky, Christian
   Beyer, Andreas
   Schroeder, Michael
TI Detection of COPB2 as a KRAS synthetic lethal partner through
   integration of functional genomics screens
SO ONCOTARGET
LA English
DT Article
DE KRAS; synthetic lethal partner; ranking; rank aggregation; functional
   screens
ID RNA INTERFERENCE; COLORECTAL-CANCER; RAS; REVEALS; AUTOPHAGY;
   IDENTIFICATION; INHIBITION; CARCINOMA; TUMORS; CELLS
AB Mutated KRAS plays an important role in many cancers. Although targeting KRAS directly is difficult, indirect inactivation via synthetic lethal partners (SLPs) is promising. Yet to date, there are no SLPs from high-throughput RNAi screening, which are supported by multiple screens. Here, we address this problem by aggregating and ranking data over three independent high-throughput screens. We integrate rankings by minimizing the displacement and by considering established methods such as RIGER and RSA.
   Our meta analysis reveals COPB2 as a potential SLP of KRAS with good support from all three screens. COPB2 is a coatomer subunit and its knock down has already been linked to disabled autophagy and reduced tumor growth. We confirm COPB2 as SLP in knock down experiments on pancreas and colorectal cancer cell lines.
   Overall, consistent integration of high throughput data can generate candidate synthetic lethal partners, which individual screens do not uncover. Concretely, we reveal and confirm that COPB2 is a synthetic lethal partner of KRAS and hence a promising cancer target. Ligands inhibiting COPB2 may, therefore, be promising new cancer drugs.
C1 [Christodoulou, Eleni G.; Beyer, Andreas; Schroeder, Michael] Tech Univ Dresden, Biotechnol Ctr, Dresden, Germany.
   [Christodoulou, Eleni G.] Natl Canc Ctr Singapore, Dept Med Oncol, Singapore, Singapore.
   [Yang, Hai; Pilarsky, Christian] Univ Klinikum Erlangen, Translat Res Ctr, Chirurg Klin, Erlangen, Germany.
   [Lademann, Franziska; Pilarsky, Christian] Tech Univ Dresden, Med Fak Carl Gustav Carus, Dresden, Germany.
   [Beyer, Andreas] Univ Cologne, Cellular Networks & Syst Biol, Cologne, Germany.
RP Beyer, A; Schroeder, M (corresponding author), Tech Univ Dresden, Biotechnol Ctr, Dresden, Germany.; Beyer, A (corresponding author), Univ Cologne, Cellular Networks & Syst Biol, Cologne, Germany.
EM andreas.beyer@uni-koeln.de; ms@biotec.tu-dresden.de
RI Beyer, Andreas/A-3352-2009; Beyer, Andreas/AAQ-5519-2020
OI Beyer, Andreas/0000-0002-3891-2123; Beyer, Andreas/0000-0002-3891-2123;
   Pilarsky, Christian/0000-0002-7968-3283; Lademann,
   Franziska/0000-0003-1059-5506
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NR 50
TC 4
Z9 5
U1 0
U2 4
PU IMPACT JOURNALS LLC
PI ORCHARD PARK
PA 6666 E QUAKER ST, STE 1, ORCHARD PARK, NY 14127 USA
EI 1949-2553
J9 ONCOTARGET
JI Oncotarget
PD MAY 23
PY 2017
VL 8
IS 21
BP 34283
EP 34297
DI 10.18632/oncotarget.16079
PG 15
WC Oncology; Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Cell Biology
GA EV8RY
UT WOS:000402051700027
PM 28415695
OA Green Published, Green Submitted, gold
DA 2022-04-25
ER

PT J
AU Xie, XL
   Liu, YB
   Liu, YP
   Du, BL
   Li, Y
   Han, M
   Li, BH
AF Xie, Xiao-Li
   Liu, Ya-Bin
   Liu, Yue-Ping
   Du, Bin-Liang
   Li, Yang
   Han, Mei
   Li, Bing-Hui
TI Reduced expression of SM22 is correlated with low autophagy activity in
   human colorectal cancer
SO PATHOLOGY RESEARCH AND PRACTICE
LA English
DT Article
DE SM22; Autophagy; p62; Colorectal cancer
ID SMOOTH-MUSCLE-CELLS; PROSTATE-CANCER; TRANSGELIN; PROTEIN; P62;
   SUPPRESSOR; BREAST; TUMORIGENESIS; ALPHA; P53
AB Colorectal cancer (CRC) is a common malignancy with a high incidence and mortality rate. Recent studies have pointed to deregulation of autophagy as a novel pathogenesis of human malignancy. SM22 is considered as a tumor suppressor. The aim of the present study was to evaluate the correlation of the SM22 expression level with the autophagy activity and the clinical characteristics in human CRC tissues. The expressions of SM22 and p62, a biomarker of autophagy activity, in paired tumor and adjacent non-tumor tissues from 43 patients with colorectal cancer were detected by western blot and immunohistochemical staining, respectively. The results showed that the SM22 level decreased significantly in 81.4% CRC tissues, while the expression of p62 increased in 79.1% cases. There was a negative correlation between p62 and SM22 expressions in colorectal cancer tissues (p = 0.004). Similarly, the negative correlation between 5M22 and p62 was verified in human CRC cell lines. The data suggest that the autophagy activity decreased in human CRC, which was associated with reduction in SM22 expression. However, the expression of SM22 was not associated with the gender, tumor site and Duke's stage of the patients. In conclusion, our findings suggest that the disruption of SM22 may be involved in tumorigenesis in CRC. The autophagic activity may be suppressed in human CRC, and SM22 may act as a positive regulator in the processes of autophagy. (C) 2013 Elsevier GmbH. All rights reserved.
C1 [Xie, Xiao-Li; Han, Mei] Hebei Med Univ, Coll Basic Med, Key Lab Med Biotechnol Hebei Prov,Minist Educ, Dept Biochem & Mol Biol,Key Lab Neural & Vasc Bio, Shijiazhuang 050017, Peoples R China.
   [Liu, Ya-Bin; Du, Bin-Liang; Li, Yang; Li, Bing-Hui] Hebei Med Univ, Affiliated Hosp 4, Dept Surg, Shijiazhuang 050017, Peoples R China.
   [Liu, Yue-Ping] Hebei Med Univ, Affiliated Hosp 4, Dept Pathol, Shijiazhuang 050017, Peoples R China.
RP Han, M (corresponding author), Hebei Med Univ, Coll Basic Med, Key Lab Med Biotechnol Hebei Prov,Minist Educ, Dept Biochem & Mol Biol,Key Lab Neural & Vasc Bio, Shijiazhuang 050017, Peoples R China.
EM hanmei@hebmu.edu.cn; lbh58@hebmu.edu.cn
OI liu, yabin/0000-0003-4970-7069
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NR 28
TC 10
Z9 12
U1 0
U2 2
PU ELSEVIER GMBH, URBAN & FISCHER VERLAG
PI JENA
PA OFFICE JENA, P O BOX 100537, 07705 JENA, GERMANY
SN 0344-0338
J9 PATHOL RES PRACT
JI Pathol. Res. Pract.
PY 2013
VL 209
IS 4
BP 237
EP 243
DI 10.1016/j.prp.2013.02.007
PG 7
WC Pathology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pathology
GA 152PN
UT WOS:000319543700007
PM 23538046
DA 2022-04-25
ER

PT J
AU Barone, R
   Bavisotto, CC
   Rappa, F
   Gargano, ML
   Macaluso, F
   Paladino, L
   Vitale, AM
   Alfano, S
   Campanella, C
   Gorska, M
   Di Felice, V
   Cappello, F
   Venturella, G
   Gammazza, AM
AF Barone, Rosario
   Caruso Bavisotto, Celeste
   Rappa, Francesca
   Gargano, Maria Letizia
   Macaluso, Filippo
   Paladino, Letizia
   Vitale, Alessandra Maria
   Alfano, Stefano
   Campanella, Claudia
   Gorska, Magdalena
   Di Felice, Valentina
   Cappello, Francesco
   Venturella, Giuseppe
   Marino Gammazza, Antonella
TI JNK pathway and heat shock response mediate the survival of C26 colon
   carcinoma bearing mice fed with the mushroom Pleurotus eryngii var.
   eryngii without affecting tumor growth or cachexia
SO FOOD & FUNCTION
LA English
DT Article
AB In the last few years, there has been emerging interest in developing treatments against human diseases using natural bioactive content. Here, the powder of the edible mushroom Pleurotus eryngii var. eryngii was mixed with the normal diet of mice bearing C26 colon carcinoma. Interestingly, it was evidenced by a significant increase in the survival rate of C26 tumor-bearing mice accompanied by a significant increase in Hsp90 and Hsp27 protein levels in the tumors. These data were paralleled by a decrease in Hsp60 levels. The mushroom introduced in the diet induced the inhibition of the transcription of the pro-inflammatory cytokines IL-6 and IL-1 exerting an anti-inflammatory action. The effects of the mushroom were mediated by the activation of c-Jun NH2-terminal kinases as a result of metabolic stress induced by the micronutrients introduced in the diet. In the tumors of C26 bearing mice fed with Pleurotus eryngii there was also a decreased expression of the mitotic regulator survivin and the anti-apoptotic factor Bcl-xL as well as an increase in the expression levels of Atg7, a protein that drives autophagy. In our hypothesis the interplay of these molecules favored the survival of the mice fed with the mushroom. These data are promising for the introduction of Pleurotus eryngii as a dietary supplement or as an adjuvant in anti-cancer therapy.
C1 [Barone, Rosario; Caruso Bavisotto, Celeste; Rappa, Francesca; Paladino, Letizia; Vitale, Alessandra Maria; Alfano, Stefano; Campanella, Claudia; Di Felice, Valentina; Cappello, Francesco; Marino Gammazza, Antonella] Univ Palermo, Dept Biomed Neurosci & Adv Diagnost, Palermo, Italy.
   [Gargano, Maria Letizia; Venturella, Giuseppe] Univ Palermo, Dept Agr Food & Forest Sci, Palermo, Italy.
   [Gargano, Maria Letizia] Univ Bari Aldo Moro, Dept Agr & Environm Sci, Bari, Italy.
   [Gargano, Maria Letizia; Venturella, Giuseppe] Italian Soc Med Mushrooms, Pisa, Italy.
   [Macaluso, Filippo] eCampus Univ, Novedrate, CO, Italy.
   [Gorska, Magdalena] Med Univ Gdansk, Dept Med Chem, Gdansk, Poland.
RP Gammazza, AM (corresponding author), Univ Palermo, Dept Biomed Neurosci & Adv Diagnost, Palermo, Italy.
EM antonella.marinogammazza@unipa.it
RI Vitale, Alessandra Maria/ABD-7894-2021; barone, rosario/ABA-6758-2021;
   Di Felice, Valentina/AAG-3740-2021; Gargano, Maria Letizia/G-8251-2015
OI Di Felice, Valentina/0000-0002-4132-1260; Gargano, Maria
   Letizia/0000-0002-0511-5363; Paladino, Letizia/0000-0001-8037-7761;
   Vitale, Alessandra Maria/0000-0002-7566-4309
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NR 82
TC 0
Z9 0
U1 3
U2 5
PU ROYAL SOC CHEMISTRY
PI CAMBRIDGE
PA THOMAS GRAHAM HOUSE, SCIENCE PARK, MILTON RD, CAMBRIDGE CB4 0WF, CAMBS,
   ENGLAND
SN 2042-6496
EI 2042-650X
J9 FOOD FUNCT
JI Food Funct.
PD APR 7
PY 2021
VL 12
IS 7
BP 3083
EP 3095
DI 10.1039/d0fo03171b
PG 13
WC Biochemistry & Molecular Biology; Food Science & Technology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Food Science & Technology
GA RM3XC
UT WOS:000639596100021
PM 33720221
DA 2022-04-25
ER

PT J
AU Yang, YP
   Zhu, F
   Wang, QM
   Ding, Y
   Ying, RB
   Zeng, LH
AF Yang, Youping
   Zhu, Feng
   Wang, Qingmei
   Ding, Yan
   Ying, Rongbiao
   Zeng, Linghui
TI Inhibition of EZH2 and EGFR produces a synergistic effect on cell
   apoptosis by increasing autophagy in gastric cancer cells
SO ONCOTARGETS AND THERAPY
LA English
DT Article
DE EZH2; EGFR; autophagy; mTOR signaling; gastric cancer
ID COLON-CANCER; EXPRESSION; PROTEIN; GROWTH; GEFITINIB; THERAPY; FAMILY;
   TUMOR; PANEL
AB Background: Numerous reports have shown that a combination of two or more drugs leads to better cancer treatment. Inhibitors of zeste homology 2 and epidermal growth factor receptor have been widely used in cancer treatments. However, the mechanisms of the combined use of these two drugs remain elusive.
   Methods: Sul forhodamine B assays and Alexa Fluor (R)-488 Annexin V/Dead Cell Apoptosis Kit were used to detect the cell proliferation and cell apoptosis in vitro, respectively. Western blotting analysis was used to detect the relative protein expression, and xenografted tumor was generated in nude mice to evaluate the effect in vivo.
   Results: Treatment with either Gefitinib ranging from 0 to 12.5 mu M or GSK126 ranging from 0 to 8.3 mu M caused adore-dependent decrease in the cell survival fraction, and the combination of Gefitinib at 12.5 mu M and GSK126 at 8.3 mu M caused further significant decrease. The combination indexes were 0.061, 0.591, 0.713, and 0.371 for MGC803, A549, PC-3, and MDB-MA-231, respectively. In MGC803 cells, the combination of GSK126 and Gefitinib synergistically induced cell apoptosis (56.2%), which was markedly higher as compared to either drug alone (7.6% and 10.6%, P<0.05). Treatment with either Gefitinib or GSK126 alone induced a significant increase in cell apoptosis in LC3-II and p-ULK, whereas the combination of the two induced a further increase. Pretreatment with an autophagy inhibitor, 3-methyladenine, prevented the apoptosis induced by the combined use of Gefitinib and GSK126. In addition, the combined use of Gefitinib and GSK126 also inhibited the activation of mammalian target of rapamycin signaling pathway. Furthermore, the combined use of GSK126 and Gefitinib synergistically inhibited xenografted tumor proliferation.
   Conclusion: The combined use of GSK126 and Gefitinib exerts a synergic effect on tumor growth inhibition both in vitro and in vivo through inducing autophagy and promoting apoptosis. Therefore, GSK126 and Gefitinib in combination may be considered as a potential strategy in treating solid tumor clinically.
C1 [Yang, Youping] First Peoples Hosp Wenling City, Dept Pathol, Wenling City 317500, Zhejiang, Peoples R China.
   [Yang, Youping; Ding, Yan; Ying, Rongbiao] Taizhou Canc Hosp, Dept Surg Oncol, Wenling City 317500, Zhejiang, Peoples R China.
   [Zhu, Feng; Wang, Qingmei; Zeng, Linghui] Zhejiang Univ City Coll, Dept Pharmacol, 50 Huzhou Rd, Hangzhou 310015, Zhejiang, Peoples R China.
RP Zeng, LH (corresponding author), Zhejiang Univ City Coll, Dept Pharmacol, 50 Huzhou Rd, Hangzhou 310015, Zhejiang, Peoples R China.
EM zenglh@zucc.edu.cn
FU Foundation of Zhejiang Health Bureau [2015 KYA148, 2015RCB004]; Zhejiang
   Provincial Foundation of National Science [LY12H16005]
FX Research reported in this publication was supported by the Foundation of
   Zhejiang Health Bureau (2015 KYA148, 2015RCB004) and Zhejiang Provincial
   Foundation of National Science (LY12H16005).
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NR 30
TC 16
Z9 17
U1 1
U2 2
PU DOVE MEDICAL PRESS LTD
PI ALBANY
PA PO BOX 300-008, ALBANY, AUCKLAND 0752, NEW ZEALAND
SN 1178-6930
J9 ONCOTARGETS THER
JI OncoTargets Ther.
PY 2018
VL 11
BP 8455
EP 8463
DI 10.2147/OTT.S186498
PG 9
WC Biotechnology & Applied Microbiology; Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biotechnology & Applied Microbiology; Oncology
GA HD0UU
UT WOS:000452225100001
PM 30555238
OA Green Published, Green Submitted, gold
DA 2022-04-25
ER

PT J
AU Asakura, K
   Izumi, Y
   Yamamoto, M
   Yamauchi, Y
   Kawai, K
   Serizawa, A
   Mizushima, T
   Ohmura, M
   Kawamura, M
   Wakui, M
   Adachi, T
   Nakamura, M
   Suematsu, M
   Nomori, H
AF Asakura, Keisuke
   Izumi, Yotaro
   Yamamoto, Michiko
   Yamauchi, Yoshikane
   Kawai, Kenji
   Serizawa, Akihiko
   Mizushima, Tomoko
   Ohmura, Mitsuyo
   Kawamura, Masafumi
   Wakui, Masatoshi
   Adachi, Takeshi
   Nakamura, Masato
   Suematsu, Makoto
   Nomori, Hiroaki
TI The Cytostatic Effects of Lovastatin on ACC-MESO-1 Cells
SO JOURNAL OF SURGICAL RESEARCH
LA English
DT Article
DE statins; mesothelioma; autophagic changes
ID PHOSPHOLIPASE C-EPSILON; BREAST-CANCER CELLS; MALIGNANT MESOTHELIOMA;
   RHO-GTPASES; INDUCED AUTOPHAGY; NITRIC-OXIDE; IN-VIVO; INHIBITION;
   ACTIVATION; STATINS
AB Background. Malignant pleural mesothelioma is known to be widely resistant to therapy, and new treatment strategies are needed. Statins are small molecules that suppress the production of multiple hydrophobic substrates in the mevalonate pathway. Although still controversial, statins may decrease the risk of certain cancers such as colon cancer, lung cancer, and prostate cancer. Since the evaluations of the direct effect of statins on malignant mesothelioma are still few, the present study was done to evaluate the effects of lovastatin on ACC-MESO-1 cells in vivo and to investigate the potential mechanisms involved in vitro.
   Materials and Methods. The in vivo effect of lovastatin was evaluated using an NOD/SCID/gamma null (NOG) mouse model of human malignant mesothelioma using ACC-MESO-1 cells. Lovastatin was also applied to ACC-MESO-1 cells in vitro and the effects were observed.
   Results. Lovastatin administration reduced primary tumor and metastasis in the NOG mouse model of human malignant mesothelioma. In vitro studies showed that lovastatin administration induced cytostatic effects as per reduced cell viability and cell migration in ACC-MESO-1 cells. These effects were suggested to be dependent on autophagic changes rather than apoptosis. Furthermore, induction of autophagic changes by lovastatin in ACC-MESO-1 cells was independent of mTOR, and was considered to be dependent at least in part on Rac/phospholipase C/inositol 1,4,5-triphosphate axis.
   Conclusions. These results suggest that it may be possible to utilize statins, or other pharmacological agents that are known to induce mTOR-independent autophagy, as an adjunct to standard treatments in malignant mesothelioma. (C) 2011 Elsevier Inc. All rights reserved.
C1 [Izumi, Yotaro] Keio Univ, Div Gen Thorac Surg, Sch Med, Dept Surg,Shinjuku Ku, Tokyo 1608582, Japan.
   [Asakura, Keisuke; Yamamoto, Michiko; Ohmura, Mitsuyo; Suematsu, Makoto] Keio Univ, Sch Med, Dept Biochem, Tokyo 1608582, Japan.
   [Wakui, Masatoshi] Keio Univ, Sch Med, Dept Lab Med, Tokyo 1608582, Japan.
   [Kawai, Kenji; Mizushima, Tomoko; Nakamura, Masato] Cent Inst Expt Anim, Kanagawa, Japan.
   [Serizawa, Akihiko] Tokai Univ Hosp, Div Diagnost Pathol, Kanagawa, Japan.
   [Adachi, Takeshi] Natl Def Med Sch, Dept Internal Med 1, Div Cardiol, Tokorozawa, Saitama, Japan.
   [Nakamura, Masato] Tokai Univ, Sch Med, Dept Pathol & Regenerat Med, Kanagawa 2591100, Japan.
RP Izumi, Y (corresponding author), Keio Univ, Div Gen Thorac Surg, Sch Med, Dept Surg,Shinjuku Ku, 35 Shinanomachi, Tokyo 1608582, Japan.
EM yotaroizumi@a2.keio.jp
RI Suematsu, Makoto/O-5762-2018; Suematsu, Makoto/I-8135-2013; Yamauchi,
   Yoshikane/I-1952-2019
OI Suematsu, Makoto/0000-0002-7165-6336; Suematsu,
   Makoto/0000-0002-7165-6336; Yamauchi, Yoshikane/0000-0002-3374-2399;
   Asakura, Keisuke/0000-0002-4491-3456
FU Ministry of Education, Culture, Sports, Science, and
   Technology-JapanMinistry of Education, Culture, Sports, Science and
   Technology, Japan (MEXT) [19790981]; Ministry of Education, Culture,
   Sports, Science and TechnologyMinistry of Education, Culture, Sports,
   Science and Technology, Japan (MEXT); School of Medicine, Keio
   University; Nateglinide Memorial Toyoshima Research and Education Fund
FX The authors thank Kei Tsujioka, Takayo Oba, Division of General Thoracic
   Surgery, and Kyoko Ishiwata, Department of Biochemistry, for their
   excellent technical assistance. This work was supported in part by grant
   in aid from the Ministry of Education, Culture, Sports, Science, and
   Technology-Japan to KA (no. 19790981), in part by Global COE Program for
   Metabolomics Systems Biology from the Ministry of Education, Culture,
   Sports, Science and Technology to MS, in part by School of Medicine,
   Keio University fund for the promotion of science to MW and YI, and in
   part by Nateglinide Memorial Toyoshima Research and Education Fund to
   TA.
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NR 45
TC 15
Z9 15
U1 0
U2 5
PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 0022-4804
EI 1095-8673
J9 J SURG RES
JI J. Surg. Res.
PD OCT
PY 2011
VL 170
IS 2
BP E197
EP E209
DI 10.1016/j.jss.2011.06.037
PG 13
WC Surgery
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Surgery
GA 823NH
UT WOS:000295128600001
PM 21816418
DA 2022-04-25
ER

PT J
AU Delmas, D
   Solary, E
   Latruffe, N
AF Delmas, D.
   Solary, E.
   Latruffe, N.
TI Resveratrol, a Phytochemical Inducer of Multiple Cell Death Pathways:
   Apoptosis, Autophagy and Mitotic Catastrophe
SO CURRENT MEDICINAL CHEMISTRY
LA English
DT Review
DE Apoptosis; cancer; chemosensitization; lipid rafts; phagocytosis;
   resveratrol
ID NF-KAPPA-B; BREAST-CANCER CELLS; PROTEIN-KINASE-C; INHIBITS
   CYCLOOXYGENASE-2 TRANSCRIPTION; CHEMOPREVENTIVE AGENT RESVERATROL;
   FAS-INDEPENDENT APOPTOSIS; NATURAL-PRODUCT PRESENT; DRUG-INDUCED
   APOPTOSIS; COLON-CARCINOMA CELLS; NITRIC-OXIDE SYNTHASE
AB Cancers are the largest cause of mortality and morbidity in industrialized countries. In the field of the medicinal chemistry of natural products, numerous studies have reported interesting properties of trans-resveratrol as a chemopreventing agent against cancers, inflammation, and viral infection. Tumor growth inhibition has been linked to the ability of resveratrol to arrest cell cycle progression and to trigger cell death. This review focuses on the pathways that mediate resveratrol-induced cell death. Resveratrol impacts on the mitochondrial functions (respiratory chain, oncoproteins, gene expression, etc), in which p53 protein can be involved and its acetylated or phosphorylated forms. This polyphenol also affects death receptor distribution in ceramide-enriched membrane platforms which serve to trap and cluster receptor molecules, and facilitates the formation of a death-inducing signaling complex in the cell. To induce apoptosis, resveratrol also activates the ceramide / sphingomyelin pathway, which promotes ceramide generation and the downstream activation of kinase cascades. Resveratrol can activate alternative pathways to cell death such as those leading to autophagy, senescence or mitotic catastrophe. Furthermore, numerous attempts have been made using resveratrol analogs to improve the molecule's ability to block cell proliferation and induce cell death. Moreover, structural modification of natural phenolics is expected to produce analogs that may be useful tools to study the structure-activity relationships. Lastly, in various cancer types, resveratrol behaves as a chemosensitizer that lowers the threshold of cell death induction by classical anticancer agents and counteracts tumor cell chemoresistance.
C1 [Delmas, D.] Fac Sci, INSERM, U866, UMR866, F-21000 Dijon, France.
   [Delmas, D.; Latruffe, N.] Univ Bourgogne, Fac Sci Gabriel, Ctr Rech Biochim Metab & Nutr LBMN, F-21000 Dijon, France.
   [Solary, E.] Univ Bourgogne, Fac Med, Ctr Rech Canc & Differenciat, F-21000 Dijon, France.
RP Delmas, D (corresponding author), Fac Sci, INSERM, U866, UMR866, 6 Blvd Gabriel, F-21000 Dijon, France.
EM ddelmas@u-bourgogne.fr
RI Delmas, Dominique/AAD-9749-2019
OI Delmas, Dominique/0000-0003-3576-0248; Delmas,
   Dominique/0000-0002-8911-8499; Solary, Eric/0000-0002-8629-1341
FU Conseil Regional de BourgogneRegion Bourgogne-Franche-Comte; Ligue
   contre le Cancer, comite grand-est
FX We thank Dr. Dominic Batt for reading the English. This study was
   supported by the "Conseil Regional de Bourgogne" and the "Ligue contre
   le Cancer, comite grand-est".
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PU BENTHAM SCIENCE PUBL LTD
PI SHARJAH
PA EXECUTIVE STE Y-2, PO BOX 7917, SAIF ZONE, 1200 BR SHARJAH, U ARAB
   EMIRATES
SN 0929-8673
EI 1875-533X
J9 CURR MED CHEM
JI Curr. Med. Chem.
PD MAR
PY 2011
VL 18
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EP 1121
DI 10.2174/092986711795029708
PG 22
WC Biochemistry & Molecular Biology; Chemistry, Medicinal; Pharmacology &
   Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Pharmacology & Pharmacy
GA 743AS
UT WOS:000288988100001
PM 21291372
DA 2022-04-25
ER

PT J
AU Coutermarsh-Ott, S
   Simmons, A
   Capria, V
   LeRoith, T
   Wilson, JE
   Heid, B
   Philipson, CW
   Qin, QZ
   Hontecillas-Magarzo, R
   Bassaganya-Riera, J
   Ting, JPY
   Dervisis, N
   Allen, IC
AF Coutermarsh-Ott, Sheryl
   Simmons, Alysha
   Capria, Vittoria
   LeRoith, Tanya
   Wilson, Justin E.
   Heid, Bettina
   Philipson, Casandra W.
   Qin, Qizhi
   Hontecillas-Magarzo, Raquel
   Bassaganya-Riera, Josep
   Ting, Jenny P-Y
   Dervisis, Nikolaos
   Allen, Irving C.
TI NLRX1 suppresses tumorigenesis and attenuates histiocytic sarcoma
   through the negative regulation of NF-lambda B signaling
SO ONCOTARGET
LA English
DT Article
DE NLR; Nod-like receptor; urethane; cancer; inflammation
ID NONSMALL CELL LUNG; TUMOR-SUPPRESSOR; COLON TUMORIGENESIS; I INTERFERON;
   CANCER; PROTEIN; GROWTH; INFLAMMATION; ACTIVATION; PATHWAY
AB Histiocytic sarcoma is an uncommon malignancy in both humans and veterinary species. Research exploring the pathogenesis of this disease is scarce; thus, diagnostic and therapeutic options for patients are limited. Recent publications have suggested a role for the NLR, NLRX1, in acting as a tumor suppressor. Based on these prior findings, we hypothesized that NLRX1 would function to inhibit tumorigenesis and thus the development of histiocytic sarcoma. To test this, we utilized Nlrx1(-/-) mice and a model of urethane-induced tumorigenesis. Nlrx1(-/-) mice exposed to urethane developed splenic histiocytic sarcoma that was associated with significant up-regulation of the NF-lambda B signaling pathway. Additionally, development of these tumors was also significantly associated with the increased regulation of genes associated with AKT signaling, cell death and autophagy. Together, these data show that NLRX1 suppresses tumorigenesis and reveals new genetic pathways involved in the pathobiology of histiocytic sarcoma.
C1 [Coutermarsh-Ott, Sheryl; Simmons, Alysha; Capria, Vittoria; LeRoith, Tanya; Heid, Bettina; Qin, Qizhi; Allen, Irving C.] Virginia Tech, VA MD Reg Coll Vet Med, Dept Biol Sci & Pathobiol, Blacksburg, VA 24061 USA.
   [Wilson, Justin E.; Ting, Jenny P-Y] Univ N Carolina, Lineberger Comprehens Canc Ctr, Dept Genet, Chapel Hill, NC 27599 USA.
   [Philipson, Casandra W.; Hontecillas-Magarzo, Raquel; Bassaganya-Riera, Josep] Virginia Tech, Virginia Bioinformat Inst, Nutr Immunol & Mol Med Lab, Blacksburg, VA USA.
   [Dervisis, Nikolaos] Virginia Tech, VA MD Reg Coll Vet Med, Dept Small Anim Clin Sci, Blacksburg, VA USA.
RP Allen, IC (corresponding author), Virginia Tech, VA MD Reg Coll Vet Med, Dept Biol Sci & Pathobiol, Blacksburg, VA 24061 USA.
EM icallen@vt.edu
RI Dervisis, Nikolaos/K-8931-2016; Philipson, Casandra/AAY-5746-2021
OI Dervisis, Nikolaos/0000-0003-2869-1483; LeRoith,
   Tanya/0000-0002-1196-6949
FU Virginia Maryland College of Veterinary Medicine through the IRC pilot
   grant program; National Institute of Allergy and Infectious Diseases
   Animal Model Research for Veterinarians (AMRV) training grant
   [T32-OD010430]; OFFICE OF THE DIRECTOR, NATIONAL INSTITUTES OF
   HEALTHUnited States Department of Health & Human ServicesNational
   Institutes of Health (NIH) - USA [T32OD010430] Funding Source: NIH
   RePORTER
FX This work was supported by the Virginia Maryland College of Veterinary
   Medicine through the IRC pilot grant program (I.C.A.). Student work on
   this publication was supported by the National Institute of Allergy and
   Infectious Diseases Animal Model Research for Veterinarians (AMRV)
   training grant (T32-OD010430) (S.C.O.). We would also like to recognize
   the Virginia Tech Initiative for Maximizing Student Development
   (VT-IMSD) Program and the Virginia Tech Maximizing Academic
   Opportunities Program for student support throughout this project. The
   content is solely the responsibility of the authors and does not
   necessarily represent the official views of the NIH or any other funding
   agency.
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NR 33
TC 24
Z9 27
U1 0
U2 4
PU IMPACT JOURNALS LLC
PI ORCHARD PARK
PA 6666 E QUAKER ST, STE 1, ORCHARD PARK, NY 14127 USA
EI 1949-2553
J9 ONCOTARGET
JI Oncotarget
PD MAY 31
PY 2016
VL 7
IS 22
BP 33096
EP 33110
DI 10.18632/oncotarget.8861
PG 15
WC Oncology; Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Cell Biology
GA DO4JP
UT WOS:000377748500116
PM 27105514
OA Green Submitted, gold, Green Published
DA 2022-04-25
ER

PT J
AU Badziul, D
   Jakubowicz-Gil, J
   Paduch, R
   Glowniak, K
   Gawron, A
AF Badziul, Dorota
   Jakubowicz-Gil, Joanna
   Paduch, Roman
   Glowniak, Kazimierz
   Gawron, Antoni
TI Combined treatment with quercetin and imperatorin as a potent strategy
   for killing HeLa and Hep-2 cells
SO MOLECULAR AND CELLULAR BIOCHEMISTRY
LA English
DT Article
DE Cancer; Cell death; Imperatorin; Quercetin
ID HEAT-SHOCK PROTEINS; MOLECULAR CHAPERONES; ANGELICA-DAHURICA; CANCER
   PREVENTION; HUMAN COLON; APOPTOSIS; DEATH; ACTIVATION; AUTOPHAGY;
   INDUCTION
AB The aim of the present study was to assess the effect of quercetin and imperatorin administered separately and in combination on apoptosis and autophagy induction in human cervical carcinoma HeLa cells and laryngeal carcinoma Hep-2 cells cultured in vitro. Conducted MTT measurements proved that quercetin and imperatorin displayed a strong antiproliferative activity manifested in markedly reduction of HeLa and Hep-2 cells viability as a result of treatment with 50 mu M of each compound. Further cell staining assays revealed that concentration mentioned above generated the highest percentage of apoptotic cells especially in the case of application of both drugs for 48 h. Simultaneous quercetin and imperatorin administration induced apoptosis remarkably stronger than treatment with single drugs. Experiments at the molecular level confirmed these results accompanied with the decreased Hsp27 and Hsp72 expression and, in addition, with increased caspases activity. Autophagy was not observed and no significant changes in the expression of beclin-1 were noticed. Additionally, experiments were performed on the above-mentioned cell lines with blocked Hsp27 and Hsp72 expression. In these cells, no significant changes in the sensitivity to apoptosis induction upon quercetin and imperatorin treatment were observed. The present study has provided evidence supporting the potential of the combination of quercetin and imperatorin drugs as a novel tool to be used in anticancer therapy. Our results have also demonstrated that blocking of the Hsp27 and Hsp72 gene expression is not enough to sensitize cancer cells to programmed cell death induction in HeLa and Hep-2 cells.
C1 [Badziul, Dorota; Jakubowicz-Gil, Joanna; Gawron, Antoni] Marie Curie Sklodowska Univ, Dept Comparat Anat & Anthropol, Inst Biol, PL-20033 Lublin, Poland.
   [Paduch, Roman] Marie Curie Sklodowska Univ, Dept Virol & Immunol, Inst Microbiol & Biotechnol, PL-20033 Lublin, Poland.
   [Glowniak, Kazimierz] Med Univ Lublin, Dept Pharmacognosy, Med Plant Unit, PL-20093 Lublin, Poland.
RP Badziul, D (corresponding author), Marie Curie Sklodowska Univ, Dept Comparat Anat & Anthropol, Inst Biol, Akad 19, PL-20033 Lublin, Poland.
EM dorota.badziul@wp.pl
RI Jakubowicz-Gil, Joanna/AAK-3561-2020
OI Jakubowicz-Gil, Joanna/0000-0003-2077-804X; Glowniak,
   Kazimierz/0000-0003-4333-0053; Badziul, Dorota/0000-0002-5044-0843;
   Paduch, Roman/0000-0001-9779-7252
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NR 65
TC 31
Z9 38
U1 0
U2 18
PU SPRINGER
PI DORDRECHT
PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS
SN 0300-8177
EI 1573-4919
J9 MOL CELL BIOCHEM
JI Mol. Cell. Biochem.
PD JUL
PY 2014
VL 392
IS 1-2
BP 213
EP 227
DI 10.1007/s11010-014-2032-4
PG 15
WC Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Cell Biology
GA AI9EW
UT WOS:000337233900020
PM 24682729
OA Green Published
DA 2022-04-25
ER

PT J
AU Thackeray, JT
   Pietzsch, S
   Stapel, B
   Ricke-Hoch, M
   Lee, CW
   Bankstahl, JP
   Scherr, M
   Heineke, J
   Scharf, G
   Haghikia, A
   Bengel, FM
   Hilfiker-Kleiner, D
AF Thackeray, James T.
   Pietzsch, Stefan
   Stapel, Britta
   Ricke-Hoch, Melanie
   Lee, Chun-Wei
   Bankstahl, Jens P.
   Scherr, Michaela
   Heineke, Jorg
   Scharf, Gesine
   Haghikia, Arash
   Bengel, Frank M.
   Hilfiker-Kleiner, Denise
TI Insulin supplementation attenuates cancer-induced cardiomyopathy and
   slows tumor disease progression
SO JCI INSIGHT
LA English
DT Article
ID HEART-FAILURE; PERIPARTUM CARDIOMYOPATHY; THERAPEUTIC TARGET; METABOLIC
   SYNDROME; DIABETES-MELLITUS; SIGNAL TRANSDUCER; GLUCOSE-UPTAKE; 2 PARTS;
   CACHEXIA; EXPRESSION
AB Advanced cancer induces fundamental changes in metabolism and promotes cardiac atrophy and heart failure. We discovered systemic insulin deficiency in cachectic cancer patients. Similarly, mice with advanced B16F10 melanoma (B16F10-TM) or colon 26 carcinoma (C26-TM) displayed decreased systemic insulin associated with marked cardiac atrophy, metabolic impairment, and function. B16F10 and C26 tumors decrease systemic insulin via high glucose consumption, lowering pancreatic insulin production and producing insulin-degrading enzyme. As tumor cells consume glucose in an insulin-independent manner, they shift glucose away from cardiomyocytes. Since cardiomyocytes in both tumor models remained insulin responsive, low-dose insulin supplementation by subcutaneous implantation of insulin-releasing pellets improved cardiac glucose uptake, atrophy, and function, with no adverse side effects. In addition, by redirecting glucose to the heart in addition to other organs, the systemic insulin treatment lowered glucose usage by the tumor and thereby decreased tumor growth and volume. Insulin corrected the cancerinduced reduction in cardiac Akt activation and the subsequent overactivation of the proteasome and autophagy. Thus, cancer-induced systemic insulin depletion contributes to cardiac wasting and failure and may promote tumor growth. Low-dose insulin supplementation attenuates these processes and may be supportive in cardio-oncologic treatment concepts.
C1 [Thackeray, James T.; Bankstahl, Jens P.; Bengel, Frank M.] Hannover Med Sch, Dept Nucl Med, Hannover, Germany.
   [Pietzsch, Stefan; Stapel, Britta; Ricke-Hoch, Melanie; Heineke, Jorg; Scharf, Gesine; Haghikia, Arash; Hilfiker-Kleiner, Denise] Hannover Med Sch, Dept Cardiol & Angiol, Div Mol Cardiol, Hannover, Germany.
   [Lee, Chun-Wei; Scherr, Michaela] Hannover Med Sch, Dept Hematol Hemostasis Oncol & Stem Cell Transpl, Hannover, Germany.
   [Haghikia, Arash] Charite, Dept Cardiol, Campus Benjamin Franklin, Berlin, Germany.
RP Hilfiker-Kleiner, D (corresponding author), Hannover Med Sch, Abt Kardiol & Angiol, Carl Neuberg Str 1, D-30625 Hannover, Germany.
EM hilfiker.denise@mh-hannover.de
RI Bengel, Frank/AAR-7353-2020; Haghikia, Arash/F-1348-2016; Thackeray,
   James/R-9350-2018
OI Dittrich, Gesine/0000-0002-9053-078X; Bengel, Frank/0000-0003-4529-7963
FU Canadian Institutes of Health ResearchCanadian Institutes of Health
   Research (CIHR); German Research Association (DFG)German Research
   Foundation (DFG) [HI-842/101, KFO 311]
FX The authors thank Martina Kasten, Silvia Gutzke, Sergej Erschow, Mirco
   M~ller, Birgit Brandt, ChunWei Lee, Silvia Eilert, Alexander Kanwischer,
   and Petra Felsch for excellent technical assistance. JTT is supported by
   a fellowship from the Canadian Institutes of Health Research. This work
   was supported by the German Research Association (DFG) (HI-842/10-1,
   KFO311, Rebirth II).
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NR 38
TC 21
Z9 21
U1 1
U2 1
PU AMER SOC CLINICAL INVESTIGATION INC
PI ANN ARBOR
PA 2015 MANCHESTER RD, ANN ARBOR, MI 48104 USA
SN 2379-3708
J9 JCI INSIGHT
JI JCI Insight
PD MAY 18
PY 2017
VL 2
IS 10
AR e93098
DI 10.1172/jci.insight.93098
PG 14
WC Medicine, Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Research & Experimental Medicine
GA EV3JM
UT WOS:000401655100011
PM 28515362
OA Green Published, gold
DA 2022-04-25
ER

PT J
AU Zhang, JW
   Zhang, SS
   Song, JR
   Sun, K
   Zong, C
   Zhao, QD
   Liu, WT
   Li, R
   Wu, MC
   Wei, LX
AF Zhang, Jian-wei
   Zhang, Shan-shan
   Song, Jian-rui
   Sun, Kai
   Zong, Chen
   Zhao, Qiu-dong
   Liu, Wen-ting
   Li, Rong
   Wu, Meng-chao
   Wei, Li-xin
TI Autophagy inhibition switches low-dose camptothecin-induced premature
   senescence to apoptosis in human colorectal cancer cells
SO BIOCHEMICAL PHARMACOLOGY
LA English
DT Article
DE Human colorectal cancer cells; Low-dose chemotherapy; DNA damage
   response; Autophagy; Senescence; Apoptosis
ID DOUBLE-STRAND BREAKS; TUMOR-CELLS; DNA-DAMAGE; CELLULAR SENESCENCE;
   IN-VITRO; CHEMOTHERAPY; P53; CHECKPOINT; DATABASE; THERAPY
AB Recently, several studies indicated that senescent tumor cells are resistant to apoptosis in chemotherapy. They may return to cell cycle, thus act as stumbling blocks in anticancer treatments. In the present study, we found that, in human colorectal cancer cells, low-dose camptothecin (CPT) simultaneously induced autophagy and premature senescence through AMPK-TSC2-mTOR pathway and ATM-Chk2-p53-p21 pathway respectively. What's important is the suppression of autophagy substantially increased apoptosis and greatly attenuated senescence possibly by blocking p53/p21 pathway, which suggests that autophagy plays an indispensable role in sustaining cell senescence caused by low-dose CPT. The combination of low-dose CPT and autophagy inhibitor, a way to lead senescent cells to die, would be potentially valuable in cancer therapy. (C) 2014 Elsevier Inc. All rights reserved.
C1 [Zhang, Jian-wei; Zhang, Shan-shan; Song, Jian-rui; Sun, Kai; Zong, Chen; Zhao, Qiu-dong; Liu, Wen-ting; Li, Rong; Wu, Meng-chao; Wei, Li-xin] Second Mil Med Univ, Eastern Hepatobiliary Surg Hosp, Tumor Immunol & Gene Therapy Ctr, Shanghai 200438, Peoples R China.
   [Song, Jian-rui] Univ Michigan, Dept Cell Biol, Ann Arbor, MI 48109 USA.
   [Song, Jian-rui] Univ Michigan, Dept Dev Biol, Ann Arbor, MI 48109 USA.
   [Sun, Kai] Shanghai Jiao Tong Univ, Sch Med, Ren Ji Hosp, Med Sci Res Ctr, Shanghai 200030, Peoples R China.
RP Wei, LX (corresponding author), Second Mil Med Univ, Eastern Hepatobiliary Surg Hosp, Tumor Immunol & Gene Therapy Ctr, 225 Changhai Rd, Shanghai 200438, Peoples R China.
EM weilixin_smmu@163.com
FU Key Basic Research Project of China [2012CBA01303, 2011CB966200,
   2010CB945600, 2011CB965100]; Key project of National Natural Science
   Foundation of ChinaNational Natural Science Foundation of China (NSFC)
   [81030041]; National Natural Science Foundation of ChinaNational Natural
   Science Foundation of China (NSFC) [31171321, 81101622, 81372330];
   Special Funds for National key Sci-Tech Sepcial Project of China
   [2012ZX10002-016, 2012ZX10002011-011]; Shanghai Science and Technology
   CommitteeShanghai Science & Technology Committee [10ZR1439600,
   11ZR1449500]; Shanghai Municipal Health Bureau [20114004]; Science Fund
   for Creative Research Groups, National Natural Science Foundation of
   China (NSFC), China [81221061]
FX This project was supported by Key Basic Research Project of China (Grant
   NO.2012CBA01303, 2011CB966200, 2010CB945600, 2011CB965100); Key project
   of National Natural Science Foundation of China (Grant NO. 81030041);
   National Natural Science Foundation of China (Grant NO. 31171321,
   81101622, 81372330); Special Funds for National key Sci-Tech Sepcial
   Project of China (Grant NO. 2012ZX10002-016, 2012ZX10002011-011);
   Shanghai Science and Technology Committee (Grant NO. 10ZR1439600,
   11ZR1449500); Shanghai Municipal Health Bureau (Grant NO.20114004) and
   Science Fund for Creative Research Groups, National Natural Science
   Foundation of China (NSFC), China (Grant NO. 81221061).
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NR 43
TC 29
Z9 30
U1 1
U2 21
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0006-2952
EI 1873-2968
J9 BIOCHEM PHARMACOL
JI Biochem. Pharmacol.
PD AUG 1
PY 2014
VL 90
IS 3
BP 265
EP 275
DI 10.1016/j.bcp.2014.05.009
PG 11
WC Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA AL6FV
UT WOS:000339228900008
PM 24858802
DA 2022-04-25
ER

PT J
AU Masuelli, L
   Di Stefano, E
   Fantini, M
   Mattera, R
   Benvenuto, M
   Marzocchella, L
   Sacchetti, P
   Focaccetti, C
   Bernardini, R
   Tresoldi, I
   Izzi, V
   Mattei, M
   Frajese, GV
   Lista, F
   Modesti, A
   Bei, R
AF Masuelli, Laura
   Di Stefano, Enrica
   Fantini, Massimo
   Mattera, Rosanna
   Benvenuto, Monica
   Marzocchella, Laura
   Sacchetti, Pamela
   Focaccetti, Chiara
   Bernardini, Roberta
   Tresoldi, Ilaria
   Izzi, Valerio
   Mattei, Maurizio
   Frajese, Giovanni Vanni
   Lista, Florigio
   Modesti, Andrea
   Bei, Roberto
TI Resveratrol potentiates the in vitro and in vivo anti-tumoral effects of
   curcumin in head and neck carcinomas
SO ONCOTARGET
LA English
DT Article
DE polyphenols; head and neck cancer; curcumin; resveratrol
ID SQUAMOUS-CELL CARCINOMA; FACTOR-KAPPA-B; MULTIPLE ERBB RECEPTORS;
   ORAL-CANCER CELLS; BCL-X-L; DIETARY POLYPHENOLS; INDUCED AUTOPHAGY;
   DOWN-REGULATION; CLINICAL-TRIAL; COLON-CANCER
AB The survival rate of head and neck squamous cell carcinomas (HNSCC) patients has not considerably changed over the last two decades. Polyphenols inhibit the growth of cancer cells. We determined whether the combination of Resveratrol (RES) and Curcumin (CUR) enhanced their in vitro and in vivo antitumor activities on HNSCC cell lines compared to the single compounds. We provide evidence that RES potentiated the apoptotic effect and reduced the IC50 of CUR on HNSCC cell lines. The model of compounds interaction indicated the onset of an additive effect of the two compounds compared to the single treatment after decrease of their concentrations. RES+CUR compared to CUR increased the PARP-1 cleavage, the Bax/Bcl-2 ratio, the inhibition of ERK1 and ERK2 phosphorylation, and the expression of LC3 II simultaneously with the formation of autophagic vacuoles. RES and CUR induced cytoplasmic NF-kappa B accumulation. RES+CUR administrations were safe in BALB/c mice and reduced the growth of transplanted salivary gland cancer cells (SALTO) more efficiently than CUR. Overall, combinations of CUR and RES was more effective in inhibiting in vivo and in vitro cancer growth than the treatment with CUR. Additional studies will be needed to define the therapeutic potential of these compounds in combination.
C1 [Masuelli, Laura; Di Stefano, Enrica; Mattera, Rosanna; Sacchetti, Pamela] Univ Roma La Sapienza, Dept Expt Med, I-00185 Rome, Italy.
   [Fantini, Massimo; Benvenuto, Monica; Marzocchella, Laura; Tresoldi, Ilaria; Izzi, Valerio; Modesti, Andrea; Bei, Roberto] Univ Roma Tor Vergata, Dept Clin Sci & Translat Med, Rome, Italy.
   [Focaccetti, Chiara; Bernardini, Roberta; Mattei, Maurizio] Univ Roma Tor Vergata, STA, Rome, Italy.
   [Frajese, Giovanni Vanni] Univ Roma, Dipartimento Sci Motorie Umane & Salute, Foro Italico, Italy.
   [Lista, Florigio] Ctr Studi & Ric Sanita & Vet Esercito, Rome, Italy.
RP Bei, R (corresponding author), Univ Roma La Sapienza, Dept Expt Med, Piazzale Aldo Moro 5, I-00185 Rome, Italy.
EM bei@med.uniroma2.it
RI Bei, Roberto/W-8023-2019; Bernardini, Roberta/AAC-1301-2019; Masuelli,
   Laura/AGW-4259-2022; Benvenuto, Monica/K-2685-2016; Focaccetti,
   Chiara/AAD-9378-2019; Izzi, Valerio/Q-5720-2019; Mattei,
   Maurizio/AAC-1303-2019
OI Bernardini, Roberta/0000-0002-1675-0645; Benvenuto,
   Monica/0000-0002-2520-1306; Focaccetti, Chiara/0000-0002-7334-3966;
   Izzi, Valerio/0000-0002-9960-4917; Mattei, Maurizio/0000-0002-0814-8873;
   MASUELLI, Laura/0000-0001-8174-8034; Fantini,
   Massimo/0000-0002-8164-2587
FU PRIN, Ricerca Universitaria "Sapienza"
FX This study was supported by a grant from PRIN (R.B.), Ricerca
   Universitaria "Sapienza" 2012 (L.M.). The authors wish to thank Barbara
   Bulgarini for help in manuscript preparation. SALTO cells were kindly
   provided by Prof. Federica Cavallo (University of Turin) and Prof.
   Patrizia Nanni (University of Bologna).
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   Zlotogorski A, 2013, ORAL ONCOL, V49, P502, DOI 10.1016/j.oraloncology.2013.02.011
NR 66
TC 72
Z9 76
U1 1
U2 10
PU IMPACT JOURNALS LLC
PI ORCHARD PARK
PA 6666 E QUAKER ST, STE 1, ORCHARD PARK, NY 14127 USA
EI 1949-2553
J9 ONCOTARGET
JI Oncotarget
PD NOV 15
PY 2014
VL 5
IS 21
BP 10745
EP 10762
DI 10.18632/oncotarget.2534
PG 18
WC Oncology; Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Cell Biology
GA AZ2AL
UT WOS:000348036900041
PM 25296980
OA Green Published, gold, Green Submitted
DA 2022-04-25
ER

PT J
AU Ha, YJ
   Kim, CW
   Roh, SA
   Cho, DH
   Park, JL
   Kim, SY
   Kim, JH
   Choi, EK
   Kim, YS
   Kim, JC
AF Ha, Ye J.
   Kim, Chan W.
   Roh, Seon A.
   Cho, Dong H.
   Park, Jong L.
   Kim, Seon Y.
   Kim, Jong H.
   Choi, Eun K.
   Kim, Yong S.
   Kim, Jin C.
TI Epigenetic Regulation of KLHL34 Predictive of Pathologic Response to
   Preoperative Chemoradiation Therapy in Rectal Cancer Patients
SO INTERNATIONAL JOURNAL OF RADIATION ONCOLOGY BIOLOGY PHYSICS
LA English
DT Article
ID SEXUAL FUNCTION; RADIOTHERAPY; INHIBITION; AUTOPHAGY
AB Purpose: Prediction of individual responsiveness to preoperative chemoradiation therapy (CRT) is urgently needed in patients with poorly responsive locally advanced rectal cancer (LARC).
   Methods and Materials: Candidate methylation genes associated with radiosensitivity were identified using a 3-step process. In the first step, genome-wide screening of methylation genes was performed in correlation with histopathologic tumor regression grade in 45 patients with LARC. In the second step, the methylation status of selected sites was analyzed by pyrosequencing in 67 LARC patients, including 24 patients analyzed in the first step. Finally, colorectal cancer cell clones with stable KLHL34 knockdown were generated and tested for cellular sensitivity to radiation.
   Results: Genome-wide screening identified 7 hypermethylated CpG sites (DZIP1 cg24107021, DZIP1 cg26886381, ZEB1 cg04430381, DKK3 cg041006961, STL cg00991794, KLHL34 cg01828474, and ARHGAP6 cg07828380) associated with preoperative CRT responses. Radiosensitivity in patients with hypermethylated KLHL34 cg14232291 was confirmed by pyrosequencing in additional cohorts. Knockdown of KLHL34 significantly reduced colony formation (KLHL34 sh#1: 20.1%, P = .0001 and KLHL34 sh#2: 15.8%, P = .0002), increased the cytotoxicity (KLHL34 sh#1: 14.8%, P = .019 and KLHL34 sh#2: 17.9%, P = .007) in LoVo cells, and increased radiation-induced caspase-3 activity and the sub-G1 population of cells.
   Conclusions: The methylation status of KLHL34 cg14232291 may be a predictive candidate of sensitivity to preoperative CRT, although further validation is needed in large cohorts using various cell types. (C) 2015 Elsevier Inc.
C1 [Ha, Ye J.; Kim, Chan W.; Roh, Seon A.; Kim, Jin C.] Univ Ulsan, Coll Med, Dept Surg, Seoul 138736, South Korea.
   [Kim, Jong H.; Choi, Eun K.] Univ Ulsan, Dept Radiat Oncol, Seoul 138736, South Korea.
   [Ha, Ye J.; Roh, Seon A.; Cho, Dong H.; Choi, Eun K.; Kim, Yong S.; Kim, Jin C.] Asan Med Ctr, Asan Inst Life Sci, Seoul, South Korea.
   [Ha, Ye J.; Roh, Seon A.; Cho, Dong H.; Choi, Eun K.; Kim, Yong S.; Kim, Jin C.] Asan Med Ctr, Inst Innovat Canc Res, Seoul, South Korea.
   [Cho, Dong H.] Kyung Hee Univ, Grad Sch East West Med Sci, Seoul, South Korea.
   [Park, Jong L.; Kim, Seon Y.; Kim, Yong S.] Med Genom Res Ctr, Korea Res Inst Bioscience & Biotechnol, Daejeon, South Korea.
RP Kim, JC (corresponding author), Univ Ulsan, Coll Med, Dept Surg, 88 Olymp Ro 43 Gil, Seoul 138736, South Korea.
EM yongsung@kribb.re.kr; jckim@amc.seoul.kr
FU Asan Institute for Life Sciences [2014-69]; National Research Foundation
   [NRF-2013R1A2A1A03070986]; Ministry of Science, ICT and Future Planning,
   the Korea Health 21 RD Project [HI06C0868, HI13C1750]; Center for
   Development and Commercialization of Anti-Cancer Therapeutics, Ministry
   of Health and Welfare, Republic of Korea [HI10C2014]
FX Supported by grants (to J.C. Kim) from the Asan Institute for Life
   Sciences (2014-69), the National Research Foundation
   (NRF-2013R1A2A1A03070986), Ministry of Science, ICT and Future Planning,
   the Korea Health 21 R&D Project (HI06C0868 and HI13C1750), and the
   Center for Development and Commercialization of Anti-Cancer Therapeutics
   (HI10C2014), Ministry of Health and Welfare, Republic of Korea.
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NR 23
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Z9 9
U1 0
U2 12
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA STE 800, 230 PARK AVE, NEW YORK, NY 10169 USA
SN 0360-3016
EI 1879-355X
J9 INT J RADIAT ONCOL
JI Int. J. Radiat. Oncol. Biol. Phys.
PD MAR 1
PY 2015
VL 91
IS 3
BP 650
EP 658
DI 10.1016/j.ijrobp.2014.11.013
PG 9
WC Oncology; Radiology, Nuclear Medicine & Medical Imaging
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Radiology, Nuclear Medicine & Medical Imaging
GA CA8YJ
UT WOS:000349206600025
PM 25680604
DA 2022-04-25
ER

PT J
AU Poluzzi, C
   Casulli, J
   Goyal, A
   Mercer, TJ
   Neill, T
   Iozzo, RV
AF Poluzzi, Chiara
   Casulli, Joshua
   Goyal, Atul
   Mercer, Thomas J.
   Neill, Thomas
   Iozzo, Renato V.
TI Endorepellin Evokes Autophagy in Endothelial Cells
SO JOURNAL OF BIOLOGICAL CHEMISTRY
LA English
DT Article
ID HEPARAN-SULFATE PROTEOGLYCAN; FIBROBLAST-GROWTH-FACTOR; PERLECAN PROTEIN
   CORE; BASEMENT-MEMBRANE PROTEOGLYCANS; DENSITY-LIPOPROTEIN-RECEPTOR;
   COLON CARCINOMA-CELLS; IMPRINTED GENE; CANCER GROWTH; TUMOR-GROWTH;
   ALPHA(2)BETA(1) INTEGRINS
AB Endorepellin, the C-terminal fragment of the heparan sulfate proteoglycan perlecan, possesses angiostatic activity via dual receptor antagonism, through concurrent binding to the alpha 2 beta 1 integrin and vascular endothelial growth factor receptor 2 (VEGFR2). Here, we discovered that soluble endorepellin induced autophagy in endothelial cells by modulating the expression of Beclin 1, LC3, and p62, three established autophagic markers. Moreover, endorepellin evoked expression of the imprinted tumor suppressor gene Peg3 and its co-localization with Beclin 1 and LC3 in autophagosomes, suggesting a major role for this gene in endothelial cell autophagy. Mechanistically, endorepellin induced autophagy by down-regulating VEGFR2 via the two LG1/2 domains, whereas the C-terminal LG3 domain, the portion responsible for binding the alpha 2 beta 1 integrin, was ineffective. Endorepellin also induced transcriptional activity of the BECN1 promoter in endothelial cells, and the VEGFR2-specific tyrosine kinase inhibitor, SU5416, blocked this effect. Finally, we found a correlation between endorepellin-evoked inhibition of capillary morphogenesis and enhanced autophagy. Thus, we have identified a new role for this endogenous angiostatic fragment in inducing autophagy through a VEGFR2-dependent but alpha 2 beta 1 integrin-independent pathway. This novel mechanism specifically targets endothelial cells and could represent a promising new strategy to potentiate the angiostatic effect of endorepellin and perhaps other angiostatic matrix proteins.
C1 [Iozzo, Renato V.] Thomas Jefferson Univ, Dept Pathol Anat & Cell Biol, Philadelphia, PA 19107 USA.
   Thomas Jefferson Univ, Canc Cell Biol & Signaling Program, Kimmel Canc Ctr, Philadelphia, PA 19107 USA.
RP Iozzo, RV (corresponding author), Thomas Jefferson Univ, Dept Pathol Anat & Cell Biol, 1020 Locust St,Ste 336 JAH, Philadelphia, PA 19107 USA.
EM renato.iozzo@jefferson.edu
RI Poluzzi, Chiara/T-3376-2019; Iozzo, Renato/AAS-1980-2020
OI Casulli, Joshua/0000-0002-3733-7614; Iozzo, Renato/0000-0002-5908-5112
FU National Institutes of HealthUnited States Department of Health & Human
   ServicesNational Institutes of Health (NIH) - USA [RO1 CA3948, RO1
   CA47282, RO1 CA164462, T32 AA07463]; NATIONAL CANCER INSTITUTEUnited
   States Department of Health & Human ServicesNational Institutes of
   Health (NIH) - USANIH National Cancer Institute (NCI) [R01CA039481,
   R01CA047282, R01CA164462, P30CA056036] Funding Source: NIH RePORTER;
   NATIONAL INSTITUTE ON ALCOHOL ABUSE AND ALCOHOLISMUnited States
   Department of Health & Human ServicesNational Institutes of Health (NIH)
   - USANIH National Institute on Alcohol Abuse & Alcoholism (NIAAA)
   [T32AA007463] Funding Source: NIH RePORTER
FX This work was supported, in whole or in part, by National Institutes of
   Health Grants RO1 CA3948, RO1 CA47282, and RO1 CA164462 (to R. V. I.).;
   Supported by National Institutes of Health Training Grant T32 AA07463.
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NR 101
TC 62
Z9 63
U1 0
U2 8
PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3996 USA
EI 1083-351X
J9 J BIOL CHEM
JI J. Biol. Chem.
PD JUN 6
PY 2014
VL 289
IS 23
BP 16114
EP 16128
DI 10.1074/jbc.M114.556530
PG 15
WC Biochemistry & Molecular Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology
GA AJ8ON
UT WOS:000337965700019
PM 24737315
OA Green Published, hybrid
DA 2022-04-25
ER

PT J
AU Liu, ML
   Zhang, Q
   Yuan, X
   Jin, L
   Wang, LL
   Fang, TT
   Wang, WB
AF Liu, Mu-Lin
   Zhang, Qiao
   Yuan, Xiao
   Jin, Long
   Wang, Li-Li
   Fang, Tao-Tao
   Wang, Wen-Bin
TI Long noncoding RNA RP4 functions as a competing endogenous RNA through
   miR-7-5p sponge activity in colorectal cancer
SO WORLD JOURNAL OF GASTROENTEROLOGY
LA English
DT Article
DE Colorectal cancer; long noncoding RNA RP4; SH3GLB1; miR-7-5p; competing
   endogenous RNA
ID MYC-DRIVEN LYMPHOMAGENESIS; CELL-PROLIFERATION; APOPTOSIS; PROGRESSION;
   MITOPHAGY; AUTOPHAGY
AB AIM
   To investigate the role of long noncoding RNA (lncRNA) RP4 in colorectal cancer.
   METHODS
   Lentivirus-mediated lncRNA RP4 overexpression and knockdown were performed in the colorectal cancer cell line SW480. Cell proliferation, tumor growth, and early apoptosis were evaluated by a cell counting kit-8 assay, an in vivo xenograft tumor model, and annexin V/propidium iodide staining, respectively. Analysis of the lncRNA RP4 mechanism involved assessment of the association of its expression with miR-7-5p and the SH3GLB1 gene. Western blot analysis was also performed to assess the effect of lncRNA RP4 on the autophagy-mediated cell death pathway and phosphatidylinositol-3-kinase (PI3K)/Akt signaling.
   RESULTS
   Cell proliferation, tumor growth, and early apoptosis in SW480 cells were negatively regulated by lncRNA RP4. Functional experiments indicated that lncRNA RP4 directly upregulated SH3GLB1 expression by acting as a competing endogenous RNA (ceRNA) for miR-7-5p. This interaction led to activation of the autophagy-mediated cell death pathway and de-repression of PI3K and Akt phosphorylation in colorectal cancer cells in vivo.
   CONCLUSION
   Our results demonstrated that lncRNA RP4 is a ceRNA that plays an important role in the pathogenesis of colorectal cancer, and could be a potential therapeutic target for colorectal cancer treatment.
C1 [Liu, Mu-Lin; Jin, Long; Wang, Li-Li; Fang, Tao-Tao] Bengbu Med Coll, Affiliated Hosp 1, Dept Gastrointestinal Surg, Bengbu 233004, Anhui, Peoples R China.
   [Zhang, Qiao] Xinxiang Med Univ, Affiliated Hosp 1, Dept Gen Surg, Xinxiang 453100, Henan, Peoples R China.
   [Yuan, Xiao; Wang, Wen-Bin] Anhui Med Univ, Affiliated Hosp 4, Dept Gen Surg, 372 Tunxi Rd, Hefei 230022, Anhui, Peoples R China.
RP Wang, WB (corresponding author), Anhui Med Univ, Affiliated Hosp 4, Dept Gen Surg, 372 Tunxi Rd, Hefei 230022, Anhui, Peoples R China.
EM surdoctor@163.com
FU Scientific Research Foundation of Anhui Education Department
   [KJ2017A219]; Scientific Research Foundation of Academic Leader of Anhui
   Province [2016H105]; education talent Foundation of universities of
   Anhui Education Department [gxbjZD2016070]; National Natural Science
   Foundation of ChinaNational Natural Science Foundation of China (NSFC)
   [81500373]; Natural Science Foundation of Anhui ProvinceNatural Science
   Foundation of Anhui Province [1608085MH193]
FX Supported by Scientific Research Foundation of Anhui Education
   Department, No. KJ2017A219 to Liu ML; Scientific Research Foundation of
   Academic Leader of Anhui Province, No. 2016H105 to Liu ML; education
   talent Foundation of universities of Anhui Education Department, No.
   gxbjZD2016070 to Liu ML; National Natural Science Foundation of China,
   No. 81500373 to Wang WB; and Natural Science Foundation of Anhui
   Province, No. 1608085MH193 to Wang WB.
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NR 32
TC 58
Z9 64
U1 1
U2 11
PU BAISHIDENG PUBLISHING GROUP INC
PI PLEASANTON
PA 8226 REGENCY DR, PLEASANTON, CA 94588 USA
SN 1007-9327
EI 2219-2840
J9 WORLD J GASTROENTERO
JI World J. Gastroenterol.
PD MAR 7
PY 2018
VL 24
IS 9
BP 1004
EP 1012
DI 10.3748/wjg.v24.i9.1004
PG 9
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA FY3BM
UT WOS:000426692100005
PM 29531464
OA Green Published, hybrid, Green Submitted
DA 2022-04-25
ER

PT J
AU Tsai, HY
   Ho, CT
   Chen, YK
AF Tsai, Hui-Yun
   Ho, Chi-Tang
   Chen, Yu-Kuo
TI Biological actions and molecular effects of resveratrol, pterostilbene,
   and 3 '-hydroxypterostilbene
SO JOURNAL OF FOOD AND DRUG ANALYSIS
LA English
DT Review
DE 3 '-hydroxypterostilbene; bioavailability; biological actions;
   pterostilbene; resveratrol; stilbenes
ID IMPROVES GLYCEMIC CONTROL; ACTIVATED PROTEIN-KINASE; CELL-CYCLE ARREST;
   COLON CARCINOGENESIS; CALORIC RESTRICTION; GENE-EXPRESSION;
   DOWN-REGULATION; CANCER CELLS; LIFE-SPAN; APOPTOSIS
AB Stilbenes are a class of polyphenolic compounds, naturally found in a wide variety of dietary sources such as grapes, berries, peanuts, red wine, and some medicinal plants. There are several well-known stilbenes including trans-resveratrol, pterostilbene, and 3'-hydroxypterostilbene. The core chemical structure of stilbene compounds is 1,2-diphenylethylene. Recently, stilbenes have attracted extensive attention and interest due to their wide range of health-beneficial effects such as anti-inflammation, -carcinogenic, -diabetes, and -dyslipidemia activities. Moreover, accumulating in vitro and in vivo studies have reported that stilbene compounds act as inducers of multiple cell-death pathways such as apoptosis, cell cycle arrest, and autophagy for chemopreventive and chemotherapeutic agents in several types of cancer cells. The aim of this review is to highlight recent molecular findings and biological actions of trans-resveratrol, pterostilbene, and 3'-hydroxypterostilbene. Copyright (C) 2016, Food and Drug Administration, Taiwan. Published by Elsevier Taiwan LLC.
C1 [Tsai, Hui-Yun; Ho, Chi-Tang] Rutgers State Univ, Dept Food Sci, 65 Dudley Rd, New Brunswick, NJ 08901 USA.
   [Chen, Yu-Kuo] Natl Pingtung Univ Sci & Technol, Dept Food Sci, 1 Shuefu Rd, Pingtung 91201, Taiwan.
RP Ho, CT (corresponding author), Rutgers State Univ, Dept Food Sci, 65 Dudley Rd, New Brunswick, NJ 08901 USA.; Chen, YK (corresponding author), Natl Pingtung Univ Sci & Technol, Dept Food Sci, 1 Shuefu Rd, Pingtung 91201, Taiwan.
EM ho@aesop.rutgers.edu; chenyk@mail.npust.edu.tw
OI Chen, Yu-Kuo/0000-0002-8031-8312
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NR 85
TC 115
Z9 123
U1 5
U2 56
PU FOOD & DRUG ADMINSTRATION
PI TAIPEI
PA 161-2 KUNYANG STREET, NANGANG, TAIPEI, 00000, TAIWAN
SN 1021-9498
J9 J FOOD DRUG ANAL
JI J. Food Drug Anal.
PD JAN
PY 2017
VL 25
IS 1
BP 134
EP 147
DI 10.1016/j.jfda.2016.07.004
PG 14
WC Food Science & Technology; Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Food Science & Technology; Pharmacology & Pharmacy
GA EJ4IM
UT WOS:000393180200015
PM 28911531
OA gold
HC Y
HP N
DA 2022-04-25
ER

PT J
AU Fu, YY
   Gu, QQ
   Luo, L
   Xu, JC
   Luo, YP
   Xia, F
   Han, FH
   Hong, L
   Yin, XM
   Huang, ZY
   Li, M
AF Fu, Yuanyuan
   Gu, Qianqian
   Luo, Li
   Xu, Jiecheng
   Luo, Yuping
   Xia, Fan
   Han, Fanghai
   Hong, Liang
   Yin, Xiao-Ming
   Huang, Zhiying
   Li, Min
TI New Anti-Cancer Strategy to Suppress Colorectal Cancer Growth Through
   Inhibition of ATG4B and Lysosome Function
SO CANCERS
LA English
DT Article
DE ATG4B; autophagy; colorectal cancer; dual-function inhibitor; lysosome
   inhibition; new anti-cancer strategy
ID AUTOPHAGY; CELLS; CHLOROQUINE; DISCOVERY; PROTEIN; TARGET; POTENT
AB Autophagy inhibition has been proposed to be a potential therapeutic strategy for cancer, however, few autophagy inhibitors have been developed. Recent studies have indicated that lysosome and autophagy related 4B cysteine peptidase (ATG4B) are two promising targets in autophagy for cancer therapy. Although some inhibitors of either lysosome or ATG4B were reported, there are limitations in the use of these single target compounds. Considering multi-functional drugs have advantages, such as high efficacy and low toxicity, we first screened and validated a batch of compounds designed and synthesized in our laboratory by combining the screening method of ATG4B inhibitors and the identification method of lysosome inhibitors. ATG4B activity was effectively inhibited in vitro. Moreover, 163N inhibited autophagic flux and caused the accumulation of autolysosomes. Further studies demonstrated that 163N could not affect the autophagosome-lysosome fusion but could cause lysosome dysfunction. In addition, 163N diminished tumor cell viability and impaired the development of colorectal cancer in vivo. The current study findings indicate that the dual effect inhibitor 163N offers an attractive new anti-cancer drug and compounds having a combination of lysosome inhibition and ATG4B inhibition are a promising therapeutic strategy for colorectal cancer therapy.
C1 [Fu, Yuanyuan; Gu, Qianqian; Luo, Li; Xu, Jiecheng; Luo, Yuping; Xia, Fan; Hong, Liang; Huang, Zhiying; Li, Min] Sun Yat Sen Univ, Sch Pharmaceut Sci, Guangzhou 510006, Peoples R China.
   [Han, Fanghai] Sun Yat Sen Univ, Dept Gastrointestinal Surg, Guangzhou 510120, Peoples R China.
   [Yin, Xiao-Ming] Tulane Univ, Sch Med, Dept Pathol & Lab Med, 1430 Tulane Ave, New Orleans, LA 70112 USA.
RP Huang, ZY; Li, M (corresponding author), Sun Yat Sen Univ, Sch Pharmaceut Sci, Guangzhou 510006, Peoples R China.
EM fuyy6@mail2.sysu.edu.cn; guqq@mail2.sysu.edu.cn;
   luoli26@mail2.sysu.edu.cn; xujch6@mail2.sysu.edu.cn;
   luoyp26@mail2.sysu.edu.cn; xiaf6@mail2.sysu.edu.cn; fh_han@163.com;
   hongliang@mail.sysu.edu.cn; xmyin@tulane.edu; hzhiying@mail.sysu.edu.cn;
   limin65@mail.sysu.edu.cn
OI li, min/0000-0002-5657-8675
FU National Natural Science Foundation of ChinaNational Natural Science
   Foundation of China (NSFC) [31970699, 31671437, 81773992, 81572925];
   Guangdong Basic and Applied Basic Research Foundation [2019A1515011030]
FX This work was supported by the National Natural Science Foundation of
   China (31970699, 31671437, 81773992, 81572925) and the Guangdong Basic
   and Applied Basic Research Foundation (2019A1515011030).
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   Satoo K, 2009, EMBO J, V28, P1341, DOI 10.1038/emboj.2009.80
   Vacante M, 2018, WORLD J CLIN CASES, V6, P869, DOI 10.12998/wjcc.v6.i15.869
   Vazquez CL, 2009, METHOD ENZYMOL, V452, P85, DOI 10.1016/S0076-6879(08)03606-9
   White E, 2012, NAT REV CANCER, V12, P401, DOI 10.1038/nrc3262
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NR 45
TC 7
Z9 7
U1 9
U2 12
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 2072-6694
J9 CANCERS
JI Cancers
PD JUN
PY 2020
VL 12
IS 6
AR 1523
DI 10.3390/cancers12061523
PG 19
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA MT4JM
UT WOS:000554937500001
PM 32532053
OA Green Published, gold
DA 2022-04-25
ER

PT J
AU Yamada, T
   Ashida, Y
   Tatebayashi, D
   Abe, M
   Himori, K
AF Yamada, Takashi
   Ashida, Yuki
   Tatebayashi, Daisuke
   Abe, Masami
   Himori, Koichi
TI Cancer Cachexia Induces Preferential Skeletal Muscle Myosin Loss When
   Combined With Denervation
SO FRONTIERS IN PHYSIOLOGY
LA English
DT Article
DE cancer cachexia; denervation; muscle atrophy; catabolism; anabolism
ID HEAVY-CHAIN; WEIGHT-LOSS; ATROPHY; ACTIVATION; EXPRESSION; AUTOPHAGY;
   CHEMOTHERAPY; DEGRADATION; PATHWAYS; MODEL
AB Patients with cancer cachexia (CCX) suffer from muscle wasting, which is often but not always accompanied by selective loss of myosin. Here we examined the effects of CCX on muscle mass and myosin heavy chain (MyHC) expression in denervated (DEN) muscles, especially focusing on the protein synthesis and degradation pathways. Male CD2F1 mice were randomly divided into control (CNT) and CCX groups and their left sciatic nerve was transected. CCX was induced by an intraperitoneal injection of colon 26 cells. After 14 days, the serum concentration of IL-6 and corticosteroid was higher in CCX mice than in CNT mice. The combination of CCX with DEN (CCX + DEN) resulted in a marked reduction of the gastrocnemius muscle weight (-69%) that was significantly lower than DEN (-53%) or CCX (-36%) alone. CCX had no effect on MyHC content, but it elicited a preferential MyHC loss when combined with DEN. The expression levels of autophagy markers cathepsin D and LC3BII/I ratio were markedly higher in the CCX + DEN group than in the CNT + DEN and the CCX groups. Paradoxically, there was an increase in protein synthesis rate and phosphorylation levels of p70S6K and rpS6, markers of mTORC1 signaling, in the CNT + DEN group, and these molecular alterations were inhibited in the CCX + DEN group. Our data indicate that CCX aggravates muscle atrophy in DEN muscles by inducing seletive loss of myosin, which involves inactivity dependent mechanisms that is likely to be a consequence of increased autophagy-mediated protein breakdown coupled with impaired protein synthesis.
C1 [Yamada, Takashi; Ashida, Yuki; Tatebayashi, Daisuke; Abe, Masami; Himori, Koichi] Sapporo Med Univ, Grad Sch Hlth Sci, Sapporo, Hokkaido, Japan.
RP Yamada, T (corresponding author), Sapporo Med Univ, Grad Sch Hlth Sci, Sapporo, Hokkaido, Japan.
EM takashi.yamada1976@sapmed.ac.jp
RI Yamada, Takashi/AAZ-6212-2021; Yamada, Takashi/U-8443-2019
OI Yamada, Takashi/0000-0003-1797-3880; Yamada, Takashi/0000-0003-1797-3880
FU Japan Society for the Promotion of ScienceMinistry of Education,
   Culture, Sports, Science and Technology, Japan (MEXT)Japan Society for
   the Promotion of Science [JP15K12585]
FX This work was supported by grants fromthe Japan Society for the
   Promotion of Science (No. JP15K12585 to TY).
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NR 48
TC 9
Z9 10
U1 2
U2 2
PU FRONTIERS MEDIA SA
PI LAUSANNE
PA AVENUE DU TRIBUNAL FEDERAL 34, LAUSANNE, CH-1015, SWITZERLAND
SN 1664-042X
J9 FRONT PHYSIOL
JI Front. Physiol.
PD APR 28
PY 2020
VL 11
AR 445
DI 10.3389/fphys.2020.00445
PG 9
WC Physiology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Physiology
GA LO1HC
UT WOS:000533378200001
PM 32425814
OA gold, Green Published
DA 2022-04-25
ER

PT J
AU Iwata, Y
   Suzuki, N
   Ohtake, H
   Kamauchi, S
   Hashimoto, N
   Kiyono, T
   Wakabayashi, S
AF Iwata, Yuko
   Suzuki, Nobuyuki
   Ohtake, Hitomi
   Kamauchi, Shinya
   Hashimoto, Naohiro
   Kiyono, Tohru
   Wakabayashi, Shigeo
TI Cancer cachexia causes skeletal muscle damage via transient receptor
   potential vanilloid 2-independent mechanisms, unlike muscular dystrophy
SO JOURNAL OF CACHEXIA SARCOPENIA AND MUSCLE
LA English
DT Article
DE TRPV2; transient receptor potential vanilloid type 2; DGC; dystrophin
   glycoprotein complex; Cancer cachexia; Muscular dystrophy; LLC; Lewis
   lung carcinoma
ID ACTIVATION; CELLS; CA2+; PATHOPHYSIOLOGY; DEGENERATION; CONTRIBUTES;
   AUTOPHAGY; MYOTUBES; CHANNELS; PATHWAY
AB BackgroundMuscle wasting during cancer cachexia contributes to patient morbidity. Cachexia-induced muscle damage may be understood by comparing its symptoms with those of other skeletal muscle diseases, but currently available data are limited.
   MethodsWe modelled cancer cachexia in mice bearing Lewis lung carcinoma/colon adenocarcinoma and compared the associated muscle damage with that in a murine muscular dystrophy model (mdx mice). We measured biochemical and immunochemical parameters: amounts/localization of cytoskeletal proteins and/or Ca2+ signalling proteins related to muscle function and abnormality. We analysed intracellular Ca2+ mobilization and compared results between the two models. Involvement of Ca2+-permeable channel transient receptor potential vanilloid 2 (TRPV2) was examined by inoculating Lewis lung carcinoma cells into transgenic mice expressing dominant-negative TRPV2.
   ResultsTumourigenesis caused loss of body and skeletal muscle weight and reduced muscle force and locomotor activity. Similar to mdx mice, cachexia muscles exhibited myolysis, reduced sarcolemmal sialic acid content, and enhanced lysosomal exocytosis and sarcolemmal localization of phosphorylated Ca2+/CaMKII. Abnormal autophagy and degradation of dystrophin also occurred. Unlike mdx muscles, cachexia muscles did not exhibit regeneration markers (centrally nucleated fibres), and levels of autophagic proteolytic pathway markers increased. While a slight accumulation of TRPV2 was observed in cachexia muscles, Ca2+ influx via TRPV2 was not elevated in cachexia-associated myotubes, and the course of cachexia pathology was not ameliorated by dominant-negative inhibition of TRPV2.
   ConclusionsThus, cancer cachexia may induce muscle damage through TRPV2-independent mechanisms distinct from those in muscular dystrophy; this may help treat patients with tumour-induced muscle wasting.
C1 [Iwata, Yuko; Ohtake, Hitomi; Kamauchi, Shinya; Wakabayashi, Shigeo] Natl Cerebral & Cardiovasc Ctr, Res Inst, Dept Mol Physiol, Suita, Osaka 5658565, Japan.
   [Suzuki, Nobuyuki] Kyowa Hakko Kirin CO Ltd, Chiyoda Ku, Tokyo, Japan.
   [Hashimoto, Naohiro] Natl Ctr Geriatr & Gerontol, Natl Inst Longev Sci, Dept Regenerat Med, Oobu, Aichi 4748522, Japan.
   [Kiyono, Tohru] Natl Canc Ctr, Viol Div, Chuo Ku, Tokyo 1040045, Japan.
RP Iwata, Y (corresponding author), Natl Cerebral & Cardiovasc Ctr, Res Inst, Dept Mol Physiol, Suita, Osaka 5658565, Japan.
EM yukoiwat@ri.ncvc.go.jp
FU Japanese Ministry of Education, Culture, Sports, Science and
   TechnologyMinistry of Education, Culture, Sports, Science and
   Technology, Japan (MEXT) [18077015, 19390080, 17659241, 18590796,
   20590874]; National Institute of Biomedical InnovationNational Institute
   of Biomedical Innovation; Japanese Ministry of Health, Labour and
   WelfareMinistry of Health, Labour and Welfare, Japan [17A-1, 16B-2,
   19A-7, 22-5]
FX This work was supported by a grant-in-aid for Priority Areas 18077015
   (to S.W.); Grants-in-Aid 19390080, 17659241 (to S.W.), 18590796, and
   20590874 (to Y.I.); a grant for the Cooperative Link for Unique Science
   and Technology for Economy Revitalization (to S. W.) from the Japanese
   Ministry of Education, Culture, Sports, Science and Technology; a grant
   for the Promotion of Fundamental Studies in Health Sciences of the
   National Institute of Biomedical Innovation; and research grants for
   Cardiovascular Diseases (17A-1; to S. W.) and Nervous and Mental
   Disorders (16B-2, 19A-7, and 22-5; to Y.I.) from the Japanese Ministry
   of Health, Labour and Welfare.
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NR 48
TC 17
Z9 17
U1 0
U2 7
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 2190-5991
EI 2190-6009
J9 J CACHEXIA SARCOPENI
JI J. Cachexia Sarcopenia Muscle
PD JUN
PY 2016
VL 7
IS 3
BP 366
EP 376
DI 10.1002/jcsm.12067
PG 11
WC Geriatrics & Gerontology; Medicine, General & Internal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Geriatrics & Gerontology; General & Internal Medicine
GA DR4JR
UT WOS:000379868200013
PM 27239414
OA Green Published, gold
DA 2022-04-25
ER

PT J
AU Bravo-San Pedro, JM
   Wei, YJ
   Sica, V
   Maiuri, MC
   Zou, ZJ
   Kroemer, G
   Levine, B
AF Bravo-San Pedro, Jose Manuel
   Wei, Yongjie
   Sica, Valentina
   Maiuri, Maria Chiara
   Zou, Zhongju
   Kroemer, Guido
   Levine, Beth
TI BAX and BAK1 are dispensable for ABT-737-induced dissociation of the
   BCL2-BECN1 complex and autophagy
SO AUTOPHAGY
LA English
DT Article
DE ABT-737; apoptosis; autophagy; BAX; BAK1; BCL2; BECN1 (Beclin 1); ACTB;
   actin; Baf A1; bafilomycin A(1); BAK1; BCL2-antagonist; killer 1; BAX;
   BCL2-associated X protein; BCL2; B-cell CLL; lymphoma 2; BECN1; Beclin
   1; autophagy-related; DKO; double-knockout; FBS; fetal bovine serum;
   GAPDH; glyceraldehyde-3-phosphate dehydrogenase; HBSS; Hanks' balanced
   salt solution; HRP; horseradish peroxidase; MAP1LC3; LC3;
   microtubule-associated protein 1 light chain 3; MCL1; myeloid cell
   leukemia 1; MEFs; mouse embryonic fibroblasts; MTOR; mechanistic target
   of rapamycin; PBS; phosphate-buffered saline; SQSTM1; sequestosome 1;
   STS; staurosporine; WT; wild type
ID BCL-2 FAMILY-MEMBERS; BECLIN 1-DEPENDENT AUTOPHAGY; 1 PHOSPHORYLATION;
   BH3-ONLY PROTEIN; MOLECULAR-BASIS; BH3 DOMAIN; X-L; APOPTOSIS;
   SUPPRESSION; PEPTIDE
AB Disruption of the complex of BECN1 with BCL2 or BCL2L1/BCL-X-L is an essential switch that turns on cellular autophagy in response to environmental stress or treatment with BH3 peptidomimetics. Recently, it has been proposed that BCL2 and BCL2L1/BCL-X-L may inhibit autophagy indirectly through a mechanism dependent on the proapoptotic BCL2 family members, BAX and BAK1. Here we report that the BH3 mimetic, ABT-737, induces autophagy in parallel with disruption of BCL2-BECN1 binding in 2 different apoptosis-deficient cell types lacking BAX and BAK1, namely in mouse embryonic fibroblasts cells and in human colon cancer HCT116 cells. We conclude that the BH3 mimetic ABT-737 induces autophagy through a BAX and BAK1-independent mechanism that likely involves disruption of BECN1 binding to antiapoptotic BCL2 family members.
C1 [Bravo-San Pedro, Jose Manuel; Sica, Valentina; Maiuri, Maria Chiara; Kroemer, Guido] Ctr Rech Cordeliers, Equipe Labellisee Ligue Natl Canc 11, Paris, France.
   [Bravo-San Pedro, Jose Manuel; Sica, Valentina; Maiuri, Maria Chiara; Kroemer, Guido] INSERM, U1138, Paris, France.
   [Bravo-San Pedro, Jose Manuel; Sica, Valentina; Maiuri, Maria Chiara; Kroemer, Guido] Univ Paris 05, Sorbonne Paris Cite, Paris, France.
   [Bravo-San Pedro, Jose Manuel; Sica, Valentina; Maiuri, Maria Chiara] Gustave Roussy Canc Campus, Villejuif, France.
   [Bravo-San Pedro, Jose Manuel; Wei, Yongjie; Sica, Valentina; Maiuri, Maria Chiara; Kroemer, Guido] Metabol & Cell Biol Platforms, Villejuif, France.
   [Zou, Zhongju; Levine, Beth] Univ Texas SW Med Ctr Dallas, Ctr Autophagy Res, Dept Internal Med, Dallas, TX 75390 USA.
   [Zou, Zhongju; Levine, Beth] Univ Texas SW Med Ctr Dallas, Howard Hughes Med Inst, Dallas, TX 75390 USA.
   [Kroemer, Guido] Hop Europeen Georges Pompidou, AP HP, Pole Biol, Paris, France.
RP Kroemer, G (corresponding author), Ctr Rech Cordeliers, Equipe Labellisee Ligue Natl Canc 11, Paris, France.
EM kroemer@orange.fr; beth.levine@utsouthwestern.edu
RI San Pedro, Jose Manuel Bravo/Q-4061-2018; Kroemer, Guido/AAY-9859-2020;
   KROEMER, Guido/B-4263-2013
OI San Pedro, Jose Manuel Bravo/0000-0002-5781-1133; KROEMER,
   Guido/0000-0002-9334-4405; Sica, Valentina/0000-0003-2770-5847
FU CPRIT [RP120718-P1]; NIHUnited States Department of Health & Human
   ServicesNational Institutes of Health (NIH) - USA [R01CA109618,
   U19AI109725]; Ligue contre le CancerLigue nationale contre le cancer;
   Agence National de la Recherche (ANR)French National Research Agency
   (ANR); Association pour la recherche sur le cancer (ARC)Fondation ARC
   pour la Recherche sur le Cancer; Canceropole Ile-de-FranceRegion
   Ile-de-France; Institut National du Cancer (INCa)Institut National du
   Cancer (INCA) France; Fondation Bettencourt-Schueller; Fondation de
   FranceFondation de France; Fondation pour la Recherche Medicale
   (FRM)Fondation pour la Recherche Medicale; European Commission
   (ArtForce)European CommissionEuropean Commission Joint Research Centre;
   European Research Council (ERC)European Research Council (ERC); LabEx
   Immuno-Oncology; SIRIC Stratified Oncology Cell DNA Repair and Tumor
   Immune Elimination (SOCRATE); SIRIC Cancer Research and Personalized
   Medicine (CARPEM); Paris Alliance of Cancer Research Institutes (PACRI);
   NATIONAL CANCER INSTITUTEUnited States Department of Health & Human
   ServicesNational Institutes of Health (NIH) - USANIH National Cancer
   Institute (NCI) [R01CA109618] Funding Source: NIH RePORTER; NATIONAL
   INSTITUTE OF ALLERGY AND INFECTIOUS DISEASESUnited States Department of
   Health & Human ServicesNational Institutes of Health (NIH) - USANIH
   National Institute of Allergy & Infectious Diseases (NIAID)
   [U19AI109725] Funding Source: NIH RePORTER
FX This work was supported by CPRIT grant RP120718-P1 (B.L.), NIH grants
   R01CA109618 and U19AI109725 (B.L.), and GK is supported by the Ligue
   contre le Cancer (equipe labelisee); Agence National de la Recherche
   (ANR); Association pour la recherche sur le cancer (ARC); Canceropole
   Ile-de-France; Institut National du Cancer (INCa); Fondation
   Bettencourt-Schueller; Fondation de France; Fondation pour la Recherche
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   Oncology Cell DNA Repair and Tumor Immune Elimination (SOCRATE); the
   SIRIC Cancer Research and Personalized Medicine (CARPEM); and the Paris
   Alliance of Cancer Research Institutes (PACRI).
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NR 31
TC 60
Z9 65
U1 0
U2 11
PU TAYLOR & FRANCIS INC
PI PHILADELPHIA
PA 530 WALNUT STREET, STE 850, PHILADELPHIA, PA 19106 USA
SN 1554-8627
EI 1554-8635
J9 AUTOPHAGY
JI Autophagy
PD MAR
PY 2015
VL 11
IS 3
BP 452
EP 459
DI 10.1080/15548627.2015.1017191
PG 8
WC Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Cell Biology
GA CG8UB
UT WOS:000353587600003
PM 25715028
OA Green Published, Bronze
DA 2022-04-25
ER

PT J
AU Singh, S
   Meena, A
   Luqman, S
AF Singh, Shilpi
   Meena, Abha
   Luqman, Suaib
TI Baicalin mediated regulation of key signaling pathways in cancer
SO PHARMACOLOGICAL RESEARCH
LA English
DT Review
DE Baicalin; Angiogenesis; Anticancer; Antiproliferative; Apoptosis;
   Pharmacokinetics
ID SHO-SAIKO-TO; PERFORMANCE LIQUID-CHROMATOGRAPHY; CELLS IN-VITRO;
   SUPERCRITICAL-FLUID EXTRACTION; SCUTELLARIA-BAICALENSIS; INDUCED
   APOPTOSIS; HERBAL MEDICINE; DOWN-REGULATION; OVARIAN-CANCER;
   BREAST-CANCER
AB Baicalin has been widely investigated against different types of malignancies both at the cellular and molecular levels over the past few years. Due to its remarkable anti-proliferative potential in numerous cancer cell lines, it has created immense interest as a potential chemotherapeutic modality compared to other flavonoids. Thus, this review focuses on the recent accomplishments of baicalin and its limitations in cancer prevention and treatment. Further, combination studies and nanoformulations using baicalin to treat cancer along with the metabolism, bioavailability, toxicity, and pharmacokinetics have been discussed. The present review explains biological source, and anti-proliferative potential of baicalin against cancers including breast, colon, hepatic, leukemia, lung, and skin, as well as the relevant mechanism of action to modulate diverse signaling pathways including apoptosis, cell cycle, invasion, and migration, angiogenesis, and autophagy. The anticancer mechanism of baicalin in orthotropic and xenograft mice models have been deliberated. The combination studies of baicalin in novel therapies as chemotherapeutic adjuvants have also been summarized. The low bioavailability, fast metabolism, and poor solubility, and other significant factors that limit the clinical use of baicalin have been examined as a challenge. The improvement in the pharmacokinetics and pharmacodynamics of baicalin with newer approaches and the gaps are highlighted, which could establish baicalin as an effective and safe compound for cancer treatment as well as help to translate its potential from bench to bedside.
C1 [Singh, Shilpi; Meena, Abha; Luqman, Suaib] CSIR Cent Inst Med & Aromat Plants, Bioprospect & Prod Dev Div, Lucknow 226015, Uttar Pradesh, India.
   [Singh, Shilpi; Meena, Abha; Luqman, Suaib] Acad Sci & Innovat Res AcSIR, Ghaziabad 201002, Uttar Pradesh, India.
RP Luqman, S (corresponding author), CSIR Cent Inst Med & Aromat Plants, Bioprospect & Prod Dev Div, Lucknow 226015, Uttar Pradesh, India.
EM s.luqman@cimap.res.in
RI Meena, Abha/AAE-2270-2022; Luqman, Suaib/M-5541-2015
OI MEENA, ABHA/0000-0002-1014-1486; Luqman, Suaib/0000-0001-6568-8107
FU CSIR-HCP [010]
FX CSIR-HCP 010.
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NR 287
TC 10
Z9 10
U1 10
U2 18
PU ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD
PI LONDON
PA 24-28 OVAL RD, LONDON NW1 7DX, ENGLAND
SN 1043-6618
EI 1096-1186
J9 PHARMACOL RES
JI Pharmacol. Res.
PD FEB
PY 2021
VL 164
AR 105387
DI 10.1016/j.phrs.2020.105387
EA FEB 2021
PG 21
WC Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA QC9LZ
UT WOS:000615153300038
PM 33352232
DA 2022-04-25
ER

PT J
AU Li, Y
   Yang, GX
   Yang, CC
   Tang, P
   Chen, JC
   Zhang, JF
   Liu, J
   Ouyang, L
AF Li, Yang
   Yang, Gaoxia
   Yang, Chengcan
   Tang, Pan
   Chen, Juncheng
   Zhang, Jifa
   Liu, Jie
   Ouyang, Liang
TI Targeting Autophagy-Related Epigenetic Regulators for Cancer Drug
   Discovery
SO JOURNAL OF MEDICINAL CHEMISTRY
LA English
DT Article
ID HISTONE METHYLTRANSFERASE ACTIVITY; INHIBITS AUTOPHAGY; GASTRIC-CANCER;
   HEPATOCELLULAR-CARCINOMA; CELL-PROLIFERATION; PROMOTES AUTOPHAGY;
   COLORECTAL-CANCER; SOMATIC MUTATIONS; INDUCE AUTOPHAGY; DNA METHYLATION
AB Existing evidence has demonstrated that epigenetic modifications (including DNA methylation, histone modifications, and microRNAs), which are associated with the occurrence and development of tumors, can directly or indirectly regulate autophagy. In particular, nuclear events induced by several epigenetic regulators can regulate the autophagic process and expression levels of tumor-associated genes, thereby promoting tumor progression. Tumor-associated microRNAs, including oncogenic and tumor-suppressive microRNAs, are of great significance to autophagy during tumor progression. Targeting autophagy with emerging epigenetic drugs is expected to be a promising therapeutic strategy for human tumors. From this perspective, we aim to summarize the role of epigenetic modification in the autophagic process and the underlying molecular mechanisms of tumorigenesis. Furthermore, the regulatory efficacy of epigenetic drugs on the autophagic process in tumors is also summarized. This perspective may provide a theoretical basis for the combined treatment of epigenetic drugs/autophagy mediators in tumors.
C1 [Li, Yang; Yang, Gaoxia; Yang, Chengcan; Tang, Pan; Chen, Juncheng; Zhang, Jifa; Liu, Jie; Ouyang, Liang] Sichuan Univ, State Key Lab Biotherapy, Natl Clin Res Ctr Geriatr, West China Hosp, Chengdu 610041, Sichuan, Peoples R China.
   [Li, Yang; Yang, Gaoxia; Yang, Chengcan; Tang, Pan; Chen, Juncheng; Zhang, Jifa; Liu, Jie; Ouyang, Liang] Sichuan Univ, Canc Ctr, Natl Clin Res Ctr Geriatr, West China Hosp, Chengdu 610041, Sichuan, Peoples R China.
RP Zhang, JF; Liu, J; Ouyang, L (corresponding author), Sichuan Univ, State Key Lab Biotherapy, Natl Clin Res Ctr Geriatr, West China Hosp, Chengdu 610041, Sichuan, Peoples R China.; Zhang, JF; Liu, J; Ouyang, L (corresponding author), Sichuan Univ, Canc Ctr, Natl Clin Res Ctr Geriatr, West China Hosp, Chengdu 610041, Sichuan, Peoples R China.
EM zjf298257@163.com; liujie2011@scu.edu.cn; ouyangliang@scu.edu.cn
RI Ouyang, Liang/A-2751-2010
OI Ouyang, Liang/0000-0001-5537-8834; Li, Yang/0000-0003-3855-7720
FU National Natural Science Foundation of ChinaNational Natural Science
   Foundation of China (NSFC) [81922064, 81874290, 81903502]; Sichuan
   Science and Technology Program [2020YJ0091]; China Postdoctoral Science
   FoundationChina Postdoctoral Science Foundation [2020M673268]; Health
   Commission of Sichuan Province [20PJ002]
FX This work was supported by the National Natural Science Foundation of
   China (grant nos. 81922064, 81874290, and 81903502), Sichuan Science and
   Technology Program (grant no. 2020YJ0091), China Postdoctoral Science
   Foundation (grant no. 2020M673268), and Scientific Research Project,
   Health Commission of Sichuan Province (grant no. 20PJ002).
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NR 154
TC 1
Z9 1
U1 5
U2 6
PU AMER CHEMICAL SOC
PI WASHINGTON
PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA
SN 0022-2623
EI 1520-4804
J9 J MED CHEM
JI J. Med. Chem.
PD AUG 26
PY 2021
VL 64
IS 16
BP 11798
EP 11815
DI 10.1021/acs.jmedchem.1c00579
EA AUG 2021
PG 18
WC Chemistry, Medicinal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA UK5LZ
UT WOS:000692012400003
PM 34378389
DA 2022-04-25
ER

PT J
AU Piepoli, A
   Palmieri, O
   Maglietta, R
   Panza, A
   Cattaneo, E
   Latiano, A
   Laczko, E
   Gentile, A
   Carella, M
   Mazzoccoli, G
   Ancona, N
   Marra, G
   Andriulli, A
AF Piepoli, Ada
   Palmieri, Orazio
   Maglietta, Rosalia
   Panza, Anna
   Cattaneo, Elisa
   Latiano, Anna
   Laczko, Endre
   Gentile, Annamaria
   Carella, Massimo
   Mazzoccoli, Gianluigi
   Ancona, Nicola
   Marra, Giancarlo
   Andriulli, Angelo
TI The expression of leucine-rich repeat gene family members in colorectal
   cancer
SO EXPERIMENTAL BIOLOGY AND MEDICINE
LA English
DT Article
DE colorectal cancer; inflammation; autophagy; bioinformatics
ID TOLL-LIKE RECEPTORS; INNATE IMMUNITY; LRR PROTEINS; RAS; TRANSCRIPTOMES;
   IDENTIFICATION; HYBRIDIZATION; PATHOGENESIS; INFLAMMATION; RECOGNITION
AB This study was conducted to evaluate the association of the leucine-rich repeat (LRR) gene family with colorectal cancer (CRC). The expression of members of the LRR gene family were analyzed in 17 CRC specimens and in 59 healthy colorectal tissues by using Human Exon1.0ST microarray, and in 25 CRC specimens and 32 healthy colorectal tissues by U133Plus2.0 microarray. An association was found for 25 genes belonging to the plant-specific (PS) class of LRR genes (P = 0.05 for Exon1.0 ST and P = 0.04 for U133Plus2.0). In both data-sets, in CRC, we found down-regulation of SHOC2 (P < 0.00003) and LRRC28 (P < 0.01) and up-regulation of LRSAM1 (P < 0.000001), while up-regulation of MFHAS1 (P = 0.0005) and down-regulation of WDFY3 (P = 0.026) were found only in the Exon1.0 ST data-set. The PS LLR gene class encodes proteins that activate immune cells and might play a key role in programmed cell death and autophagy. SHOC2 and LRRC28 genes involved in RAS-mediated signaling, which hinders nutrient deprivation-induced autophagy, might be a possible link between the negative control of autophagy and tumorigenesis.
C1 [Piepoli, Ada; Palmieri, Orazio; Panza, Anna; Latiano, Anna; Gentile, Annamaria; Andriulli, Angelo] IRCCS Casa Sollievo Sofferenza, Lab Gastroenterol, I-71013 San Giovanni Rotondo, FG, Italy.
   [Piepoli, Ada; Palmieri, Orazio; Panza, Anna; Latiano, Anna; Gentile, Annamaria; Andriulli, Angelo] IRCCS Casa Sollievo Sofferenza, Div Gastroenterol, I-71013 San Giovanni Rotondo, FG, Italy.
   [Maglietta, Rosalia; Ancona, Nicola] CNR, Ist Sistemi Intelligenti Automaz, I-70126 Bari, Italy.
   [Carella, Massimo] IRCCS Casa Sollievo Sofferenza, Med Genet Serv, I-71013 San Giovanni Rotondo, Italy.
   [Cattaneo, Elisa; Marra, Giancarlo] Univ Zurich, Inst Mol Canc Res, CH-8006 Zurich, Switzerland.
   [Laczko, Endre] Funct Genom Ctr Zurich, CH-8057 Zurich, Switzerland.
   [Mazzoccoli, Gianluigi] IRCCS Casa Sollievo Sofferenza, Div Internal Med, I-71013 San Giovanni Rotondo, FG, Italy.
   [Mazzoccoli, Gianluigi] IRCCS Casa Sollievo Sofferenza, Chronobiol Unit, I-71013 San Giovanni Rotondo, FG, Italy.
RP Piepoli, A (corresponding author), IRCCS Casa Sollievo Sofferenza, Lab Gastroenterol, Viale Cappuccini 1, I-71013 San Giovanni Rotondo, FG, Italy.
EM a.piepoli@operapadrepio.it
RI Latiano, Anna/R-1965-2016; Palmieri, Orazio/J-7697-2012; Andriulli,
   Angelo/B-5027-2017; Ancona, Nicola/E-9971-2013; Ancona,
   Nicola/AAD-4772-2022; Maglietta, Rosalia/AAE-8546-2020; Piepoli,
   Ada/K-9299-2016; Panza, Anna/K-1989-2016; Carella, Massimo/A-2804-2014;
   Mazzoccoli, Gianluigi/H-2447-2016
OI Latiano, Anna/0000-0003-3719-2061; Palmieri, Orazio/0000-0002-0019-7929;
   Andriulli, Angelo/0000-0001-8862-7083; Ancona,
   Nicola/0000-0003-0065-0321; Maglietta, Rosalia/0000-0001-8580-4806;
   Piepoli, Ada/0000-0001-7487-8754; Panza, Anna/0000-0001-5840-0849;
   Carella, Massimo/0000-0002-6830-6829; Mazzoccoli,
   Gianluigi/0000-0003-3535-7635; Laczko, Endre/0000-0003-0271-3971
FU Italian Ministry of HealthMinistry of Health, Italy [RC1003GA53]; '5 x
   1000' voluntary contributions; Progetto Strategico [PS_012]; Regione
   PugliaRegione Puglia; Swiss National Science FoundationSwiss National
   Science Foundation (SNSF)European Commission [31003A-122186]
FX This work was supported by a grant from Italian Ministry of Health
   (RC1003GA53), by the '5 x 1000' voluntary contributions, by the
   'Progetto Strategico' (grant PS_012) funded by the 'Regione Puglia', and
   by Swiss National Science Foundation (grant no. 31003A-122186). The
   microarrays data are accessible through Array Express (accession number
   E-MTAB-829) and GEO (accession number GSE21962).
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Z9 14
U1 2
U2 11
PU ROYAL SOC MEDICINE PRESS LTD
PI LONDON
PA 1 WIMPOLE STREET, LONDON W1G 0AE, ENGLAND
SN 1535-3702
J9 EXP BIOL MED
JI Exp. Biol. Med.
PD OCT
PY 2012
VL 237
IS 10
BP 1123
EP 1128
DI 10.1258/ebm.2012.012042
PG 6
WC Medicine, Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Research & Experimental Medicine
GA 043DY
UT WOS:000311524300002
PM 23045723
DA 2022-04-25
ER

PT J
AU Farrall, AL
   Whitelaw, ML
AF Farrall, A. L.
   Whitelaw, M. L.
TI The HIF1 alpha-inducible pro-cell death gene BNIP3 is a novel target of
   SIM2s repression through cross-talk on the hypoxia response element
SO ONCOGENE
LA English
DT Article
DE SIM2; BNIP3; HIF1 alpha; hypoxia; cell death; cancer
ID DRUG-THERAPY TARGET; SINGLE-MINDED GENE; PANCREATIC-CANCER;
   PROSTATE-CANCER; COLORECTAL-CANCER; UP-REGULATION; EXPRESSION;
   AUTOPHAGY; PROTEIN; APOPTOSIS
AB The short isoform of single-minded 2 (SIM2s), a basic helix-loop-helix/PAS (bHLH/PAS) transcription factor, is upregulated in pancreatic and prostate tumours; however, a mechanistic role for SIM2s in these cancers is unknown. Microarray studies in prostate DU145 cells identified the pro-cell death gene, BNIP3 (Bcl-2/adenovirus E1B 19 kDa interacting protein 3), as a novel putative target of SIM2s repression. Further validation showed BNIP3 repression in several prostate and pancreatic carcinoma-derived cell lines with ectopic expression of human SIM2s. BNIP3 levels are enhanced in prostate carcinoma cells upon short interfering (si) RNA-mediated knockdown of endogenous SIM2s. Chromatin immunoprecipitation and promoter studies show that SIM2s represses BNIP3 through its activities at the proximal promoter hypoxia response element (HRE), the site through which the bHLH/PAS family member, hypoxia-inducible factor 1 alpha (HIF1 alpha), induces BNIP3. SIM2s attenuates BNIP3 hypoxic induction via the HRE, and increased hypoxic induction of BNIP3 occurs with siRNA knockdown of endogenous SIM2s in prostate PC3AR+ cells. BNIP3 is implicated in hypoxia-induced cell death processes. Prolonged treatment of PC3AR+ cells with hypoxia mimetics, DP and DMOG, confers hypoxia-induced autophagy, measured by enhanced LC3-II levels and SQSTM1/p62 turnover. We show that PC3AR+ cells expressing ectopic SIM2s have enhanced survival in these conditions. Induction of LC3-II and turnover of SQSTM1/p62 are attenuated in PC3AR+/SIM2s DMOG and hypoxia-treated cells, suggesting that SIM2s may attenuate autophagic cell death processes, perhaps through BNIP3 repression. These data show, for the first time, SIM2s cross-talk on an endogenous HRE. SIM2s' functional interference with HIF1 alpha activities on BNIP3 may indicate a novel role for SIM2s in promoting tumourigenesis. Oncogene (2009) 28, 3671-3680; doi: 10.1038/onc.2009.228; published online 10 August 2009
C1 [Farrall, A. L.; Whitelaw, M. L.] Univ Adelaide, Discipline Biochem, Sch Mol & Biomed Sci, Adelaide, SA 5005, Australia.
   [Farrall, A. L.; Whitelaw, M. L.] Ctr Mol Genet Dev, Adelaide, SA, Australia.
RP Farrall, AL (corresponding author), Univ Adelaide, Discipline Biochem, Sch Mol & Biomed Sci, Adelaide, SA 5005, Australia.
EM alexandra.farrall@adelaide.edu.au
RI Farrall, Alexandra/ABD-2079-2020
OI Farrall, Alexandra/0000-0002-0909-8978
FU Australian Cancer Research Foundation; Australian Research
   CouncilAustralian Research Council; Cancer Council South AustraliaCancer
   Council South Australia
FX We thank M van Bekkum and C Bindloss for their kind technical
   assistance, and Dr S Woods for reagents and critical reading of the
   manuscript. PC3AR+ cells were a kind gift from Prof W Tilley, Hanson
   Research Institute, Adelaide, Australia. Tet-inducible lentiviral
   vectors were a kind gift from Dr S Barry, Children's Health Research
   Institute, SA, Australia (Drabsch et al., 2007). Anti-HIF1 alpha-CAD
   antibody was obtained from the laboratory of Prof J Pouyssegur, CNRS
   UMR6543, University of Nice, France (Richard et al., 1999). We
   acknowledge the contribution of the Australian Cancer Research
   Foundation for their support of the Adelaide Microarray Facility,
   Adelaide, Australia, which supplied, processed and analysed the
   microarrays. This work was supported by grants from the Australian
   Research Council and the Cancer Council South Australia.
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U1 0
U2 11
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0950-9232
EI 1476-5594
J9 ONCOGENE
JI Oncogene
PD OCT 15
PY 2009
VL 28
IS 41
BP 3671
EP 3680
DI 10.1038/onc.2009.228
PG 10
WC Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics &
   Heredity
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics &
   Heredity
GA 507KJ
UT WOS:000270851800008
PM 19668230
OA Bronze
DA 2022-04-25
ER

PT J
AU Giannopoulou, E
   Nikolakopoulos, A
   Kotsirilou, D
   Lampropoulou, A
   Raftopoulou, S
   Papadimitriou, E
   Theocharis, AD
   Makatsoris, T
   Fasseas, K
   Kalofonos, HP
AF Giannopoulou, Efstathia
   Nikolakopoulos, Achilleas
   Kotsirilou, Dimitra
   Lampropoulou, Angeliki
   Raftopoulou, Sofia
   Papadimitriou, Evangelia
   Theocharis, Achilleas D.
   Makatsoris, Thomas
   Fasseas, Konstantinos
   Kalofonos, Haralabos P.
TI Epidermal growth factor receptor status and Notch inhibition in
   non-small cell lung cancer cells
SO JOURNAL OF BIOMEDICAL SCIENCE
LA English
DT Article
DE Notch intracellular domain; Epidermal growth factor receptor; Non-small
   cell lung cancer cells; Apoptosis; Autophagy; Cell cycle arrest
ID HUMAN BREAST-CANCER; SECRETASE INHIBITOR; ACQUIRED-RESISTANCE; SIGNALING
   PATHWAY; COLON-CANCER; CROSS-TALK; EGFR; ACTIVATION; EXPRESSION;
   INDUCTION
AB Background: Notch may behave as an oncogene or a tumor suppressor gene in lung cancer cells. Notch receptor undergoes cleavage by enzymes, including gamma-secretase, generating the active Notch intracellular domain (NICD). The aim of the present study was to investigate the effect of DAPT, gamma-secretase inhibitor, in non-small cell lung cancer (NSCLC) cells, as well as the impact of epidermal growth factor (EGF) that is over-expressed by NSCLC cells, on Notch signaling. H23, A549, H661 and HCC827 human NSCLC cell lines were used, expressing various NICD and EGF receptor (EGFR) protein levels.
   Results: DAPT decreased the number of H661 cells in a concentration-dependent manner, while it had a small effect on H23 and A549 cells and no effect on HCC827 cells that carry mutated EGFR. Notch inhibition did not affect the stimulatory effect of EGF on cell proliferation, while EGF prevented DAPT-induced NICD decrease in H23 and H661 cells. The type of cell death induced by DAPT seems to depend on the cell type.
   Conclusions: Our data indicate that inhibition of Notch cleavage may not affect cell number in the presence of EGFR mutations and that EGFR may affect Notch signalling suggesting that a dual inhibition of these pathways might be promising in NSCLC.
C1 [Giannopoulou, Efstathia; Nikolakopoulos, Achilleas; Kotsirilou, Dimitra; Lampropoulou, Angeliki; Makatsoris, Thomas; Kalofonos, Haralabos P.] Univ Patras, Patras Med Sch, Dept Med, Div Oncol,Clin Oncol Lab, Rion 26504, Greece.
   [Kotsirilou, Dimitra; Papadimitriou, Evangelia] Univ Patras, Sch Hlth Sci, Dept Pharm, Mol Pharmacol Lab, Rion 26504, Greece.
   [Lampropoulou, Angeliki; Theocharis, Achilleas D.] Univ Patras, Dept Chem, Biochem Lab, Rion 26504, Greece.
   [Raftopoulou, Sofia; Fasseas, Konstantinos] Agr Univ Athens, Fac Crop Prod, Electron Microscopy Lab, GR-11855 Athens, Greece.
RP Kalofonos, HP (corresponding author), Univ Patras, Patras Med Sch, Dept Med, Div Oncol,Clin Oncol Lab, Rion 26504, Greece.
EM kalofonos@upatras.gr
RI Papadimitriou, Evangelia/ABG-1356-2020
OI Papadimitriou, Evangelia/0000-0001-6429-4325; Nikolakopoulos,
   Achilleas/0000-0003-1681-8520; Kalofonos, Haralabos/0000-0002-3286-778X
FU EOGE Oncological Research Fund
FX We would like to thank EOGE Oncological Research Fund for financial
   support.
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NR 42
TC 15
Z9 15
U1 0
U2 10
PU BIOMED CENTRAL LTD
PI LONDON
PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND
SN 1021-7770
EI 1423-0127
J9 J BIOMED SCI
JI J. Biomed. Sci.
PD OCT 24
PY 2015
VL 22
AR 98
DI 10.1186/s12929-015-0196-1
PG 11
WC Cell Biology; Medicine, Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Cell Biology; Research & Experimental Medicine
GA CU1SH
UT WOS:000363301100002
PM 26497899
OA Green Published, gold
DA 2022-04-25
ER

PT J
AU Hu, FQ
   Song, D
   Yan, YM
   Huang, CS
   Shen, CT
   Lan, J
   Chen, YQ
   Liu, AY
   Wu, Q
   Sun, L
   Xu, F
   Hu, FY
   Chen, LS
   Luo, XL
   Feng, YD
   Huang, SY
   Hu, JB
   Wang, GH
AF Hu, Fuqing
   Song, Da
   Yan, Yumeng
   Huang, Changsheng
   Shen, Chentao
   Lan, Jingqin
   Chen, Yaqi
   Liu, Anyi
   Wu, Qi
   Sun, Li
   Xu, Feng
   Hu, Fayong
   Chen, Lisheng
   Luo, Xuelai
   Feng, Yongdong
   Huang, Shengyou
   Hu, Junbo
   Wang, Guihua
TI IL-6 regulates autophagy and chemotherapy resistance by promoting BECN1
   phosphorylation
SO NATURE COMMUNICATIONS
LA English
DT Article
ID BECLIN 1; COLORECTAL-CANCER; DRUG-RESISTANCE; INTERLEUKIN-6;
   INFLAMMATION; STAT3; MICROENVIRONMENT; FIBROBLASTS; PROGRESSION;
   IMMUNITY
AB Extracellular cytokines are enriched in the tumor microenvironment and regulate various important properties of cancers, including autophagy. However, the precise molecular mechanisms underlying the link between autophagy and extracellular cytokines remain to be elucidated. In the present study, we demonstrate that IL-6 activates autophagy through the IL-6/JAK2/BECN1 pathway and promotes chemotherapy resistance in colorectal cancer (CRC). Mechanistically, IL-6 triggers the interaction between JAK2 and BECN1, where JAK2 phosphorylates BECN1 at Y333. We demonstrate that BECN1 Y333 phosphorylation is crucial for BECN1 activation and IL-6-induced autophagy by regulating PI3KC3 complex formation. Furthermore, we investigate BECN1 Y333 phosphorylation as a predictive marker for poor CRC prognosis and chemotherapy resistance. Combination treatment with autophagy inhibitors or pharmacological agents targeting the IL-6/JAK2/BECN1 signaling pathway may represent a potential strategy for CRC cancer therapy. IL-6 is an important cytokine in the tumour microenvironment, but its role in regulating autophagy in cancer cells is unclear. Here the authors show that IL-6 activates autophagy in colorectal cancer through the interaction between JAK2 and autophagy regulator, BECN1, which leads to chemotherapeutic resistance.
C1 [Hu, Fuqing; Song, Da; Huang, Changsheng; Shen, Chentao; Lan, Jingqin; Chen, Yaqi; Liu, Anyi; Wu, Qi; Xu, Feng; Hu, Fayong; Chen, Lisheng; Luo, Xuelai; Feng, Yongdong; Hu, Junbo; Wang, Guihua] Huazhong Univ Sci & Technol, Tongji Hosp, GI Canc Res Inst, Wuhan, Peoples R China.
   [Yan, Yumeng; Huang, Shengyou] Huazhong Univ Sci & Technol, Sch Phys, Wuhan, Hubei, Peoples R China.
   [Sun, Li] Huazhong Univ Sci & Technol, Tongji Hosp, Dept Oncol, Wuhan, Peoples R China.
RP Hu, JB; Wang, GH (corresponding author), Huazhong Univ Sci & Technol, Tongji Hosp, GI Canc Res Inst, Wuhan, Peoples R China.
EM jbhu@tjh.tjmu.edu.cn; ghwang@tjh.tjmu.edu.cn
RI Wang, Guihua/AAX-3130-2021
FU NSFCNational Natural Science Foundation of China (NSFC) [81773113,
   81874186, 81922053]; Tongji Hospital
FX We are grateful to Dr. Weina Zhang, Dr. Peijing Zhang, Dr. Min Wang, and
   Dr. Guoxiang Jin for the suggestions on this project. We thank Shengyou
   Huang and his lab members for the great favor of performing protein
   structure data analysis and project suggestions. We thank all the health
   workers for help against COVID-19 in Wuhan City and all coauthors for
   your great work during this difficult period. This work is supported by
   NSFC (No. 81773113G.W., No. 81874186J.H., and No. 81922053G.W.) and
   startup funding from Tongji Hospital for G.W.
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NR 48
TC 6
Z9 6
U1 14
U2 24
PU NATURE RESEARCH
PI BERLIN
PA HEIDELBERGER PLATZ 3, BERLIN, 14197, GERMANY
SN 2041-1723
J9 NAT COMMUN
JI Nat. Commun.
PD JUN 15
PY 2021
VL 12
IS 1
AR 3651
DI 10.1038/s41467-021-23923-1
PG 14
WC Multidisciplinary Sciences
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Science & Technology - Other Topics
GA SX2EE
UT WOS:000665022900006
PM 34131122
OA Green Published, gold
DA 2022-04-25
ER

PT J
AU Zhang, YY
   Xu, MF
   Chen, JH
   Chen, K
   Zhuang, JF
   Yang, YF
   Liu, X
   Guan, GX
AF Zhang, Yiyi
   Xu, Meifang
   Chen, Jianhua
   Chen, Kui
   Zhuang, Jinfu
   Yang, Yuanfeng
   Liu, Xing
   Guan, Guoxian
TI Prognostic Value of the FOXK Family Expression in Patients with Locally
   Advanced Rectal Cancer Following Neoadjuvant Chemoradiotherapy
SO ONCOTARGETS AND THERAPY
LA English
DT Article
DE rectal cancer; neoadjuvant chemoradiotherapy; FOXK1; FOXK2; prognosis
ID CELL-GROWTH; PROLIFERATION; APOPTOSIS; SYSTEM; KNOCKDOWN; AUTOPHAGY;
   BINDING; PREDICT; GENES
AB Purpose: To assess the role of the expression levels of FOXK family members, FOXK1 and FOXK2, in predicting response to neo-chemoradiotherapy (NCRT) and prognosis in locally advanced rectal cancer (LARC).
   Methods: A total of 256 LARC patients who underwent NCRT and radical resection between 2011 and 2017 were enrolled in the present study. The patients were divided into a training dataset (n=169, 2011-2015) and a validation dataset (n=87, 2016-2017). Tumor tissues were collected before NCRT and post-surgery and were used for immunohistochemical analysis.
   Results: Oncomine database analysis revealed that FOXK1 and FOXK2 were overexpressed in most cancers especially in colorectal cancer. Additionally, overexpression of FOXK1 and FOXK2 was associated with poorer prognosis by the R2 database. In both our training and validation datasets, the expression of FOXK1 and FOXK2 was lower in the pathological complete response (pCR) group compared with the non-pCR group (P<0.05). Cox regression analysis demonstrated that pathological N stage (HR=1.810, 95% CI 1.159-2.827, P=0.009), FOXK1 expression (HR=5.831, 95% CI 2.925-11.625, P<0.001), and FOXK2 expression (HR=2.390, 95% CI 11.272-4.491, P=0.007) were independent predictors of disease-free survival (DFS). Based on the Cox multivariate analysis, we constructed a risk score model that served as a prognostic biomarker and had a powerful ability to predict pCR in LARC patients upon NCRT in both training and validation groups.
   Conclusion: Expression levels of FOXK family members were associated with chemoradiotherapy resistance and prognosis of LARC patients following NCRT and were used to construct a risk score model that is a promising biomarker for LARC.
C1 [Zhang, Yiyi; Zhuang, Jinfu; Yang, Yuanfeng; Liu, Xing; Guan, Guoxian] Fujian Med Univ, Dept Colorectal Surg, Affiliated Hosp 1, Fuzhou 350001, Fujian, Peoples R China.
   [Xu, Meifang] Fujian Med Univ, Dept Pathol, Union Hosp, Fuzhou, Peoples R China.
   [Chen, Jianhua] Fujian Med Univ, Dept Radiol, Union Hosp, Fuzhou, Peoples R China.
   [Chen, Kui] Fujian Med Univ, Dept Gen Surg, Hosp Fuzhou City 1, Fuzhou, Peoples R China.
RP Liu, X; Guan, GX (corresponding author), Fujian Med Univ, Dept Colorectal Surg, Affiliated Hosp 1, Fuzhou 350001, Fujian, Peoples R China.
EM fjmufylx@163.com; fjxhggx@163.com
OI Guan, Guoxian/0000-0001-9883-3139
FU Science Foundation of the Fujian ProvinceNatural Science Foundation of
   Fujian Province [2016J01602, 2019J0105]; Special Financial Foundation of
   Fujian Provincial [2015-1297]; Young and middle-aged backbone training
   project in the health system of Fujian province [2016-ZQN-26]; Startup
   Fund for Scientific Research, Fujian Medical University [2018QH2027,
   2018S0130]; Professor Development Foundation of Fujian Medical
   University [JS11006]
FX This study was supported by the Science Foundation of the Fujian
   Province, (No. 2016J01602; 2019J0105), Special Financial Foundation of
   Fujian Provincial (No.2015-1297), Young and middle-aged backbone
   training project in the health system of Fujian province (2016-ZQN-26),
   the Startup Fund for Scientific Research, Fujian Medical University
   (2018QH2027, 2018S0130) and Professor Development Foundation of Fujian
   Medical University (No.JS11006).
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NR 48
TC 4
Z9 4
U1 2
U2 6
PU DOVE MEDICAL PRESS LTD
PI ALBANY
PA PO BOX 300-008, ALBANY, AUCKLAND 0752, NEW ZEALAND
SN 1178-6930
J9 ONCOTARGETS THER
JI OncoTargets Ther.
PY 2020
VL 13
BP 9185
EP 9201
DI 10.2147/OTT.S255956
PG 17
WC Biotechnology & Applied Microbiology; Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biotechnology & Applied Microbiology; Oncology
GA NU5BH
UT WOS:000573656200004
PM 32982306
OA Green Published, gold
DA 2022-04-25
ER

PT J
AU Yang, Y
   Luo, H
   Hui, KY
   Ci, YL
   Shi, KJ
   Chen, G
   Shi, L
   Xu, CM
AF Yang, Yang
   Luo, Hui
   Hui, Kaiyuan
   Ci, Yali
   Shi, Kejian
   Chen, Ge
   Shi, Lei
   Xu, Caimin
TI Selenite-induced autophagy antagonizes apoptosis in colorectal cancer
   cells in vitro and in vivo
SO ONCOLOGY REPORTS
LA English
DT Article
DE selenite; apoptosis; autophagy; colorectal cancer cells; reactive oxygen
   species
ID PROSTATE-CANCER; MEDIATED APOPTOSIS; SODIUM SELENITE; VITAMIN-E;
   CROSSTALK; INHIBITION; PREVENTION; RISK
AB In the present study, we aimed to investigate the relationship between autophagy and apoptosis in selenite-treated colorectal cancer (CRC) cells. The effects of selenite on HCT116 and SW480 cell apoptosis were investigated with an Annexin V/propidium iodide (PI) double staining kit by flow cytometry. The punctate of LC3 protein following treatment with selenite was observed by a laser scanning confocal microscope and by transmission electron microscopy. Using western blot assays, we detected the apoptotic and autophagic markers in both CRC cells and mouse xenograft tumor models. We found that sodium selenite induced autophagy in the two CRC cell lines. Consistent with the in vitro results, we observed that the expression of autophagy marker LC3 was increased. Finally, we discovered that modulation of reactive oxygen species by MnTMPyP inhibited autophagy, while H2O2 activated autophagy. These results help to elucidate the anticancer effect of selenium, providing further evidence to exploit novel anticancer drugs targeting selenium.
C1 [Yang, Yang; Hui, Kaiyuan; Ci, Yali; Shi, Kejian; Shi, Lei; Xu, Caimin] Chinese Acad Med Sci, Peking Union Med Coll, Sch Basic Med, Inst Basic Med Sci,Dept Biochem & Mol Biol,State, Beijing 100005, Peoples R China.
   [Luo, Hui] Shenzhen Univ, Hlth Sci Ctr, Shenzhen 518060, Peoples R China.
   [Chen, Ge] CAMS, PUMC Hosp, Dept Gen Surg, Beijing 100730, Peoples R China.
RP Shi, L (corresponding author), Chinese Acad Med Sci, Peking Union Med Coll, Sch Basic Med, Inst Basic Med Sci,Dept Biochem & Mol Biol,State, 5 Dong Dan San Tiao, Beijing 100005, Peoples R China.
EM shilei@ibms.pumc.edu.cn; cmxu@ibms.pumc.edu.cn
RI Shi, Lei/AAX-9455-2021
FU National Natural Science Foundation of ChinaNational Natural Science
   Foundation of China (NSFC) [31170788, 31340037, 31271565]; National
   Natural Science FoundationNational Natural Science Foundation of China
   (NSFC) [31101018]; State Key Laboratory Special Fund [2060204]; Natural
   Science Foundation of BeijingBeijing Natural Science Foundation
   [5082015]
FX The present study was supported by the National Natural Science
   Foundation of China (nos. 31170788, 31340037 and 31271565), the National
   Natural Science Foundation for Young Scholars of China (no. 31101018),
   the State Key Laboratory Special Fund (no. 2060204), and the Natural
   Science Foundation of Beijing (no. 5082015).
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NR 31
TC 16
Z9 17
U1 3
U2 31
PU SPANDIDOS PUBL LTD
PI ATHENS
PA POB 18179, ATHENS, 116 10, GREECE
SN 1021-335X
EI 1791-2431
J9 ONCOL REP
JI Oncol. Rep.
PD MAR
PY 2016
VL 35
IS 3
BP 1255
EP 1264
DI 10.3892/or.2015.4484
PG 10
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA DB0WP
UT WOS:000368228900004
PM 26676801
OA Green Published, hybrid, Green Submitted
DA 2022-04-25
ER

PT J
AU Li, CM
   Pan, B
   Liu, XX
   Qin, J
   Wang, XH
   He, BS
   Pan, YQ
   Sun, HL
   Xu, T
   Xu, XN
   Zeng, KX
   Wang, SK
AF Li, Chenmeng
   Pan, Bei
   Liu, Xiangxiang
   Qin, Jian
   Wang, Xuhong
   He, Bangshun
   Pan, Yuqin
   Sun, Huiling
   Xu, Tao
   Xu, Xueni
   Zeng, Kaixuan
   Wang, Shukui
TI Long intergenic non-coding RNA LINC00485 exerts tumor-suparessive
   activity by regulating miR-581/EDEM1 axis in colorectal cancer
SO AGING-US
LA English
DT Article
DE linc00485; microRNA-581; EDEM1; colorectal cancer
ID EPITHELIAL-MESENCHYMAL TRANSITION; AUTOPHAGY; MICRORNAS
AB Long non-coding RNAs (lncRNA) play a vital role in colorectal cancer (CRC) progression. To investigate the role of long intergenic non-coding RNA LINC00485 in CRC, we performed in vitro functional experiments. LoVo tumor-bearing and liver metastasis mice were used as in vivo models. We found that LINC00485 expression was significantly lower in CRC tissues and cancer cells than in paired normal samples and human normal colonic epithelial cells. Lower expression of LINC00485 predicted poor prognosis in CRC patients. LINC00485 knockdown promoted the proliferation, migration, and invasion of FHC cells, while LINC00485 overexpression weakened these abilities of LoVo cells. MicroRNA miR-581 was the downstream target of LINC00485, which was downregulated in CRC samples and cancer cells compared to normal tissues and normal colonic epithelial cells. MiR-581 overexpression induced proliferation, migration, and invasion of FHC cells, while miR-581 antagomir treatment produced opposite results. MiR-581 directly targeted the 3'UTR of EDEM1 and inhibited its expression and induction of epithelial-mesenchymal transition of CRC. In mouse models, LINC00485 knockdown or down-regulation of miR-581 significantly repressed CRC cell growth and prevented CRC liver metastasis. Overall, LINC00485 suppressed CRC tumorigenesis and progression by targeting the miR-581/EDEM1 axis. LINC00485 may be a potential therapeutic target for CRC.
C1 [Li, Chenmeng; Pan, Bei; Liu, Xiangxiang; Wang, Xuhong; Xu, Xueni; Zeng, Kaixuan; Wang, Shukui] Southeast Univ, Sch Med, Nanjing 210009, Peoples R China.
   [Li, Chenmeng; Pan, Bei; Liu, Xiangxiang; Qin, Jian; Wang, Xuhong; He, Bangshun; Pan, Yuqin; Sun, Huiling; Xu, Tao; Xu, Xueni; Zeng, Kaixuan; Wang, Shukui] Nanjing Med Univ, Nanjing Hosp 1, Gen Clin Res Ctr, Nanjing 210006, Peoples R China.
   [Wang, Shukui] Nanjing Med Univ, Jiangsu Collaborat Innovat Ctr Canc Personalized, Nanjing 211100, Peoples R China.
RP Wang, SK (corresponding author), Southeast Univ, Sch Med, Nanjing 210009, Peoples R China.; Wang, SK (corresponding author), Nanjing Med Univ, Nanjing Hosp 1, Gen Clin Res Ctr, Nanjing 210006, Peoples R China.; Wang, SK (corresponding author), Nanjing Med Univ, Jiangsu Collaborat Innovat Ctr Canc Personalized, Nanjing 211100, Peoples R China.
EM sk_wang@njmu.edu.cn
FU National Nature Science Foundation of ChinaNational Natural Science
   Foundation of China (NSFC) [81972806]; Jiangsu Provincial Key Research
   and Development Plan [BE2019614]; Key Project of Science and Technology
   Development of Nanjing Medicine [ZDX16001, ZKX18030]; The National
   Nature Science Foundation of ChinaNational Natural Science Foundation of
   China (NSFC) [81802093]; Innovation team of Jiangsu provincial
   health-strengthening engineering by science and education
   [CXTDB20170080]; Jiangsu Youth Medical Talents Training Project
   [QNRC2016066, QNRC2016074]; Jiangsu 333 High-level Talents Cultivating
   Project [BRA201702]; Jiangsu Cancer Personalized Medicine Collaborative
   Innovation Center
FX This project was supported by grants from The National Nature Science
   Foundation of China (No. 81972806), Jiangsu Provincial Key Research and
   Development Plan (BE2019614), Key Project of Science and Technology
   Development of Nanjing Medicine (ZDX16001) to SKW; The National Nature
   Science Foundation of China (No. 81802093) to HLS; Innovation team of
   Jiangsu provincial health-strengthening engineering by science and
   education (CXTDB20170080); Jiangsu Youth Medical Talents Training
   Project to BSH (QNRC2016066) and YQP (QNRC2016074); Key Project of
   Science and Technology Development of Nanjing Medicine (ZKX18030, breast
   cancer); Jiangsu 333 High-level Talents Cultivating Project (Gastric
   cancer, no. BRA201702) and Jiangsu Cancer Personalized Medicine
   Collaborative Innovation Center.
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NR 38
TC 2
Z9 2
U1 1
U2 2
PU IMPACT JOURNALS LLC
PI ORCHARD PARK
PA 6666 E QUAKER ST, STE 1, ORCHARD PARK, NY 14127 USA
SN 1945-4589
J9 AGING-US
JI Aging-US
PD FEB 15
PY 2021
VL 13
IS 3
BP 3866
EP 3885
DI 10.18632/aging.202354
PG 20
WC Cell Biology; Geriatrics & Gerontology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Cell Biology; Geriatrics & Gerontology
GA QI2UY
UT WOS:000618834100018
PM 33461166
OA Green Published, gold
DA 2022-04-25
ER

PT J
AU Zaytseva, YY
   Harris, JW
   Mitov, MI
   Kim, JT
   Butterfield, DA
   Lee, EY
   Weiss, HL
   Gao, T
   Evers, BM
AF Zaytseva, Yekaterina Y.
   Harris, Jennifer W.
   Mitov, Mihail I.
   Kim, Ji Tae
   Butterfield, D. Allan
   Lee, Eun Y.
   Weiss, Heidi L.
   Gao, Tianyan
   Evers, B. Mark
TI Increased expression of fatty acid synthase provides a survival
   advantage to colorectal cancer cells via upregulation of cellular
   respiration
SO ONCOTARGET
LA English
DT Article
DE FASN; colorectal cancer; energy homeostasis; metastasis; metabolic
   stress
ID ACTIVATED PROTEIN-KINASE; PROSTATE-CANCER; LIPID-SYNTHESIS;
   TUMOR-GROWTH; METABOLISM; INHIBITION; AUTOPHAGY; TARGETS; AMPK;
   METASTASIS
AB Fatty acid synthase (FASN), a lipogenic enzyme, is upregulated in colorectal cancer (CRC). Increased de novo lipid synthesis is thought to be a metabolic adaptation of cancer cells that promotes survival and metastasis; however, the mechanisms for this phenomenon are not fully understood. We show that FASN plays a role in regulation of energy homeostasis by enhancing cellular respiration in CRC. We demonstrate that endogenously synthesized lipids fuel fatty acid oxidation, particularly during metabolic stress, and maintain energy homeostasis. Increased FASN expression is associated with a decrease in activation of energy-sensing pathways and accumulation of lipid droplets in CRC cells and orthotopic CRCs. Immunohistochemical evaluation demonstrated increased expression of FASN and p62, a marker of autophagy inhibition, in primary CRCs and liver metastases compared to matched normal colonic mucosa. Our findings indicate that overexpression of FASN plays a crucial role in maintaining energy homeostasis in CRC via increased oxidation of endogenously synthesized lipids. Importantly, activation of fatty acid oxidation and consequent downregulation of stress-response signaling pathways may be key adaptation mechanisms that mediate the effects of FASN on cancer cell survival and metastasis, providing a strong rationale for targeting this pathway in advanced CRC.
C1 [Zaytseva, Yekaterina Y.; Harris, Jennifer W.; Mitov, Mihail I.; Kim, Ji Tae; Butterfield, D. Allan; Lee, Eun Y.; Weiss, Heidi L.; Gao, Tianyan; Evers, B. Mark] Univ Kentucky, Markey Canc Ctr, Lexington, KY 40508 USA.
   [Harris, Jennifer W.; Evers, B. Mark] Univ Kentucky, Dept Surg, Lexington, KY USA.
   [Butterfield, D. Allan] Univ Kentucky, Dept Chem, Lexington, KY 40506 USA.
   [Lee, Eun Y.] Univ Kentucky, Pathol & Lab Med, Lexington, KY USA.
RP Evers, BM (corresponding author), Univ Kentucky, Markey Canc Ctr, Lexington, KY 40508 USA.
EM mark.evers@uky.edu
FU NIHUnited States Department of Health & Human ServicesNational
   Institutes of Health (NIH) - USA [T32 CA165990]; NCIUnited States
   Department of Health & Human ServicesNational Institutes of Health (NIH)
   - USANIH National Cancer Institute (NCI) [P30 CA177558]; NATIONAL CANCER
   INSTITUTEUnited States Department of Health & Human ServicesNational
   Institutes of Health (NIH) - USANIH National Cancer Institute (NCI)
   [T32CA160003, T32CA165990, P30CA177558] Funding Source: NIH RePORTER
FX This research was supported by NIH grant T32 CA165990 and NCI grant P30
   CA177558 (for shared resource facilities).
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PU IMPACT JOURNALS LLC
PI ORCHARD PARK
PA 6666 E QUAKER ST, STE 1, ORCHARD PARK, NY 14127 USA
EI 1949-2553
J9 ONCOTARGET
JI Oncotarget
PD AUG 7
PY 2015
VL 6
IS 22
BP 18891
EP 18904
DI 10.18632/oncotarget.3783
PG 14
WC Oncology; Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Cell Biology
GA CO7RS
UT WOS:000359360000017
PM 25970773
OA Green Published, gold, Green Submitted
DA 2022-04-25
ER

PT J
AU Wu, YH
   Wu, YR
   Li, B
   Yan, ZY
AF Wu, Yan-Hong
   Wu, Yu-Rui
   Li, Bo
   Yan, Zhu-Yun
TI Cryptotanshinone: A review of its pharmacology activities and molecular
   mechanisms
SO FITOTERAPIA
LA English
DT Review
DE Cryptotanshinone; Pharmacology; Anti-tumor; Molecular mechanisms;
   Signaling pathways
ID AUTOPHAGIC CELL-DEATH; COLON-CANCER CELLS; SALVIA-MILTIORRHIZA; CARDIAC
   FIBROSIS; SIGNALING PATHWAY; INDUCED APOPTOSIS; HERBAL COMPOUND;
   DOWN-REGULATION; TANSHINONE IIA; CYCLE ARREST
AB As a natural quinone compound, the medicinal value of cryptotanshinone (CT) has received increasing attentions, but there is no systematic literature review that describes the pharmacological activity of CT. This paper reviewed the pharmacology researches of CT, with a primary focus on its anti-tumor activity. We also discussed the underlying molecular mechanisms, and proposed future outlooks. In addition to anti-tumor activity, CT was found to have anti-inflammatory, neuroprotective, cardioprotective, visceral protective, anti-metabolic disorders and other abilities. Furthermore, the potential molecular mechanisms contributing to the anti-tumor effect of CT likely involve the following aspects: the induction of apoptosis, targeting of ER and AR, reversion of MDR, combined pharmacotherapy, and the inhibition of cell proliferation, migration, and invasion. We also found that different pharmacological effects involved various signaling pathways. Among them, STAT3-related signaling pathways played a vital role in the CT-mediated induction of tumor cell apoptosis and proliferation, while NF-kappa B signal pathway also was essential for inhibition of inflammation by CT. Furthermore, CT could significantly enhance the activities of several anticancer drugs and reverse their resistances in tumors. Therefore, we proposed suggestions for future studies of CT, including enhancing anti-tumor activity by targeting STAT3-related receptors, targeting NF-kappa B-related pathways to inhibit inflammatory responses, enhancing anti-tumor efficacy by combining with anti-tumor drugs, and further studying the dose-effect relationship to ensure safer and more effective applications of CT.
C1 [Wu, Yan-Hong; Wu, Yu-Rui; Li, Bo; Yan, Zhu-Yun] Chengdu Univ Tradit Chinese Med, Sch Pharm, Key Lab Characterist Chinese Med Resources Southw, Chengdu, Peoples R China.
RP Yan, ZY (corresponding author), Chengdu Univ Tradit Chinese Med, Sch Pharm, Chengdu, Peoples R China.
EM yanzhuyun@cdutcm.edu.cn
FU National Natural Science Foundation of ChinaNational Natural Science
   Foundation of China (NSFC) [81573537, 81973416]
FX This study was supported by grants from the National Natural Science
   Foundation of China (81573537, 81973416).
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NR 140
TC 14
Z9 14
U1 2
U2 28
PU ELSEVIER
PI AMSTERDAM
PA RADARWEG 29, 1043 NX AMSTERDAM, NETHERLANDS
SN 0367-326X
EI 1873-6971
J9 FITOTERAPIA
JI Fitoterapia
PD SEP
PY 2020
VL 145
AR 104633
DI 10.1016/j.fitote.2020.104633
PG 12
WC Chemistry, Medicinal; Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA LY7ME
UT WOS:000540710700011
PM 32445662
DA 2022-04-25
ER

PT J
AU Su, YY
   Yao, SW
   Zhao, S
   Li, JC
   Li, HY
AF Su, Yanyan
   Yao, Shuwen
   Zhao, Shill
   Li, Jinchun
   Li, Hongyan
TI LncRNA CCAT1 functions as apoptosis inhibitor in podocytes via autophagy
   inhibition
SO JOURNAL OF CELLULAR BIOCHEMISTRY
LA English
DT Article
DE autophagy; lncRNA CCAT1; PI3K; Akt signaling; podocyte
ID LONG NONCODING RNA; NECROSIS-FACTOR-ALPHA; CELL-PROLIFERATION; C-MYC;
   EXPRESSION; INJURY
AB Podocyte apoptosis importantly contributes to various kidney diseases. Long noncoding RNAs Colon cancer-associated transcript-1 (CCAT-1) has been demonstrated for a critical role in cell proliferation. In the present study, the relationship between CCAT1 and popdocyte impairment, and the underlying mechanism was investigated. Podocytes were isolated from mice and then treated with tumor necrosis factor-alpha to simulate podocyte injury. After developed CCAT1 overexpression or knockdown, cell viabilities were determined with the CCK-8 assay, apoptosis was examined with Flow cytometry, the autophagy was observed by Western blot. Furthermore, phosphorylated PI3K and Akt expressions were examined. We found that after CCAT1 overexpression, the cell viability was significantly increased, apoptosis was significantly decreased, and autophagy was significantly inhibited, which was indicated by induced P62, LC3B-I and decreased LC3B-II. In addition, CCAT1 overexpression induced the levels of phosphorylated PI3K and Akt. With Rap treatment, these effects by CCAT1 were reversed. Furthermore, the results contrary to the effects by CCAT1 overexpression were presented after CCAT1 knockdown, and this was inhibited by 3-MA. Taken together, our results suggested that CCAT1 induction critically participated in apoptosis inhibition in podocytes through autophagy inhibition via increasing PI3K/Akt signaling. This might act as a promising therapeutic intervention for renal diseases associated with podocyte apoptosis.
C1 [Su, Yanyan; Yao, Shuwen; Zhao, Shill; Li, Jinchun; Li, Hongyan] Southern Med Univ, Huadu Dist Peoples Hosp Guangzhou, Dept Nephrol, 22 Baohua Rd, Guangzhou, Guangdong, Peoples R China.
RP Li, HY (corresponding author), Southern Med Univ, Huadu Dist Peoples Hosp Guangzhou, Dept Nephrol, 22 Baohua Rd, Guangzhou, Guangdong, Peoples R China.
EM lihy0726@126.com
FU Guangzhou Medical Key Discipline Construction Project [2017-2019]
FX Guangzhou Medical Key Discipline Construction Project, Grant/Award
   Number: 2017-2019
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PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0730-2312
EI 1097-4644
J9 J CELL BIOCHEM
JI J. Cell. Biochem.
PD JAN
PY 2020
VL 121
IS 1
BP 621
EP 631
DI 10.1002/jcb.29307
EA AUG 2019
PG 11
WC Biochemistry & Molecular Biology; Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Cell Biology
GA JQ1VC
UT WOS:000484291500001
PM 31468575
OA hybrid, Green Published
DA 2022-04-25
ER

PT J
AU Douglass, S
   Goyal, A
   Iozzo, RV
AF Douglass, Stephen
   Goyal, Atul
   Iozzo, Renato V.
TI The role of perlecan and endorepellin in the control of tumor
   angiogenesis and endothelial cell autophagy
SO CONNECTIVE TISSUE RESEARCH
LA English
DT Review
DE Angiogenesis; autophagy; perlecan; LG domains; Peg3
ID HEPARAN-SULFATE PROTEOGLYCAN; SCHWARTZ-JAMPEL-SYNDROME;
   FIBROBLAST-GROWTH-FACTOR; COLON-CARCINOMA-CELLS; BASEMENT-MEMBRANE
   PROTEOGLYCANS; EXTRACELLULAR-MATRIX; PROTEIN CORE; FACTOR-RECEPTOR;
   IN-VIVO; SIGNALING PATHWAYS
AB During tumor growth and angiogenesis there is a dynamic remodeling of tissue architecture often accompanied by the release of extracellular matrix constituents full of biological activity. One of the key constituents of the tumor microenvironment is the large heparan sulfate proteoglycan perlecan. This proteoglycan, strategically located at cell surfaces and within basement membranes, is a well-defined pro-angiogenic molecule when intact. However, when partially processed by proteases released during cancer remodeling and invasion, the C-terminal fragment of perlecan, known as endorepellin, has opposite effects than its parent molecule. Endorepellin is a potent inhibitor of angiogenesis by exerting a dual receptor antagonism by simultaneously engaging VEGFR2 and alpha 2 beta 1 integrin. Signaling through the a2b1 integrin leads to actin disassembly and block of endothelial cell migration, necessary for capillary morphogenesis. Signaling through the VEGFR2 induces dephosphorylation of the receptor via activation of SHP-1 and suppression of downstream proangiogenic effectors, especially attenuating VEGFA expression. A novel and emerging role of endorepellin is its ability to evoke autophagy by activating Peg3 and various canonical autophagic markers. This effect is specific for endothelial cells as these are the primary cells expressing both VEGFR2 and a2b1 integrin. Thus, an endogenous fragment of a ubiquitous proteoglycan can regulate both angiogenesis and autophagy through a dual receptor antagonism. The biological properties of this natural endogenous protein place endorepellin as a potential therapeutic agent against cancer or diseases where angiogenesis is prominent.
C1 Thomas Jefferson Univ, Sidney Kimmel Med Coll, Kimmel Canc Ctr, Dept Pathol Anat & Cell Biol, Philadelphia, PA 19107 USA.
   Thomas Jefferson Univ, Sidney Kimmel Med Coll, Kimmel Canc Ctr, Canc Cell Biol & Signalling Program, Philadelphia, PA 19107 USA.
RP Iozzo, RV (corresponding author), Thomas Jefferson Univ, Sidney Kimmel Med Coll, Dept Pathol Anat & Cell Biol, 1020 Locust St,Suite 336 JAH, Philadelphia, PA 19107 USA.
EM renato.iozzo@jefferson.edu
RI Douglass, Stephen/ABH-4878-2020; Iozzo, Renato/AAS-1980-2020
OI Douglass, Stephen/0000-0003-1562-2235; Iozzo, Renato/0000-0002-5908-5112
FU National Institutes of HealthUnited States Department of Health & Human
   ServicesNational Institutes of Health (NIH) - USA [RO1 CA39481, RO1
   CA47282, RO1 CA164462]; NATIONAL CANCER INSTITUTEUnited States
   Department of Health & Human ServicesNational Institutes of Health (NIH)
   - USANIH National Cancer Institute (NCI) [R01CA039481, R01CA047282,
   R01CA164462] Funding Source: NIH RePORTER
FX The authors declare that they have no competing interests. All the
   authors were involved in drafting the article, and approved the final
   version to be published. The original research was supported in part by
   National Institutes of Health Grants RO1 CA39481, RO1 CA47282 and RO1
   CA164462.
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NR 153
TC 49
Z9 49
U1 1
U2 5
PU TAYLOR & FRANCIS INC
PI PHILADELPHIA
PA 530 WALNUT STREET, STE 850, PHILADELPHIA, PA 19106 USA
SN 0300-8207
EI 1607-8438
J9 CONNECT TISSUE RES
JI Connect. Tissue Res.
PY 2015
VL 56
IS 5
SI SI
BP 381
EP 391
DI 10.3109/03008207.2015.1045297
PG 11
WC Cell Biology; Orthopedics
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Cell Biology; Orthopedics
GA DD3KY
UT WOS:000369822300005
PM 26181327
OA Green Submitted, Green Accepted
DA 2022-04-25
ER

PT J
AU Keles, U
   Iscan, E
   Yilmaz, HE
   Karakulah, G
   Suner, A
   Bal, E
   Tasdemir, N
   Cavga, AD
   Ekin, U
   Mutlu, Z
   Kahyaoglu, S
   Serdar, MA
   Atabey, N
   Ozturk, M
AF Keles, Umur
   Iscan, Evin
   Yilmaz, Huriye Erbak
   Karakulah, Gokhan
   Suner, Asli
   Bal, Erhan
   Tasdemir, Nilgun
   Cavga, Ayse Derya
   Ekin, Umut
   Mutlu, Zeynep
   Kahyaoglu, Sila
   Serdar, Muhittin A.
   Atabey, Nese
   Ozturk, Mehmet
TI Differential expression of full-length and NH2 terminally truncated
   FAM134B isoforms in normal physiology and cancer
SO AMERICAN JOURNAL OF PHYSIOLOGY-GASTROINTESTINAL AND LIVER PHYSIOLOGY
LA English
DT Article
DE autophagy; endoplasmic reticulum; ER-phagy; gene expression; gene
   knockout; hepatocellular carcinoma; reticulophagy
ID GOLGI PROTEIN; MICE; METABOLISM; AUTOPHAGY; CHOLESTEROL; INHIBITION;
   STARVATION
AB Selective autophagy of the endoplasmic reticulum (ER), namely ER-phagy, is mediated by ER-localized receptors, which are recognized and sequestered by GABARAP/LC3B-decorated phagophores and transferred to lysosomes for degradation. Being one such receptor, FAM134B plays critical roles in cellular processes such as protein quality control and neuronal survival. FAM134B has also been associated with different cancers, although its exact role remains elusive. We report here that the FAM134B gene encodes not one but at least two different protein isoforms: the full-length and the NH2 terminally truncated forms. Their relative expression shows extreme variation, both within normal tissues and among cancer types. Expression of full-length FAM134B is restricted to the brain, testis, spleen, and prostate. In contrast, NH2 terminally truncated FAM134B is dominant in the heart, skeletal muscle, kidney, pancreas, and liver. We compared wild-type and knockout mice to study the role of the Fam134b gene in starvation. NH2 terminally truncated FAM134B-2 was induced in the liver, skeletal muscle, and heart but not in the pancreas and stomach following starvation. Upon starvation, Fam134b(-/-) mice differed from wild-type mice by less weight loss and less hyperaminoacidemic and hypocalcemic response but increased levels of serum albumin, total serum proteins, and a-amylase. Interestingly, either NH2 terminally truncated FAM134B or both isoforms were downregulated in liver, lung, and colon cancers. In contrast, upregulation was observed in stomach and chromophobe kidney cancers.
   NEW & NOTEWORTHY We reported tissues expressing FAM134B2 such as the kidney, muscle, heart, and pancreas, some of which exhibit stimulated expression upon nutrient starvation. We also demonstrated the effect of Fam134b deletion during ad libitum and starvation conditions. Resistance to weight loss and hypocalcemia, accompanied by an increase in serum albumin and alpha-amylase levels, indicate critical roles of Fam134b in physiology. Furthermore, the differential expression of FAM134B isoforms was shown to be significantly dysregulated in human cancers.
C1 [Keles, Umur; Iscan, Evin; Karakulah, Gokhan; Bal, Erhan; Ekin, Umut; Mutlu, Zeynep; Kahyaoglu, Sila; Atabey, Nese; Ozturk, Mehmet] Izmir Biomed & Genome Ctr, Izmir, Turkey.
   [Keles, Umur; Iscan, Evin; Yilmaz, Huriye Erbak; Karakulah, Gokhan; Ekin, Umut] Dokuz Eylul Univ, Izmir Int Biomed & Genome Inst, Izmir, Turkey.
   [Suner, Asli] Ege Univ, Dept Biostat & Med Informat, Izmir, Turkey.
   [Tasdemir, Nilgun; Cavga, Ayse Derya] Bilkent Univ, Dept Mol Biol & Genet, Ankara, Turkey.
   [Serdar, Muhittin A.] Acibadem Univ, Dept Biochem, Istanbul, Turkey.
RP Ozturk, M (corresponding author), Izmir Biomed & Genome Ctr, Izmir, Turkey.
EM mehmet.orturk@ibg.edu.tr
RI Atabey, Nese/A-1853-2018; İşcan, Evin/AAA-4818-2022; SUNER,
   ASLI/C-1032-2012; OZTURK, MEHMET/AAS-7241-2021
OI Atabey, Nese/0000-0003-4966-2980; SUNER, ASLI/0000-0002-6872-9901;
   OZTURK, MEHMET/0000-0002-6092-9706; Cavga, Ayse
   Derya/0000-0001-5017-5042; Keles, Umur/0000-0002-6771-3721
FU Dokuz Eylul University, Department of Scientific Research ProjectsDokuz
   Eylul University [2014.KB.SAG.047]; Izmir Biomedicine and Genome
   Center's (IBG) institutional funds; Common Fund of the Office of the
   Director of the National Institutes of Health; National Cancer
   InstituteUnited States Department of Health & Human ServicesNational
   Institutes of Health (NIH) - USANIH National Cancer Institute (NCI);
   National Human Genome Research InstituteUnited States Department of
   Health & Human ServicesNational Institutes of Health (NIH) - USANIH
   National Human Genome Research Institute (NHGRI); National Heart, Lung,
   and Blood InstituteUnited States Department of Health & Human
   ServicesNational Institutes of Health (NIH) - USANIH National Heart Lung
   & Blood Institute (NHLBI); National Institute on Drug AbuseUnited States
   Department of Health & Human ServicesNational Institutes of Health (NIH)
   - USANIH National Institute on Drug Abuse (NIDA)European Commission;
   National Institute of Mental HealthUnited States Department of Health &
   Human ServicesNational Institutes of Health (NIH) - USANIH National
   Institute of Mental Health (NIMH); National Institute of Neurological
   Disorders and StrokeUnited States Department of Health & Human
   ServicesNational Institutes of Health (NIH) - USANIH National Institute
   of Neurological Disorders & Stroke (NINDS)
FX This study is supported by Dokuz Eylul University, Department of
   Scientific Research Projects (with the Project code 2014.KB.SAG.047),
   and Izmir Biomedicine and Genome Center's (IBG) institutional funds. The
   GenotypeTissue Expression (GTEx) Project was supported by the Common
   Fund of the Office of the Director of the National Institutes of Health
   and by the National Cancer Institute, National Human Genome Research
   Institute, National Heart, Lung, and Blood Institute, National Institute
   on Drug Abuse, National Institute of Mental Health, and National
   Institute of Neurological Disorders and Stroke. The data used for the
   analyses described in this article were obtained from the GTEx Portal on
   11/14/2018 and/or dbGaP Accession No. phs000424.v3.p1.
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NR 46
TC 2
Z9 2
U1 0
U2 0
PU AMER PHYSIOLOGICAL SOC
PI Rockville
PA 6120 Executive Blvd, Suite 600, Rockville, MD, UNITED STATES
SN 0193-1857
EI 1522-1547
J9 AM J PHYSIOL-GASTR L
JI Am. J. Physiol.-Gastroint. Liver Physiol.
PD DEC
PY 2020
VL 319
IS 6
BP G733
EP G747
DI 10.1152/ajpgi.00094.2020
PG 15
WC Gastroenterology & Hepatology; Physiology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology; Physiology
GA RC3LQ
UT WOS:000632705700001
PM 33052704
OA Green Submitted, Green Published
DA 2022-04-25
ER

PT J
AU Nicoli, ER
   Dumitrescu, T
   Uscatu, CD
   Popescu, FD
   Streata, I
   Sosoi, SS
   Ivanov, P
   Dumitrescu, A
   Barbalan, A
   Lungulescu, D
   Petrescu, F
   Schenker, M
   Verdes, D
   Saftoiu, A
AF Nicoli, Elena-Raluca
   Dumitrescu, Theodor
   Uscatu, Constantin-Daniel
   Popescu, Florin-Dan
   Streata, Ioana
   Sosoi, Simona Serban
   Ivanov, Petar
   Dumitrescu, Alexandra
   Barbalan, Alexandru
   Lungulescu, Dan
   Petrescu, Florin
   Schenker, Michael
   Verdes, Doina
   Saftoiu, Adrian
TI Determination of autophagy gene ATG16L1 polymorphism in human colorectal
   cancer
SO ROMANIAN JOURNAL OF MORPHOLOGY AND EMBRYOLOGY
LA English
DT Article
DE ATG16L1; gene polymorphism; colorectal cancer; autophagy
ID GENOME-WIDE ASSOCIATION; CROHNS-DISEASE; SUSCEPTIBILITY; INFLAMMATION;
   CELLS; IL23R; PHENOTYPE; INFECTION; IMMUNITY; VARIANT
AB Autophagy has emerged not only as an essential repair mechanism to degrade damaged organelles and proteins but also as a major player in protection of tumor cells from multiple stresses. It was shown that autophagy gene polymorphisms are correlated with development of chronic inflammatory lesions, which represent a risk factor for colorectal tumors. In this study, we aimed to determine if ATG16L1 +898A>G (Thr300Ala) polymorphism is associated with an increased risk of developing colorectal cancer (CRC) and to establish correlations between ATG16L1 genotypes and the major clinical and morphological parameters. We observed that subjects carrying GG genotype were at a higher risk for CRC (OR 1.99, 95% Cl: 1.02-3.91, p=0.039) when compared with the more frequent AA genotype, furthermore this was even more consistent in male subjects (OR 2.72, 95% Cl: 1.11-6.63, p=0.019) but not in female subjects (OR 1.29, 95% Cl: 0.43-3.86, p=0.652). In addition, we noticed a correlation between ATG16L1 GO genotype and tumor stage in moderately and poorly differentiated CRC cases. GG genotype carrying patients were at a higher risk for CRC (OR 5.19, 95% Cl: 1.50-17.87, p=0.002) when compared with the more frequent AA genotype. Such correlation suggests a possible role of autophagy gene polymorphisms in the development of human colorectal cancer.
C1 [Nicoli, Elena-Raluca; Uscatu, Constantin-Daniel; Streata, Ioana; Sosoi, Simona Serban] Univ Med & Pharm Craiova, Human Genom Lab, Craiova 200638, Romania.
   [Nicoli, Elena-Raluca; Ivanov, Petar] Univ Med & Pharm Craiova, Dept Pharmacol, Craiova 200638, Romania.
   [Dumitrescu, Theodor] Univ Med & Pharm Craiova, Dept Surg, Craiova 200638, Romania.
   [Dumitrescu, Theodor; Barbalan, Alexandru] Emergency Cty Hosp, Med Surg Clin 2, Craiova, Romania.
   [Uscatu, Constantin-Daniel] Emergency Cty Hosp, Dept Pathol, Craiova, Romania.
   [Popescu, Florin-Dan] Carol Davila Univ Med & Pharm, Dept Allergy & Clin Immunol, Bucharest, Romania.
   [Dumitrescu, Alexandra] Emergency Cty Hosp, Clin Med Oncol, Craiova, Romania.
   [Barbalan, Alexandru; Saftoiu, Adrian] Univ Med & Pharm Craiova, Res Ctr Gastroenterol & Hepatol, Craiova 200638, Romania.
   [Lungulescu, Dan] OncoLab Med Ctr, Craibva, Romania.
   [Petrescu, Florin] Univ Med & Pharm Craiova, Dept Med Semiol, Craiova 200638, Romania.
   [Schenker, Michael] Univ Med & Pharm Craiova, Dept Oncol, Craiova 200638, Romania.
   [Verdes, Doina] Victor Babes Univ Med & Pharm, Dept Cellular & Mol Biol, Timisoara, Romania.
   [Saftoiu, Adrian] Univ Copenhagen, Fac Med & Hlth Sci, DK-1168 Copenhagen, Denmark.
   [Saftoiu, Adrian] Univ Copenhagen, Herlev Hosp, Gastrointestinal Unit, DK-1168 Copenhagen, Denmark.
RP Nicoli, ER (corresponding author), Univ Med & Pharm Craiova, Human Genom Lab, 66 1 May Ave, Craiova 200638, Romania.
EM raluca@nicoli.ro
RI Schenker, Michael/AAD-6920-2022; Nicoli, Elena-Raluca/F-3968-2011;
   Popescu, Florin-Dan/AAL-4750-2021; Saftoiu, Adrian/C-2792-2011;
   Lungulescu, Dan/F-4085-2017
OI Schenker, Michael/0000-0003-2645-6391; Nicoli,
   Elena-Raluca/0000-0002-5545-630X; Popescu,
   Florin-Dan/0000-0001-6316-3155; Saftoiu, Adrian/0000-0001-7993-8269;
   Dumitrescu, Theodor Viorel/0000-0002-2485-7821; Calota,
   Firmilian/0000-0002-2689-5477
FU Sectorial Operational Programme Human Resources Development; European
   Social FundEuropean Social Fund (ESF); Romanian GovernmentRomanian
   Government; Romanian National Authority for Scientific Research,
   CNCS-UEFISCDIConsiliul National al Cercetarii Stiintifice (CNCS)Unitatea
   Executiva pentru Finantarea Invatamantului Superior, a Cercetarii,
   Dezvoltarii si Inovarii (UEFISCDI) [PNII-CT-ERC-2012-1]; 
   [POSDRU/107/1.5/S/82705]
FX Elena-Raluca Nicoli acknowledges the support of the research grant
   POSDRU/107/1.5/S/82705 project, supported by Sectorial Operational
   Programme Human Resources Development, financed by the European Social
   Fund and the Romanian Government. First author also acknowledges that
   this work was supported by a grant of the Romanian National Authority
   for Scientific Research, CNCS-UEFISCDI, project ID PNII-CT-ERC-2012-1.
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NR 42
TC 25
Z9 26
U1 0
U2 12
PU EDITURA ACAD ROMANE
PI BUCURESTI
PA CALEA 13 SEPTEMBRIE NR 13, SECTOR 5, BUCURESTI 050711, ROMANIA
SN 1220-0522
J9 ROM J MORPHOL EMBRYO
JI Rom. J. Morphol. Embryol.
PY 2014
VL 55
IS 1
BP 57
EP 62
PG 6
WC Developmental Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Developmental Biology
GA AF4BL
UT WOS:000334656300008
PM 24715166
DA 2022-04-25
ER

PT J
AU Gabryanczyk, A
   Klimczak, S
   Szymczak-Pajor, I
   Sliwinska, A
AF Gabryanczyk, Anna
   Klimczak, Sylwia
   Szymczak-Pajor, Izabela
   Sliwinska, Agnieszka
TI Is Vitamin D Deficiency Related to Increased Cancer Risk in Patients
   with Type 2 Diabetes Mellitus?
SO INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
LA English
DT Review
DE vitamin D deficiency; type 2 diabetes (T2DM); cancer
ID CIRCULATING 25-HYDROXYVITAMIN D; HUMAN-COLON-CANCER;
   NECROSIS-FACTOR-ALPHA; ROR-GAMMA EXPRESSION; PROTEIN-KINASE CK2;
   D-BINDING PROTEIN; CELL LUNG-CANCER; D-RECEPTOR FOKI; FACTOR-KAPPA-B;
   PROSTATE-CANCER
AB There is mounting evidence that type 2 diabetes mellitus (T2DM) is related with increased risk for the development of cancer. Apart from shared common risk factors typical for both diseases, diabetes driven factors including hyperinsulinemia, insulin resistance, hyperglycemia and low grade chronic inflammation are of great importance. Recently, vitamin D deficiency was reported to be associated with the pathogenesis of numerous diseases, including T2DM and cancer. However, little is known whether vitamin D deficiency may be responsible for elevated cancer risk development in T2DM patients. Therefore, the aim of the current review is to identify the molecular mechanisms by which vitamin D deficiency may contribute to cancer development in T2DM patients. Vitamin D via alleviation of insulin resistance, hyperglycemia, oxidative stress and inflammation reduces diabetes driven cancer risk factors. Moreover, vitamin D strengthens the DNA repair process, and regulates apoptosis and autophagy of cancer cells as well as signaling pathways involved in tumorigenesis i.e., tumor growth factor beta (TGF beta), insulin-like growth factor (IGF) and Wnt-beta-Cathenin. It should also be underlined that many types of cancer cells present alterations in vitamin D metabolism and action as a result of Vitamin D Receptor (VDR) and CYP27B1 expression dysregulation. Although, numerous studies revealed that adequate vitamin D concentration prevents or delays T2DM and cancer development, little is known how the vitamin affects cancer risk among T2DM patients. There is a pressing need for randomized clinical trials to clarify whether vitamin D deficiency may be a factor responsible for increased risk of cancer in T2DM patients, and whether the use of the vitamin by patients with diabetes and cancer may improve cancer prognosis and metabolic control of diabetes.
C1 [Gabryanczyk, Anna; Szymczak-Pajor, Izabela; Sliwinska, Agnieszka] Med Univ Lodz, Dept Nucle Acid Biochem, 251 Pomorska Str, PL-92213 Lodz, Poland.
   [Klimczak, Sylwia] Med Univ Lodz, Student Sci Soc Civilizat Dis, 251 Pomorska, PL-92213 Lodz, Poland.
RP Sliwinska, A (corresponding author), Med Univ Lodz, Dept Nucle Acid Biochem, 251 Pomorska Str, PL-92213 Lodz, Poland.
EM anna.gabryanczyk@umed.lodz.pl; sylwia.cichuta@stud.umed.lodz.pl;
   izabela.szymczak@umed.lodz.pl; agnieszka.sliwinska@umed.lodz.pl
OI Szymczak-Pajor, Izabela/0000-0002-6545-579X; Sliwinska,
   Agnieszka/0000-0002-6864-0704
FU Medical University of Lodz [503/1-15901/503-21-001]
FX This paper was supported by the grant from Medical University of Lodz
   (No. 503/1-15901/503-21-001)
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IS 12
AR 6444
DI 10.3390/ijms22126444
PG 33
WC Biochemistry & Molecular Biology; Chemistry, Multidisciplinary
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Chemistry
GA SZ0SB
UT WOS:000666285300001
PM 34208589
OA gold, Green Published
DA 2022-04-25
ER

PT J
AU Huang, XM
   Huang, JJ
   Du, JJ
   Zhang, N
   Long, Z
   Yang, Y
   Zhong, FF
   Zheng, BW
   Shen, YF
   Huang, Z
   Qin, X
   Chen, JH
   Lin, QY
   Lin, WJ
   Ma, WZ
AF Huang, Xiao-ming
   Huang, Jia-jun
   Du, Jing-jing
   Zhang, Na
   Long, Ze
   Yang, You
   Zhong, Fang-fang
   Zheng, Bo-wen
   Shen, Yun-fu
   Huang, Zhe
   Qin, Xiang
   Chen, Jun-he
   Lin, Qian-yu
   Lin, Wan-jun
   Ma, Wen-zhe
TI Autophagy inhibitors increase the susceptibility of KRAS-mutant human
   colorectal cancer cells to a combined treatment of 2-deoxy-D-glucose and
   lovastatin
SO ACTA PHARMACOLOGICA SINICA
LA English
DT Article
DE human colorectal cancers; lovastatin; 2DG; glycolysis; OXPHOS;
   autophagy; chloroquine; hydroxychloroquine
AB RAS-driven colorectal cancer relies on glucose metabolism to support uncontrolled growth. However, monotherapy with glycolysis inhibitors like 2-deoxy-D-glucose causes limited effectiveness. Recent studies suggest that anti-tumor effects of glycolysis inhibition could be improved by combination treatment with inhibitors of oxidative phosphorylation. In this study we investigated the effect of a combination of 2-deoxy-D-glucose with lovastatin (a known inhibitor of mevalonate pathway and oxidative phosphorylation) on growth of KRAS-mutant human colorectal cancer cell lines HCT116 and LoVo. A combination of lovastatin (>3.75 mu M) and 2-deoxy-D-glucose (>1.25 mM) synergistically reduced cell viability, arrested cells in the G(2)/M phase, and induced apoptosis. The combined treatment also reduced cellular oxygen consumption and extracellular acidification rate, resulting in decreased production of ATP and lower steady-state ATP levels. Energy depletion markedly activated AMPK, inhibited mTOR and RAS signaling pathways, eventually inducing autophagy, the cellular pro-survival process under metabolic stress, whereas inhibition of autophagy by chloroquine (6.25 mu M) enhanced the cytotoxic effect of the combination of lovastatin and 2-deoxy-D-glucose. These in vitro experiment results were reproduced in a nude mouse xenograft model of HCT116 cells. Our findings suggest that concurrently targeting glycolysis, oxidative phosphorylation, and autophagy may be a promising regimen for the management of RAS-driven colorectal cancers.
C1 [Huang, Xiao-ming; Huang, Jia-jun; Du, Jing-jing; Zhang, Na; Long, Ze; Yang, You; Zhong, Fang-fang; Zheng, Bo-wen; Shen, Yun-fu; Huang, Zhe; Qin, Xiang; Chen, Jun-he; Lin, Qian-yu; Lin, Wan-jun; Ma, Wen-zhe] Macau Univ Sci & Technol, State Key Lab Qual Res Chinese Med, Macau, Peoples R China.
RP Ma, WZ (corresponding author), Macau Univ Sci & Technol, State Key Lab Qual Res Chinese Med, Macau, Peoples R China.
EM wzma@must.edu.mo
RI /AAS-7015-2021
FU Science and Technology Development Fund, Macau SAR, China [0036/2020/A1,
   0013/2019/A1, 0039/2020/A]
FX This work was funded by the Science and Technology Development Fund,
   Macau SAR, China (File no. 0036/2020/A1, 0013/2019/A1 and 0039/2020/A).
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NR 61
TC 8
Z9 8
U1 5
U2 20
PU NATURE PUBL GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 1671-4083
EI 1745-7254
J9 ACTA PHARMACOL SIN
JI Acta Pharmacol. Sin.
PD NOV
PY 2021
VL 42
IS 11
BP 1875
EP 1887
DI 10.1038/s41401-021-00612-9
EA FEB 2021
PG 13
WC Chemistry, Multidisciplinary; Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Chemistry; Pharmacology & Pharmacy
GA WQ9BZ
UT WOS:000619696700001
PM 33608672
DA 2022-04-25
ER

PT J
AU Zhou, CX
   Gu, J
   Zhang, G
   Dong, D
   Yang, QY
   Chen, MB
   Xu, DF
AF Zhou, Chunxian
   Gu, Jun
   Zhang, Gang
   Dong, Da
   Yang, Qunying
   Chen, Min-Bin
   Xu, Dongfeng
TI AMPK-autophagy inhibition sensitizes icaritin-induced anti-colorectal
   cancer cell activity
SO ONCOTARGET
LA English
DT Article
DE colorectal cancer; icaritin; autophagy; AMPK; chemosensitization
ID ACTIVATED PROTEIN-KINASE; SMALL-MOLECULE ACTIVATOR; COMPOUND 13;
   PRECLINICAL EVALUATION; THERAPEUTIC TARGET; ANTICANCER AGENT;
   PHOSPHORYLATION; GROWTH; PATHWAY; DEATH
AB The current research studied the potential effect of autophagy on icaritin-induced anti-colorectal cancer (CRC) cell activity. Treatment of icaritin in both primary and established (HT-29) CRC cells induced feedback activation of autophagy, evidenced by p62 degradation, Beclin-1 and autophagy-related gene-5 (ATG-5) upregulation, as well as light chain 3B (LC3B)-GFP puncta formation. Pharmacological inhibiting of autophagy dramatically potentiated icaritin-induced CRC cell death and apoptosis. Meanwhile, shRNA-mediated knockdown of Beclin-1 or ATG-5 also sensitized icaritin-induced CRC cell death and apoptosis. Icaritin activated AMP-activated protein kinase (AMPK) signaling in CRC cells, functioning as the upstream signaling for autophagy activation. shRNA/siRNA-mediated knockdown of AMPKa1inhibited icaritin-induced autophagy activation, but exacerbated CRC cell death. On the other hand, the AMPK activator compound 13 (C13) or the autophagy activator MHY1485 attenuated icaritin-induced cytotoxicity. In nude mice, icaritin (oral administration)-induced HT-29 tumor growth inhibition was potentiated when combined with AMPKa1 shRNA knockdown in tumors. We conclude that feedback activation of AMPK-autophagy pathway could be a primary resistance factor of icaritin.
C1 [Zhou, Chunxian; Zhang, Gang; Dong, Da; Yang, Qunying; Xu, Dongfeng] Nantong Univ, Wujiang Hosp, Dept Intervent Radiol, Suzhou, Peoples R China.
   [Gu, Jun] Soochow Univ, Affiliated Hosp 2, Dept Orthoped, Suzhou, Peoples R China.
   [Chen, Min-Bin] Jiangsu Univ, Kunshan Peoples Hosp 1, Dept Oncol, Kunshan 215300, Peoples R China.
RP Xu, DF (corresponding author), Nantong Univ, Wujiang Hosp, Dept Intervent Radiol, Suzhou, Peoples R China.; Chen, MB (corresponding author), Jiangsu Univ, Kunshan Peoples Hosp 1, Dept Oncol, Kunshan 215300, Peoples R China.
EM cmb1981@163.com; drxudongfeng6@126.com
FU WuJiang Science Bureau; National Natural Science Foundation of
   ChinaNational Natural Science Foundation of China (NSFC) [81472786];
   Foundation of tumor clinical and basic research team of Kunshan First
   People's Hospital [KYC005]
FX The study was supported by WuJiang Science Bureau and the National
   Natural Science Foundation of China (81472786), the Foundation of tumor
   clinical and basic research team of Kunshan First People's Hospital
   (KYC005).
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NR 48
TC 25
Z9 28
U1 1
U2 11
PU IMPACT JOURNALS LLC
PI ORCHARD PARK
PA 6666 E QUAKER ST, STE 1, ORCHARD PARK, NY 14127 USA
EI 1949-2553
J9 ONCOTARGET
JI Oncotarget
PD FEB 28
PY 2017
VL 8
IS 9
BP 14736
EP 14747
DI 10.18632/oncotarget.14718
PG 12
WC Oncology; Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Cell Biology
GA EN4YV
UT WOS:000396013700042
PM 28103582
OA gold, Green Submitted, Green Published
DA 2022-04-25
ER

PT J
AU Ferro, F
   Servais, S
   Besson, P
   Roger, S
   Dumas, JF
   Brisson, L
AF Ferro, Fabio
   Servais, Stephane
   Besson, Pierre
   Roger, Sebastien
   Dumas, Jean-Francois
   Brisson, Lucie
TI Autophagy and mitophagy in cancer metabolic remodelling
SO SEMINARS IN CELL & DEVELOPMENTAL BIOLOGY
LA English
DT Review
DE Cancer metabolism; Autophagy; Mitophagy; ROS; Mitochondria; Ion channel
ID HYPOXIA-INDUCED AUTOPHAGY; TUMOR-SUPPRESSOR GENE; CELL-DEATH; OXIDATIVE
   STRESS; MITOCHONDRIAL DYSFUNCTION; HEPATOCELLULAR-CARCINOMA; REGULATE
   AUTOPHAGY; COLORECTAL-CANCER; LIPID-METABOLISM; CA2+ TRANSFER
AB Metabolic reprogramming in tumours is now recognized as a hallmark of cancer, participating both in tumour growth and cancer progression. Cancer cells develop global metabolic adaptations allowing them to survive in the low oxygen and nutrient tumour microenvironment. Among these metabolic adaptations, cancer cells use glycolysis but also mitochondrial oxidations to produce ATP and building blocks needed for their high proliferation rate. Another particular adaptation of cancer cell metabolism is the use of autophagy and specific forms of autophagy like mitophagy to recycle intracellular components in condition of metabolic stress or during anticancer treatments. The plasticity of cancer cell metabolism is a major limitation of anticancer treatments and could participate to therapy resistances. The aim of this review is to report recent advances in the understanding of the relationship between tumour metabolism and autophagy/mitophagy in order to propose new therapeutic strategies.
C1 [Ferro, Fabio; Servais, Stephane; Besson, Pierre; Dumas, Jean-Francois; Brisson, Lucie] Univ Tours, INSERM, UMR1069, Nutr Croissance & Canc, Tours, France.
   [Roger, Sebastien] Univ Tours, EA4245, Transplantat Immunol & Inflammat, Tours, France.
RP Brisson, L (corresponding author), Univ Tours, INSERM, UMR 1069, 10 Blvd Tonnelle, F-37032 Tours, France.
EM lucie.brisson@univ-tours.fr
RI Dumas, Jean-François/S-7486-2017; Servais, Stephane/Q-6057-2017; Dumas,
   Jean-François/AAN-5035-2020; Brisson, Lucie/R-1179-2016
OI Dumas, Jean-François/0000-0002-2293-6606; Servais,
   Stephane/0000-0002-3127-9679; Dumas, Jean-François/0000-0002-2293-6606;
   Brisson, Lucie/0000-0001-7811-1382
FU InsermInstitut National de la Sante et de la Recherche Medicale
   (Inserm)European Commission; Ligue Nationale Contre le Cancer
   -Inter-region Grand-Ouest; Fondation ARC; Canceropole Grand-Ouest
FX We thank all our colleagues from the Universite de Tours-Inserm UMR1069
   for all constructive discussion and Ms. Catherine Le Roy for secretary
   and administrative assistance. The work performed at the Universite de
   Tours-Inserm UMR1069 was supported by the Inserm, the "Ligue Nationale
   Contre le Cancer -Inter-region Grand-Ouest", the Fondation ARC and the
   "Canceropole Grand-Ouest".; Finally, we wish to apologize to all
   researchers whose relevant works, owing to the limited length of this
   article format, could not be cited in this review.
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NR 169
TC 44
Z9 43
U1 3
U2 73
PU ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD
PI LONDON
PA 24-28 OVAL RD, LONDON NW1 7DX, ENGLAND
SN 1084-9521
J9 SEMIN CELL DEV BIOL
JI Semin. Cell Dev. Biol.
PD FEB
PY 2020
VL 98
SI SI
BP 129
EP 138
DI 10.1016/j.semcdb.2019.05.029
PG 10
WC Cell Biology; Developmental Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Cell Biology; Developmental Biology
GA KD5XE
UT WOS:000507938200015
PM 31154012
OA Green Submitted, Bronze
DA 2022-04-25
ER

PT J
AU Parashar, K
   Sood, S
   Mehaidli, A
   Curran, C
   Vegh, C
   Nguyen, C
   Pignanelli, C
   Wu, JZ
   Liang, G
   Wang, Y
   Pandey, S
AF Parashar, Krishan
   Sood, Siddhartha
   Mehaidli, Ali
   Curran, Colin
   Vegh, Caleb
   Nguyen, Christopher
   Pignanelli, Christopher
   Wu, Jianzhang
   Liang, Guang
   Wang, Yi
   Pandey, Siyaram
TI Evaluating the Anti-cancer Efficacy of a Synthetic Curcumin Analog on
   Human Melanoma Cells and Its Interaction with Standard Chemotherapeutics
SO MOLECULES
LA English
DT Article
DE melanoma; curcumin analog; apoptosis; oxidative stress; drug-drug
   interaction; tamoxifen; taxol; cisplatin
ID MITOCHONDRIAL DYSFUNCTION; PROOXIDANT ACTIVITY; APOPTOSIS PATHWAYS;
   CANCER-CELLS; COMPLEX-I; MECHANISMS; INDUCTION; TAMOXIFEN; AUTOPHAGY;
   SURVIVAL
AB Melanoma is the leading cause of skin-cancer related deaths in North America. Metastatic melanoma is difficult to treat and chemotherapies have limited success. Furthermore, chemotherapies lead to toxic side effects due to nonselective targeting of normal cells. Curcumin is a natural product of Curcuma longa (turmeric) and has been shown to possess anti-cancer activity. However, due to its poor bioavailability and stability, natural curcumin is not an effective cancer treatment. We tested synthetic analogs of curcumin that are more stable. One of these derivatives, Compound A, has shown significant anti-cancer efficacy in colon, leukemia, and triple-negative inflammatory breast cancer cells. However, the effects of Compound A against melanoma cells have not been studied before. In this study, for the first time, we demonstrated the efficacy of Compound A for the selective induction of apoptosis in melanoma cells and its interaction with tamoxifen, taxol, and cisplatin. We found that Compound A induced apoptosis selectively in human melanoma cells by increasing oxidative stress. The anti-cancer activity of Compound A was enhanced when combined with tamoxifen and the combination treatment did not result in significant toxicity to noncancerous cells. Additionally, Compound A did not interact negatively with the anti-cancer activity of taxol and cisplatin. These results indicate that Compound A could be developed as a selective and effective melanoma treatment either alone or in combination with other non-toxic agents like tamoxifen.
C1 [Parashar, Krishan; Sood, Siddhartha; Mehaidli, Ali; Curran, Colin; Vegh, Caleb; Nguyen, Christopher; Pignanelli, Christopher; Pandey, Siyaram] Univ Windsor, Dept Chem & Biochem, 401 Sunset Ave, Windsor, ON N9B 3P4, Canada.
   [Wu, Jianzhang; Liang, Guang; Wang, Yi] Whenzhou Med Univ, Chem Biol Res Ctr, Sch Pharmaceut Sci, Wenzhou 325035, Peoples R China.
RP Pandey, S (corresponding author), Univ Windsor, Dept Chem & Biochem, 401 Sunset Ave, Windsor, ON N9B 3P4, Canada.
EM spandey@uwindsor.ca
RI Pandey, Siyaram/AAI-5491-2020
OI Pignanelli, Christopher/0000-0001-7120-4818; Sood,
   Siddhartha/0000-0003-3531-5961
FU National Natural Science Foundation of ChinaNational Natural Science
   Foundation of China (NSFC) [81472307]
FX Funding for this work was by generous donations by the Windsor Mold
   Group (Windsor, Ontario), Lotte and John Hecht Foundation, and Natural
   Science and Engineering Council of Canada. A grant from the National
   Natural Science Foundation of China (81472307) was used to fund the
   synthesis of each analog.
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NR 48
TC 7
Z9 7
U1 0
U2 3
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 1420-3049
J9 MOLECULES
JI Molecules
PD JUL 1
PY 2019
VL 24
IS 13
AR 2483
DI 10.3390/molecules24132483
PG 17
WC Biochemistry & Molecular Biology; Chemistry, Multidisciplinary
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Chemistry
GA IK6MH
UT WOS:000476700300137
PM 31284561
OA Green Published, Green Submitted
DA 2022-04-25
ER

PT J
AU Mihanfar, A
   Darband, SG
   Sadighparvar, S
   Kaviani, M
   Mirza-Aghazadeh-Attari, M
   Yousefi, B
   Majidinia, M
AF Mihanfar, Ainaz
   Darband, Saber Ghazizadeh
   Sadighparvar, Shirin
   Kaviani, Mojtaba
   Mirza-Aghazadeh-Attari, Mohammad
   Yousefi, Bahman
   Majidinia, Maryam
TI In vitro and in vivo anticancer effects of syringic acid on colorectal
   cancer: Possible mechanistic view
SO CHEMICO-BIOLOGICAL INTERACTIONS
LA English
DT Article
DE Colorectal cancer; Syringic acid; Proliferation; Apoptosis; Autophagy
ID CAFFEIC ACID; CELLS; PROLIFERATION; AUTOPHAGY; BREAST; GROWTH; ESTER
AB This study aimed to evaluate the in vitro effects of syringic acid on human colorectal cancer cells (SW-480) and the effect of orally administered syringic acid on in vivo models of colorectal cancer induced in rats by administration of 1,2-dimethylhydrazine (DMH). In vitro effects of syringic acid treatment on human colorectal cancer SW-480 cell lines were assessed by performing cell proliferation assay (MTT and Trypan Blue staining), apoptosis assays (TUNEL assay, Annexin-V/PI flowcytometry and lactate dehydrogenase release assay), measuring reactive oxygen species (ROS), antioxidant enzymes and DNA damage, and evaluating protein levels of proliferative genes, and autophagy markers. In vitro anti-cancer roles of syringic acid were studied in rats with DMH-induced colorectal cancer cells. The effect of orally administered syringic acid (50 mg/kg) on tumor growth and incidence was studied in four groups (n = 6) of animals injected with DMH and treated for 15 weeks. Syringic acid treatment resulted in a significant dose-dependent inhibition of cellular proliferation, induction of apoptosis through increasing cellular ROS and DNA damage levels, as well as downregulating major proliferative genes. In vivo, treatment of rats with syringic acid demonstrated a statistically significant tumor volume and incidence reduction when compared to the control. This is the first study demonstrating an in vivo growth inhibitory effect of orally administered syringic acid on colorectal tumors in rats.
C1 [Mihanfar, Ainaz] Urmia Univ Med Sci, Fac Med, Dept Biochem, Orumiyeh, Iran.
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   [Kaviani, Mojtaba] Acadia Univ, Sch Nutr & Dietet, Wolfville, NS B4P 2R6, Canada.
   [Mirza-Aghazadeh-Attari, Mohammad] Tabriz Univ Med Sci, Student Res Comm, Tabriz, Iran.
   [Mirza-Aghazadeh-Attari, Mohammad] Tabriz Univ Med Sci, Aging Res Inst, Tabriz, Iran.
   [Yousefi, Bahman] Tabriz Univ Med Sci, Immunol Res Ctr, Tabriz, Iran.
   [Majidinia, Maryam] Urmia Univ Med Sci, Solid Tumor Res Ctr, Orjhans St,Resalat Blvd, Orumiyeh, Iran.
RP Majidinia, M (corresponding author), Urmia Univ Med Sci, Solid Tumor Res Ctr, Orjhans St,Resalat Blvd, Orumiyeh, Iran.
EM majidinia.m@umsu.ac.ir
OI Mirza-Aghazadeh-Attari, Mohammad/0000-0001-7927-6912
FU Urmia University of Medical Sciences [273]
FX This study was funded by Urmia University of Medical Sciences (grant
   number: 273).
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NR 38
TC 2
Z9 2
U1 1
U2 5
PU ELSEVIER IRELAND LTD
PI CLARE
PA ELSEVIER HOUSE, BROOKVALE PLAZA, EAST PARK SHANNON, CO, CLARE, 00000,
   IRELAND
SN 0009-2797
EI 1872-7786
J9 CHEM-BIOL INTERACT
JI Chem.-Biol. Interact.
PD MAR 1
PY 2021
VL 337
AR 109337
DI 10.1016/j.cbi.2020.109337
EA FEB 2021
PG 11
WC Biochemistry & Molecular Biology; Pharmacology & Pharmacy; Toxicology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Pharmacology & Pharmacy; Toxicology
GA QL2OE
UT WOS:000620918900001
PM 33548266
DA 2022-04-25
ER

PT J
AU Ye, YQ
   Zhang, PJ
   Qian, YH
   Yin, BX
   Yan, MJ
AF Ye, Yongqi
   Zhang, Pengju
   Qian, Yuhang
   Yin, Baoxin
   Yan, Meijuan
TI The Effect of Pyrroloquinoline Quinone on the Expression of WISP1 in
   Traumatic Brain Injury
SO STEM CELLS INTERNATIONAL
LA English
DT Article
ID SIGNALING PATHWAY PROTEIN-1; INDUCED CARDIOMYOCYTE DEATH; BETA-CATENIN;
   ALZHEIMERS-DISEASE; GROWTH-FACTOR; AUTOPHAGY; CELLS; SURVIVAL; PQQ;
   NEUROPROTECTION
AB WISP1, as a member of the CCN4 protein family, has cell protective effects of promoting cell proliferation and inhibiting cell apoptosis. Although some studies have confirmed that WISP1 is concerned with colon cancer and lung cancer, there is little report about the influence of WISP1 in traumatic brain injury. Here, we found that the expression of WISP1 mRNA and protein decreased at 3 d and then increased at 5 d after traumatic brain injury (TBI). Meanwhile, immunofluorescence demonstrated that there was little colocation of WISP1 with GFAP, Iba1, and WISP1 colocalized with NeuN partly. WISP1 colocalized with LC3, but there was little of colocation about WISP1 with cleaved caspase-3. Subsequent study displayed that the expression of beta-catenin protein was identical to that of WISP1 after TBI. WISP1 was mainly located in cytoplasm of PC12 or SHSY5Y cells. Compared with the negative control group, WISP1 expression reduced obviously in SHSY5Y cells transfected with WISP1 si-RNA. CCK-8 assay showed that pyrroloquinoline quinone (PQQ) had little influence on viability of PC12 and SHSY5Y cells. These results suggested that WISP1 played a protective role after traumatic brain injury in rats, and this effect might be relative to autophagy caused by traumatic brain injury.
C1 [Ye, Yongqi; Zhang, Pengju; Qian, Yuhang; Yin, Baoxin; Yan, Meijuan] Nantong Univ, Jiangsu Key Lab Neuroregenerat, 19 Qixiu Rd, Nantong 226001, Peoples R China.
RP Yan, MJ (corresponding author), Nantong Univ, Jiangsu Key Lab Neuroregenerat, 19 Qixiu Rd, Nantong 226001, Peoples R China.
EM ymz@ntu.edu.cn
RI yan, mei/AAA-1379-2022
FU National Natural Scientific Foundation of ChinaNational Natural Science
   Foundation of China (NSFC) [31370803]; Application Study Program of
   Nantong City [BK2013004]; Early Pre-research Program of Nantong
   University [10ZY013]; Doctoral Program of Nantong University [12B035]
FX This work was supported by the National Natural Scientific Foundation of
   China (31370803), Application Study Program of Nantong City (BK2013004),
   Early Pre-research Program of Nantong University (10ZY013), and Doctoral
   Program of Nantong University (12B035).
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TC 11
Z9 11
U1 2
U2 5
PU HINDAWI LTD
PI LONDON
PA ADAM HOUSE, 3RD FLR, 1 FITZROY SQ, LONDON, W1T 5HF, ENGLAND
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EI 1687-9678
J9 STEM CELLS INT
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PY 2017
VL 2017
AR 4782820
DI 10.1155/2017/4782820
PG 16
WC Cell & Tissue Engineering
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Cell Biology
GA FE8KM
UT WOS:000408454000001
PM 28883836
OA Green Submitted, Green Published, gold
DA 2022-04-25
ER

PT J
AU Papatsirou, M
   Artemaki, PI
   Scorilas, A
   Kontos, CK
AF Papatsirou, Maria
   Artemaki, Pinelopi, I
   Scorilas, Andreas
   Kontos, Christos K.
TI The role of circular RNAs in therapy resistance of patients with solid
   tumors
SO PERSONALIZED MEDICINE
LA English
DT Review
DE apoptosis regulation; breast cancer; chemoresistance; circRNAs;
   colorectal cancer; EMT; epithelial-mesenchymal transition; gastric
   cancer; lung cancer; prostate cancer; radioresistance
ID EPITHELIAL-MESENCHYMAL TRANSITION; CANCER-CELLS; CISPLATIN RESISTANCE;
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   RESISTANCE; PROMISING BIOMARKER; COLORECTAL-CANCER; PROSTATE-CANCER
AB Circular RNAs (circRNAs) are a type of single-stranded RNA molecules forming a covalently closed, continuous structure, lacking 5 '-3 ' polarity and polyadenylated tails. Recent advances in high-throughput sequencing technologies have revealed that these molecules are abundant, resistant to degradation and often expressed in a tissue- or developmental stage-specific manner. circRNAs are produced by back-splicing circularization of primary transcripts and exhibit a variety of functions, including regulation of transcription, translation and cellular localization. This review focuses on differentially expressed circRNAs conferring therapy resistance or sensitivity of solid tumors, such as carcinomas, sarcomas and lymphomas. Deregulated circRNAs can participate in the development of resistance to treatment by modulating regulatory pathways and cellular processes, including the mitogen-activated protein kinase pathway, epithelial-mesenchymal transition, apoptosis and autophagy.
C1 [Papatsirou, Maria; Artemaki, Pinelopi, I; Scorilas, Andreas; Kontos, Christos K.] Natl & Kapodistrian Univ Athens, Fac Biol, Dept Biochem & Mol Biol, Athens 15701, Greece.
RP Kontos, CK (corresponding author), Natl & Kapodistrian Univ Athens, Fac Biol, Dept Biochem & Mol Biol, Athens 15701, Greece.
EM chkontos@biol.uoa.gr
RI Kontos, Christos/C-2757-2012
OI Kontos, Christos/0000-0002-9935-8461; Papatsirou,
   Maria/0000-0002-0227-9258; Artemaki, Pinelopi/0000-0001-5002-0390;
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NR 150
TC 18
Z9 18
U1 2
U2 5
PU FUTURE MEDICINE LTD
PI LONDON
PA UNITEC HOUSE, 3RD FLOOR, 2 ALBERT PLACE, FINCHLEY CENTRAL, LONDON, N3
   1QB, ENGLAND
SN 1741-0541
EI 1744-828X
J9 PERS MED
JI Pers. Med.
PD NOV
PY 2020
VL 17
IS 06
BP 469
EP 490
DI 10.2217/pme-2020-0103
EA OCT 2020
PG 22
WC Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA OI1IN
UT WOS:000577575100001
PM 33052780
DA 2022-04-25
ER

PT J
AU Gil, J
   Ramsey, D
   Pawlowski, P
   Szmida, E
   Leszczynski, P
   Bebenek, M
   Sasiadek, MM
AF Gil, J.
   Ramsey, D.
   Pawlowski, P.
   Szmida, E.
   Leszczynski, P.
   Bebenek, M.
   Sasiadek, M. M.
TI INTERDEPENDENCE BETWEEN AN EXPRESSION OF THE ATG9A GENE AND THE BAX GENE
   IN COLORECTAL CANCER
SO JOURNAL OF BIOLOGICAL REGULATORS AND HOMEOSTATIC AGENTS
LA English
DT Article
DE autophagy; apoptosis; colorectal cancer; relative expression; ATG genes
ID AUTOPHAGY
AB Despite great progress in colorectal cancer (CRC) prevention, early recognition and treatment, a high frequency of morbidity and mortality of CRC patients is still observed even in developed countries. Molecular characterization of this tumor becomes a standard procedure allowing for application of personalized therapy. However, searching for new biomarkers and for new individual therapeutic strategies is increasingly desirable. In this study on molecular background of CRC, we focused on analyses of mRNA levels of autophagy gene ATG9A and pro-apoptotic gene BAX. Genes involved in autophagy, that is the catabolic and conservative cellular process, have been revealed as a promising new cancer biomarker as well as anti-cancer target. Under normal circumstances autophagy occurs at a low, basal level in most human cells, however in cancer cells its expression varies from down- to upregulation. Despite the fact that the complex link between autophagy and apoptosis is well documented, these interrelations have not yet been fully uncovered. The relative expression of mRNA values of ATG9A and BAX genes in colorectal cancer samples vs normal adjacent tissues was assessed by Real-time PCR with Universal Probe Library. The results of our study revealed a statistically significant correlation between the expression of BAX and ATG9A genes, showing that in CRC a higher expression of BAX gene is connected with lower expression of ATG9A.
C1 [Gil, J.; Pawlowski, P.; Szmida, E.; Sasiadek, M. M.] Wroclaw Med Univ, Dept Genet, Ul Marcinkowskiego 1, PL-50368 Wroclaw, Poland.
   [Ramsey, D.] Wroclaw Univ kchnol, Dept Operat Res, Wroclaw, Poland.
   [Leszczynski, P.] Wroclaw Med Univ, Dept Biol & Med Parasitol, Wroclaw, Poland.
   [Bebenek, M.] Lower Silesian Oncol Ctr, Dept Surg Oncol 1, Wroclaw, Poland.
RP Gil, J (corresponding author), Wroclaw Med Univ, Dept Genet, Ul Marcinkowskiego 1, PL-50368 Wroclaw, Poland.
EM justyna.gil@umed.wroc.pl
RI /L-5618-2019
OI /0000-0003-0991-7686; Sasiadek, Maria/0000-0002-7599-7074; Leszczynski,
   Przemyslaw/0000-0002-4181-4997; Szmida, Elzbieta/0000-0003-3108-0165;
   Bebenek, Marek/0000-0001-7716-5960
FU National Science Centre (Poland) [DEC-2012/07/D/NZ5/04305]
FX This work was financed from the funds of the National Science Centre
   (Poland), decision number DEC-2012/07/D/NZ5/04305.
CR Banerjee R, 2010, TRENDS NEUROSCI, V33, P541, DOI 10.1016/j.tins.2010.09.001
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NR 12
TC 1
Z9 1
U1 0
U2 2
PU BIOLIFE SAS
PI SILVA MARINA (TE)
PA VIA S STEFANO 39 BIS, 64029 SILVA MARINA (TE), ITALY
SN 0393-974X
EI 1724-6083
J9 J BIOL REG HOMEOS AG
JI J. Biol. Regul. Homeost. Agents
PD JAN-FEB
PY 2019
VL 33
IS 1
BP 183
EP 185
PG 3
WC Endocrinology & Metabolism; Immunology; Medicine, Research &
   Experimental; Physiology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Endocrinology & Metabolism; Immunology; Research & Experimental
   Medicine; Physiology
GA HT6TS
UT WOS:000464697500025
PM 30761869
DA 2022-04-25
ER

PT J
AU Abdel-Rafei, MK
   Thabet, NM
   Maksoud, MIAA
   Abd Elkodous, M
   Kawamura, G
   Matsuda, A
   Ashour, AH
   El-Batal, AI
   El-Sayyad, GS
AF Abdel-Rafei, Mohamed K.
   Thabet, Noura M.
   Abdel Maksoud, M. I. A.
   Abd Elkodous, M.
   Kawamura, Go
   Matsuda, Atsunori
   Ashour, A. H.
   El-Batal, Ahmed I.
   El-Sayyad, Gharieb S.
TI Influence of Ce3+ Substitution on Antimicrobial and Antibiofilm
   Properties of ZnCexFe2-xO4 Nanoparticles (X=0.0, 0.02, 0.04, 0.06, and
   0.08) Conjugated with Ebselen and Its Role Subsidised with
   gamma-Radiation in Mitigating Human TNBC and Colorectal Adenocarcinoma
   Proliferation In Vitro
SO INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
LA English
DT Article
DE MDA-MB-231; HT-29; ebselen; cerium; ERK1; 2; STAT-6; IL-4; STAT-1;
   antimicrobial activity
ID CERIUM OXIDE NANOPARTICLES; MAGNETIC-PROPERTIES; FERRITE NANOPARTICLES;
   CELL-CYCLE; DIELECTRIC-PROPERTIES; ELECTRICAL-PROPERTIES; PATHOGENIC
   BACTERIA; CATION DISTRIBUTION; CEO2 NANOPARTICLES; IONIC-STRENGTH
AB Cancers are a major challenge to health worldwide. Spinel ferrites have attracted attention due to their broad theranostic applications. This study aimed at investigating the antimicrobial, antibiofilm, and anticancer activities of ebselen (Eb) and cerium-nanoparticles (Ce-NPs) in the form of ZnCexFe2-XO4 on human breast and colon cancer cell lines. Bioassays of the cytotoxic concentrations of Eb and ZnCexFe2-XO4, oxidative stress and inflammatory milieu, autophagy, apoptosis, related signalling effectors, the distribution of cells through the cell-cycle phases, and the percentage of cells with apoptosis were evaluated in cancer cell lines. Additionally, the antimicrobial and antibiofilm potential have been investigated against different pathogenic microbes. The ZOI, and MIC results indicated that ZnCexFe2-XO4; X = 0.06 specimen reduced the activity of a wide range of bacteria and unicellular fungi at low concentration including P. aeruginosa (9.5 mm; 6.250 mu g/mL), S. aureus (13.2 mm; 0.390 mu g/mL), and Candida albicans (13.5 mm; 0.195 mu g/mL). Reaction mechanism determination indicated that after ZnCexFe2-xO4; X = 0.06 treatment, morphological differences in S. aureus were apparent with complete lysis of bacterial cells, a concomitant decrease in the viable number, and the growth of biofilm was inhibited. The combination of Eb with ZFO or ZnCexFe2-XO4 with gamma-radiation exposure showed marked anti-proliferative efficacy in both cell lines, through modulating the oxidant/antioxidant machinery imbalance, restoring the fine-tuning of redox status, and promoting an anti-inflammatory milieu to prevent cancer progression, which may be a valuable therapeutic approach to cancer therapy and as a promising antimicrobial agent to reduce the pathogenic potential of the invading microbes.
C1 [Abdel-Rafei, Mohamed K.; Thabet, Noura M.] Natl Ctr Radiat Res & Technol NCRRT, Egyptian Atom Energy Author EAEA, Radiat Biol Dept, Cairo 11787, Egypt.
   [Abdel Maksoud, M. I. A.; Ashour, A. H.] Natl Ctr Radiat Res & Technol NCRRT, Egyptian Atom Energy Author EAEA, Mat Sci Lab, Cairo 11787, Egypt.
   [Abd Elkodous, M.; Kawamura, Go; Matsuda, Atsunori] Toyohashi Univ Technol, Dept Elect & Elect Informat Engn, 1-1 Hibarigaoka,Tempaku Cho, Toyohashi, Aichi 441, Japan.
   [El-Batal, Ahmed I.; El-Sayyad, Gharieb S.] Natl Ctr Radiat Res & Technol NCRRT, Egyptian Atom Energy Author EAEA, Drug Microbiol Lab, Drug Radiat Res Dept, Cairo 11787, Egypt.
RP Thabet, NM (corresponding author), Natl Ctr Radiat Res & Technol NCRRT, Egyptian Atom Energy Author EAEA, Radiat Biol Dept, Cairo 11787, Egypt.; Matsuda, A (corresponding author), Toyohashi Univ Technol, Dept Elect & Elect Informat Engn, 1-1 Hibarigaoka,Tempaku Cho, Toyohashi, Aichi 441, Japan.
EM mohamed.marawan2011@yahoo.com; noura_magdy@hotmail.com;
   muhamadmqsod@gmail.com; mohamed.hamada.abdlekodous.xi@tut.jp;
   kawamura.go.km@tut.jp; matsuda@ee.tut.ac.jp; ashourvip3@hotmail.com;
   aelbatal2020@gmail.com; Gharieb.S.Elsayyad@eaea.org.eg
RI Thabet, Noura Magdy/P-8402-2015; Abdel Maksoud, Muhammad Ibrahim
   Ahmed/S-7676-2018
OI Thabet, Noura Magdy/0000-0003-0073-7347; Abdel Maksoud, Muhammad Ibrahim
   Ahmed/0000-0001-7708-9646; Abd Elkodous, Mohamed/0000-0002-9408-9178;
   matsuda, atsunori/0000-0002-6493-1205
FU Japan Society for Promotion of Science (JSPS) KAKENHIMinistry of
   Education, Culture, Sports, Science and Technology, Japan (MEXT)Japan
   Society for the Promotion of ScienceGrants-in-Aid for Scientific
   Research (KAKENHI) [18H03841, 21K18823]
FX This study was partly funded by Japan Society for Promotion of Science
   (JSPS) KAKENHI Grant No. 18H03841 and No. 21K18823.
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NR 149
TC 4
Z9 4
U1 4
U2 5
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 1422-0067
J9 INT J MOL SCI
JI Int. J. Mol. Sci.
PD SEP
PY 2021
VL 22
IS 18
AR 10171
DI 10.3390/ijms221810171
PG 40
WC Biochemistry & Molecular Biology; Chemistry, Multidisciplinary
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Chemistry
GA UW6JN
UT WOS:000700259700001
PM 34576334
OA Green Published, gold
DA 2022-04-25
ER

PT J
AU Zhou, HY
   Yuan, M
   Yu, QF
   Zhou, XY
   Min, WP
   Gao, D
AF Zhou, Huangyan
   Yuan, Min
   Yu, Qiongfang
   Zhou, Xiaoyan
   Min, Weiping
   Gao, Dian
TI Autophagy regulation and its role in gastric cancer and colorectal
   cancer
SO CANCER BIOMARKERS
LA English
DT Review
DE Autophagy; gastric cancer; colorectal cancer
ID TUMOR-SUPPRESSOR; FRAMESHIFT MUTATION; THERAPEUTIC TARGET; HUMAN HEALTH;
   IN-VITRO; EXPRESSION; BECLIN-1; PATHWAYS; KRAS; RAS
AB BACKGROUND: Autophagy is associated with the occurrence, development, cellular adaptation, progression, treatment and prognosis of gastric cancer (GC) and colorectal cancer (CRC). The effect of autophagy in these two cancers has attracted our attention.
   OBJECTIVE: The aim of this study was to describe the functional and regulatory mechanisms associated with autophagy in GC and CRC.
   METHODS: We reviewed recent publications describing the role of autophagy in GC and CRC, including the functional characteristics, clinical significance and regulatory mechanisms.
   RESULTS: Autophagy plays context-dependent dual roles in the development and progression of GC and CRC. It can either promote tumor growth and cell survival or can contribute to tumor suppression and promote cell death. Both of these effects employ complex regulatory networks, such as those mediated by p53, PI3K/Akt/mTOR, Ras and microRNA. Among the cellular process associated with these pathways, autophagy is a potential target for anti-tumor therapy.
   CONCLUSION: Autophagy is associated with both tumorigenic and protective effects in cancer. However, the role of autophagy in GC and CRC remains unclear. Although the translation of the basic science of autophagy into clinical practice is a long process, the modulation of autophagy as a potential therapeutic approach in GC and CRC merits further investigation.
C1 [Zhou, Huangyan; Min, Weiping; Gao, Dian] Nanchang Univ, Coll Med, Dept Pathogen Biol & Immunol, 461 Bayi Rd, Nanchang 330006, Jiangxi, Peoples R China.
   [Zhou, Huangyan; Min, Weiping; Gao, Dian] Jiangxi Acad Med Sci, Nanchang, Jiangxi, Peoples R China.
   [Zhou, Huangyan; Min, Weiping; Gao, Dian] Nanchang Univ, Inst Immunotherapy, Nanchang, Jiangxi, Peoples R China.
   [Yuan, Min] Nanchang Univ, Affiliated Hosp 2, Dept Neurol, Nanchang, Jiangxi, Peoples R China.
   [Yu, Qiongfang] Nanchang Univ, Affiliated Hosp 2, Dept Gastroenterol & Hepatol, Nanchang, Jiangxi, Peoples R China.
   [Zhou, Xiaoyan] Nanchang Univ, Coll Med, Dept Pathophysiol, Nanchang, Jiangxi, Peoples R China.
RP Gao, D (corresponding author), Nanchang Univ, Coll Med, Dept Pathogen Biol & Immunol, 461 Bayi Rd, Nanchang 330006, Jiangxi, Peoples R China.
EM gaodian@ncu.edu.cn
RI Yuan, Min/ABF-7560-2020
OI Yuan, Min/0000-0002-1190-5337; Gao, Dian/0000-0002-9391-1756
FU National Natural Science Foundation of ChinaNational Natural Science
   Foundation of China (NSFC) [31460696, 81460462, 81460126]; Technology
   Pedestal and Society Development Project of Jiangxi Province
   [20141BBG70040]; Foundation of Jiangxi Educational Committee [86283702];
   Department of Health of Jiangxi Province [20155629]
FX The authors thank Dr. Wirnkar S. Jadwiga for his help in English
   language editing. This work is supported by grants from National Natural
   Science Foundation of China (No. 31460696, 81460462, 81460126),
   Technology Pedestal and Society Development Project of Jiangxi Province
   (No. 20141BBG70040), Foundation of Jiangxi Educational Committee (No.
   86283702), Department of Health of Jiangxi Province (No. 20155629).
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NR 105
TC 56
Z9 58
U1 5
U2 28
PU IOS PRESS
PI AMSTERDAM
PA NIEUWE HEMWEG 6B, 1013 BG AMSTERDAM, NETHERLANDS
SN 1574-0153
EI 1875-8592
J9 CANCER BIOMARK
JI Cancer Biomark.
PY 2016
VL 17
IS 1
BP 1
EP 10
DI 10.3233/CBM-160613
PG 10
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA DS9OZ
UT WOS:000381114300001
PM 27314289
DA 2022-04-25
ER

PT J
AU Ryoo, IG
   Choi, BH
   Kwak, MK
AF Ryoo, In-geun
   Choi, Bo-hyun
   Kwak, Mi-Kyoung
TI Activation of NRF2 by p62 and proteasome reduction in sphere-forming
   breast carcinoma cells
SO ONCOTARGET
LA English
DT Article
DE mammospheres; cancer stem cell; resistance; NRF2; p62
ID CANCER STEM-CELLS; ANTIOXIDANT RESPONSE ELEMENT; TRANSCRIPTION FACTOR
   NRF2; IN-VITRO PROPAGATION; INITIATING CELLS; SELF-RENEWAL; SUBUNIT
   EXPRESSION; OXIDATIVE STRESS; AUTOPHAGY; KEAP1
AB Cancer stem cells (CSCs) express high levels of drug efflux transporters and antioxidant genes, and are therefore believed to be responsible for cancer recurrence following chemo/radiotherapy intervention. In this study, we investigated the role of NF-E2-related factor 2 (NRF2), a master regulator of antioxidant gene expression, in the growth and stress resistance of CSC-enriched mammosphere. The MCF7 mammospheres expressed significantly higher levels of the NRF2 protein and target gene expression compared to the monolayer. As underlying mechanisms, we observed that proteolytic activity and expression of the proteasome catalytic subunits were decreased in the mammospheres. Additionally, mammospheres retained a high level of p62 and the silencing of p62 was observed to attenuate NRF2 activation. NRF2 increase was confirmed in sphere-cultures of the colon and ovarian cancer cells. The functional implication of NRF2 was demonstrated in NRF2-knockdown mammospheres. NRF2-silenced mammospheres demonstrated increased cell death and retarded sphere growth as a result of target gene repression. Moreover, unlike the control mammospheres, NRF2-knockdown mammospheres did not develop anticancer drug resistance. Collectively, these results indicated that altered proteasome function and p62 expression caused NRF2 activation in CSC-enriched mammospheres. In addition, NRF2 appeared to play a role in CSC survival and anticancer drug resistance.
C1 [Ryoo, In-geun; Choi, Bo-hyun; Kwak, Mi-Kyoung] Catholic Univ Korea, Coll Pharm, Bucheon, Gyeonggi Do, South Korea.
RP Kwak, MK (corresponding author), Catholic Univ Korea, Coll Pharm, Bucheon, Gyeonggi Do, South Korea.
EM mkwak@catholic.ac.kr
FU National Research Foundation (NRF) - Ministry of Science, ICT & Future
   Planning [NRF-2013R1A2A2A01015497]
FX This study was financially supported by the National Research Foundation
   (NRF) funded by the Ministry of Science, ICT & Future Planning
   (NRF-2013R1A2A2A01015497).
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NR 59
TC 51
Z9 54
U1 0
U2 4
PU IMPACT JOURNALS LLC
PI ORCHARD PARK
PA 6666 E QUAKER ST, STE 1, ORCHARD PARK, NY 14127 USA
EI 1949-2553
J9 ONCOTARGET
JI Oncotarget
PD APR 10
PY 2015
VL 6
IS 10
BP 8167
EP 8184
DI 10.18632/oncotarget.3047
PG 18
WC Oncology; Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Cell Biology
GA CI6QJ
UT WOS:000354885300059
PM 25717032
OA Green Submitted, Green Published, gold
DA 2022-04-25
ER

PT J
AU Ren, YC
   Yuan, BC
   Hou, SH
   Sui, YL
   Yang, TH
   Lv, ML
   Zhou, YL
   Yu, H
   Li, S
   Peng, HS
   Chang, ND
   Liu, Y
AF Ren, Yachao
   Yuan, Bingchuan
   Hou, Shenghua
   Sui, Yilei
   Yang, Tinghui
   Lv, Meilin
   Zhou, Yulong
   Yu, Hui
   Li, Sen
   Peng, Haisheng
   Chang, Naidan
   Liu, Yang
TI Delivery of RGD-modified liposome as a targeted colorectal carcinoma
   therapy and its autophagy mechanism
SO JOURNAL OF DRUG TARGETING
LA English
DT Article
DE RGD peptide; liposomes; colorectal drug targeting; targeting mechanism;
   autophagy
ID DRUG-DELIVERY; ALPHA-V-BETA-3 INTEGRIN; NANOPARTICLES; CANCER; SYSTEM;
   EXPRESSION; PEPTIDE; CELLS
AB Liposomes are among the most extensively applied drug carriers due to their excellent biocompatibility, controllable size and ease of modification. In the present study, we prepared untargeted liposomes (LP) and targeting liposomes modified with Arg-Gly-Asp (RGD-LP), and Doxorubicin Hydrochloride (DOX) or fluorescent probe was loaded. RGD-LP/DOX was identified to be uniformly spherical in size 131.2 +/- 2.7 nm. Based on flow cytometry analysis and the confocal laser scanning microscopy, RGD-LP had a higher uptake into HRT-18 colorectal cancer cells than LP. Further, in vivo imaging study further suggested that RGD-LP could significantly increase the liposome accumulation in the tumour tissues of the mice bearing subcutaneous tumours. By investigating the targeting mechanism of RGD-LP, we found that they entered the cell via macropinocytosis. When loaded with DOX, RGD-LP exerted stronger tumour growth inhibitory activity against tumours of colorectal carcinoma compared to LP. Moreover, RGD-LP induced autophagy. Therefore, RGD-LP have the potential to be applied as a targeted colorectal carcinoma therapy.
C1 [Ren, Yachao; Yuan, Bingchuan; Hou, Shenghua; Sui, Yilei; Yang, Tinghui; Lv, Meilin; Yu, Hui; Li, Sen; Peng, Haisheng; Chang, Naidan] Harbin Med Univ Daqing, Dept Pharm, Daqing 163319, Peoples R China.
   [Zhou, Yulong] Heilongjiang Bayi Agr Univ, Coll Anim Sci & Technol, Daqing, Peoples R China.
   [Liu, Yang] Zhengzhou Univ, Sch Pharmaceut Sci, Zhengzhou 450001, Peoples R China.
RP Peng, HS; Chang, ND (corresponding author), Harbin Med Univ Daqing, Dept Pharm, Daqing 163319, Peoples R China.; Liu, Y (corresponding author), Zhengzhou Univ, Sch Pharmaceut Sci, Zhengzhou 450001, Peoples R China.
EM fisher1688@163.com; changnaidan@126.com; liuyang8016@126.com
FU National Natural Science Foundation of ChinaNational Natural Science
   Foundation of China (NSFC) [81703426]; Natural Science Foundation of
   Heilongjiang ProvinceNatural Science Foundation of Heilongjiang Province
   [LH2019H010, H2018018]; China Postdoctoral Science FoundationChina
   Postdoctoral Science Foundation [2019M651312]; Heilongjiang Postdoctoral
   Fund [LBH-Z18106]; Health Commission of Heilongjiang Province
   [2017-170]; Mentor Found of Daqing campus, Harbin Medical University
   [XQJJ2016003]; Innovation and Entrepreneurship Programme for College
   Students in Heilongjiang Province [201910226137]; Key research and
   development and promotion projects of Henan Province [192102310154];
   Innovation and entrepreneurship training program of Zhengzhou University
   [202010459148]
FX This work was supported by National Natural Science Foundation of China
   (81703426); Natural Science Foundation of Heilongjiang Province
   (LH2019H010); Natural Science Foundation of Heilongjiang Province
   (H2018018); China Postdoctoral Science Foundation (2019M651312);
   Heilongjiang Postdoctoral Fund (LBH-Z18106); Health Commission of
   Heilongjiang Province (2017-170); the Mentor Found (XQJJ2016003) of
   Daqing campus, Harbin Medical University; and Innovation and
   Entrepreneurship Programme for College Students in Heilongjiang Province
   (201910226137); Key research and development and promotion projects of
   Henan Province (192102310154); Innovation and entrepreneurship training
   program of Zhengzhou University (202010459148).
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NR 62
TC 3
Z9 3
U1 7
U2 7
PU TAYLOR & FRANCIS LTD
PI ABINGDON
PA 2-4 PARK SQUARE, MILTON PARK, ABINGDON OR14 4RN, OXON, ENGLAND
SN 1061-186X
EI 1029-2330
J9 J DRUG TARGET
JI J. Drug Target.
PD SEP 14
PY 2021
VL 29
IS 8
BP 863
EP 874
DI 10.1080/1061186X.2021.1882469
EA FEB 2021
PG 12
WC Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA UB2PH
UT WOS:000618265600001
PM 33507113
DA 2022-04-25
ER

PT J
AU Lee, J
   Zhou, W
   Na, M
   Oh, S
AF Lee, Jaehoo
   Zhou, Wei
   Na, MinKyun
   Oh, Sangtaek
TI Cytotoxic Activity of Aplykurodin A Isolated From Aplysia kurodai
   against AXIN1-Mutated Hepatocellular Carcinoma Cells by Promoting
   Oncogenic beta-Catenin Degradation
SO MARINE DRUGS
LA English
DT Article
DE hepatocellular carcinoma (HCC); aplykurodin A; Wnt; beta-catenin
   signaling; apoptosis; autophagy
ID DOWN-REGULATION; COLON-CANCER; SEA HARE; PROTEIN; TARGET; AUTOPHAGY;
   PATHWAY; COMPLEX; AXIN; PHOSPHORYLATION
AB Dysregulation of the Wnt/beta-catenin signaling pathway is involved in the development of human hepatocellular carcinoma and has thus emerged as a therapeutic target for this malignant tumor. In this study, we employed sensitive cell-based assays to identify aplykurodin A isolated from Aplysia kurodai as an antagonist of Wnt/beta-catenin signaling. Aplykurodin A inhibited beta-catenin responsive transcription, which was stimulated by a Wnt3a-conditioned medium or a glycogen synthase kinase 3 beta inhibitor by accelerating intracellular beta-catenin degradation. Aplykurodin A downregulated the level of oncogenic beta-catenin and decreased the expression of beta-catenin-dependent gene, leading to inhibition of human hepatoma Hep3B and SNU475 cell proliferation. Moreover, apoptosis and autophagy were elicited by aplykurodin A, as indicated by an increase the number of Annexin V-FITC-stained cells and the formation of microtubule-associated protein 1 light chain 3 puncta, respectively, in Hep3B and SNU475 cells. Our findings suggest that aplykurodin A provides a novel therapeutic strategy for human hepatocellular carcinoma via stimulation of oncogenic beta-catenin degradation.
C1 [Lee, Jaehoo; Oh, Sangtaek] Kookmin Univ, Dept Bio & Fermentat Convergence Technol, BK21 PLUS Program, Seoul 136702, South Korea.
   [Zhou, Wei] Yanbian Univ, Coll Pharm, Yanji 133002, Peoples R China.
   [Na, MinKyun] Chungnam Natl Univ, Coll Pharm, Daejeon 34134, South Korea.
RP Oh, S (corresponding author), Kookmin Univ, Dept Bio & Fermentat Convergence Technol, BK21 PLUS Program, Seoul 136702, South Korea.; Na, M (corresponding author), Chungnam Natl Univ, Coll Pharm, Daejeon 34134, South Korea.
EM wogn1208@gmail.com; zhouwei8452@163.com; mkna@cnu.ac.kr;
   ohsa@kookmin.ac.kr
OI Na, MinKyun/0000-0002-4865-6506
FU Basic Science Research Program through the National Research Foundation
   of Korea (NRF) grant - Korean Government [NRF-2018R1D1A1B07048208,
   NRF-2020R1A2B5B01002415]; World Class 300 Project R&D grant, Korea Small
   and Medium Business Administration (SMBA)
FX This work was supported by the Basic Science Research Program
   (NRF-2018R1D1A1B07048208; NRF-2020R1A2B5B01002415) through the National
   Research Foundation of Korea (NRF) grant funded by the Korean Government
   and by the World Class 300 Project R&D grant provided by the Korea Small
   and Medium Business Administration (SMBA).
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NR 41
TC 3
Z9 3
U1 0
U2 1
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 1660-3397
J9 MAR DRUGS
JI Mar. Drugs
PD APR
PY 2020
VL 18
IS 4
AR 210
DI 10.3390/md18040210
PG 12
WC Chemistry, Medicinal; Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA LO8XP
UT WOS:000533909300031
PM 32294900
OA Green Published, gold
DA 2022-04-25
ER

PT J
AU Huang, YC
   Hung, WC
   Chen, WT
   Yu, HS
   Chai, CY
AF Huang, Ya-Chun
   Hung, Wen-Chun
   Chen, Wan-Tzu
   Yu, Hsin-Su
   Chai, Chee-Yin
TI Sodium arsenite-induced DAPK promoter hypermethylation and autophagy via
   ERK1/2 phosphorylation in human uroepithelial cells
SO CHEMICO-BIOLOGICAL INTERACTIONS
LA English
DT Article
DE Arsenite; SV-HUC-1 cells; ERK1/2; Autophagy; Beclin-1; DAPK
ID COLON-CANCER CELLS; ACTIVATED PROTEIN-KINASES; GROWTH-FACTOR RECEPTOR;
   DNA METHYLTRANSFERASE; GLIOMA-CELLS; DEATH; METHYLATION; TRIOXIDE;
   PATHWAY; INHIBITION
AB Arsenic compounds or arsenicals are well-known toxic and carcinogenic agents. The toxic effects of arsenic that are of most concern to humans are those that occur from chronic, low-level exposure, and are associated with various human malignancies, including skin, lung and bladder cancers. In addition, arsenic could induce cell death, including apoptosis or autophagy in malignant cells. Previously, we have demonstrated that arsenite can induce autophagy and death-associated protein kinase (DAPK) promoter hypermethylation in the SV-40 immortalized human uroepithelial cell line (SV-HUC-1). However, the underlying mechanism of arsenite-induced autophagy is still unclear. In the present study, we demonstrate that arsenite can activate the extracellular signaling-regulated protein kinase 1/2 (ERK1/2) signaling pathway after treatment in SV-HUC-1 cells by using immunocytochemistry and Western blotting. In addition, our results also show an increase of autophagosomes was produced in arsenite-treated SV-HUC-1 cells by using electron microscopy. We found that, by incrementally increasing the dosages, microtubule-associated protein light chain 3B (LOB) and Beclin-1 are important regulators for the formation of autophagosomes, in a dose-dependent manner. When the cells were pretreated with inhibitors 5-aza-CdR or U0126 for 24 h, the effect of arsenite on ERK1/2, LC3B, Beclin-1 and DAPK proteins expression is suppressed. Furthermore, Our results support the notion that arsenite can induce the ERK1/2 signaling pathway to stimulate autophagy and DAPK promoter hypermethylation in human uroepithelial SV-HUC-1 cells. These findings may contribute to a better understanding of the carcinogenesis of arsenite. (C) 2009 Elsevier Ireland Ltd. All rights reserved.
C1 [Chen, Wan-Tzu; Chai, Chee-Yin] Kaohsiung Med Univ Hosp, Dept Pathol, Kaohsiung 807, Taiwan.
   [Yu, Hsin-Su] Kaohsiung Med Univ Hosp, Dept Dermatol, Kaohsiung 807, Taiwan.
   [Huang, Ya-Chun] Kaohsiung Med Univ, Coll Med, Grad Inst Med, Kaohsiung, Taiwan.
   [Huang, Ya-Chun; Chen, Wan-Tzu; Chai, Chee-Yin] Kaohsiung Med Univ, Coll Med, Dept Pathol, Kaohsiung, Taiwan.
   [Hung, Wen-Chun; Chai, Chee-Yin] Natl Sun Yat Sen Univ, Inst Biomed Sci, Kaohsiung 80424, Taiwan.
   [Hung, Wen-Chun; Chai, Chee-Yin] Kaohsiung Med Univ, Natl Sun Yat Sen Univ, Joint Res Ctr, Kaohsiung, Taiwan.
   [Yu, Hsin-Su] Kaohsiung Med Univ, Coll Med, Dept Dermatol, Kaohsiung, Taiwan.
   [Yu, Hsin-Su; Chai, Chee-Yin] Kaohsiung Med Univ, Ctr Excellence Environm Med, Kaohsiung, Taiwan.
RP Chai, CY (corresponding author), Kaohsiung Med Univ Hosp, Dept Pathol, 100 Tzyou 1st Rd, Kaohsiung 807, Taiwan.
EM cychai@kmu.edu.tw
RI Hung, Wen-Chun/F-4846-2011; Chai, Chee-Yin/D-5523-2009
OI Chai, Chee-Yin/0000-0003-0486-9742
FU National Sun Yat-Sen University-Kaohsiung Medical University Joint
   Research Center, Kaohsiung, Taiwan; Center of Excellence for
   Environmental Medicine, Kaohsiung Medical University [KMU-EM-98-2-3]
FX This work was supported by a research grant from the National Sun
   Yat-Sen University-Kaohsiung Medical University Joint Research Center,
   Kaohsiung, Taiwan and Center of Excellence for Environmental Medicine,
   Kaohsiung Medical University (KMU-EM-98-2-3).
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NR 52
TC 28
Z9 32
U1 0
U2 7
PU ELSEVIER IRELAND LTD
PI CLARE
PA ELSEVIER HOUSE, BROOKVALE PLAZA, EAST PARK SHANNON, CO, CLARE, 00000,
   IRELAND
SN 0009-2797
EI 1872-7786
J9 CHEM-BIOL INTERACT
JI Chem.-Biol. Interact.
PD OCT 7
PY 2009
VL 181
IS 2
BP 254
EP 262
DI 10.1016/j.cbi.2009.06.020
PG 9
WC Biochemistry & Molecular Biology; Pharmacology & Pharmacy; Toxicology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Pharmacology & Pharmacy; Toxicology
GA 499IO
UT WOS:000270212800013
PM 19577553
DA 2022-04-25
ER

PT J
AU Liang, D
   Khoonkari, M
   Avril, T
   Chevet, E
   Kruyt, FAE
AF Liang, Dong
   Khoonkari, Mohammad
   Avril, Tony
   Chevet, Eric
   Kruyt, Frank A. E.
TI The unfolded protein response as regulator of cancer stemness and
   differentiation: Mechanisms and implications for cancer therapy
SO BIOCHEMICAL PHARMACOLOGY
LA English
DT Review
DE Unfolded protein response; Cancer stem cells; Tumor formation; Therapy;
   PERK; IRE1
ID ENDOPLASMIC-RETICULUM STRESS; BREAST-CANCER; BONE-MARROW; CELLS;
   ACTIVATION; GSK2606414; DISCOVERY; AUTOPHAGY; SURVIVAL; TARGET
AB The unfolded protein response (UPR) is an adaptive mechanism that regulates protein and cellular homeostasis. Three endoplasmic reticulum (ER) membrane localized stress sensors, IRE1, PERK and ATF6, coordinate the UPR in order to maintain ER proteostasis and cell survival, or induce cell death when homeostasis cannot be restored. However, recent studies have identified alternative functions for the UPR in developmental biology processes and cell fate decisions under both normal and cancerous conditions. In cancer, increasing evidence points to-wards the involvement of the three UPR sensors in oncogenic reprogramming and the regulation of tumor cells endowed with stem cell properties, named cancer stem cells (CSCs), that are considered to be the most malignant cells in tumors. Here we review the reported roles and underlying molecular mechanisms of the three UPR sensors in regulating stemness and differentiation, particularly in solid tumor cells, processes that have a major impact on tumor aggressiveness. Mainly PERK and IRE1 branches of the UPR were found to regulate CSCs and tumor development and examples are provided for breast cancer, colon cancer and aggressive brain tumors, glioblastoma. Although the underlying mechanisms and interactions between the different UPR branches in regulating stemness in cancer need to be further elucidated, we propose that PERK and IRE1 targeted therapy could inhibit self-renewal of CSCs or induce differentiation that is predicted to have therapeutic benefit. For this, more specific UPR modulators need to be developed with favorable pharmacological properties that together with patient stratification will allow optimal evaluation in clinical studies.
C1 [Liang, Dong; Khoonkari, Mohammad; Kruyt, Frank A. E.] Univ Groningen, Univ Med Ctr Groningen, Dept Med Oncol, Hanzepl 1, NL-9713 GZ Groningen, Netherlands.
   [Avril, Tony; Chevet, Eric] Univ Rennes, INSERM U1242, Rennes, France.
   [Avril, Tony; Chevet, Eric] Ctr Lutte Canc Eugene Marquis, Rennes, France.
RP Kruyt, FAE (corresponding author), Univ Groningen, Univ Med Ctr Groningen, Dept Med Oncol, Hanzepl 1, NL-9713 GZ Groningen, Netherlands.
EM f.a.e.kruyt@umcg.nl
OI Kruyt, Frank/0000-0002-2445-9380; Liang, Dong/0000-0002-7145-5569
FU China Scholarship CouncilChina Scholarship Council; University of
   Groningen; Zernike Institute for Advanced Materials at the University of
   Groningen; Bonus Incentive Scheme (Dutch Ministry for Education, Culture
   and Science (OCW)); La Ligue contre le cancer (comite 35); l'Institut
   des Neurosciences Cliniques de Rennes (AAP 2020); Fondation pour la
   Recherche Medicale (FRM equipe labellisee 2018); Institut National du
   Cancer (INCa; PLBIO)Institut National du Cancer (INCA) France; Agence
   Nationale de la Recherche (ANR; ERAAT)French National Research Agency
   (ANR); La Ligue contre le cancer (comite 56); La Ligue contre le cancer
   (comite 85)
FX DL was supported by the China Scholarship Council and the University of
   Groningen. MK was financially supported by the Zernike Institute for
   Advanced Materials at the University of Groningen, including funding
   from the Bonus Incentive Scheme (of the Dutch Ministry for Education,
   Culture and Science (OCW)). T. Avril was supported by La Ligue contre le
   cancer (comites 35, 56 and 85) and by l'Institut des Neurosciences
   Cliniques de Rennes (AAP 2020). EC was funded by Grants from Fondation
   pour la Recherche Medicale (FRM equipe labellisee 2018), Institut
   National du Cancer (INCa; PLBIO), Agence Nationale de la Recherche (ANR;
   ERAAT).
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NR 73
TC 2
Z9 2
U1 1
U2 2
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0006-2952
EI 1873-2968
J9 BIOCHEM PHARMACOL
JI Biochem. Pharmacol.
PD OCT
PY 2021
VL 192
AR 114737
DI 10.1016/j.bcp.2021.114737
EA AUG 2021
PG 7
WC Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA US9US
UT WOS:000697771600011
PM 34411568
OA Green Published, hybrid
DA 2022-04-25
ER

PT J
AU Zhang, JT
   Yi, M
   Zha, LY
   Chen, SQ
   Li, ZJ
   Li, C
   Gong, MX
   Deng, H
   Chu, XW
   Chen, JH
   Zhang, ZQ
   Mao, LM
   Sun, SX
AF Zhang, Jintao
   Yi, Man
   Zha, Longying
   Chen, Siqiang
   Li, Zhijia
   Li, Cheng
   Gong, Mingxing
   Deng, Hong
   Chu, Xinwei
   Chen, Jiehua
   Zhang, Zheqing
   Mao, Limei
   Sun, Suxia
TI Sodium Butyrate Induces Endoplasmic Reticulum Stress and Autophagy in
   Colorectal Cells: Implications for Apoptosis
SO PLOS ONE
LA English
DT Article
ID CHAIN FATTY-ACIDS; CYCLE ARREST; CANCER; DEATH; PATHWAYS; PROLIFERATION;
   INFLAMMATION; INHIBITOR; MECHANISM; TARGET
AB Purpose
   Butyrate, a short-chain fatty acid derived from dietary fiber, inhibits proliferation and induces cell death in colorectal cancer cells. However, clinical trials have shown mixed results regarding the anti-tumor activities of butyrate. We have previously shown that sodium butyrate increases endoplasmic reticulum stress by altering intracellular calcium levels, a well-known autophagy trigger. Here, we investigated whether sodium butyrate-induced endoplasmic reticulum stress mediated autophagy, and whether there was crosstalk between autophagy and the sodium butyrate-induced apoptotic response in human colorectal cancer cells.
   Methods
   Human colorectal cancer cell lines (HCT-116 and HT-29) were treated with sodium butyrate at concentrations ranging from 0.5-5mM. Cell proliferation was assessed using MTT tetrazolium salt formation. Autophagy induction was confirmed through a combination of Western blotting for associated proteins, acridine orange staining for acidic vesicles, detection of autolysosomes (MDC staining), and electron microscopy. Apoptosis was quantified by flow cytometry using standard annexinV/propidium iodide staining and by assessing PARP-1 cleavage by Western blot.
   Results
   Sodium butyrate suppressed colorectal cancer cell proliferation, induced autophagy, and resulted in apoptotic cell death. The induction of autophagy was supported by the accumulation of acidic vesicular organelles and autolysosomes, and the expression of autophagya-ssociated proteins, including microtubule-associated protein II light chain 3 (LC3-II), beclin-1, and autophagocytosis-associated protein (Atg)3. The autophagy inhibitors 3-methyladenine (3-MA) and chloroquine inhibited sodium butyrate induced autophagy. Furthermore, sodium butyrate treatment markedly enhanced the expression of endoplasmic reticulum stress-associated proteins, including BIP, CHOP, PDI, and IRE-1a. When endoplasmic reticulum stress was inhibited by pharmacological (cycloheximide and mithramycin) and genetic (siRNA targeting BIP and CHOP) methods, the induction of BIP, PDI, IRE1a, and LC3-II was blocked, but PARP cleavage was markedly enhanced.
   Discussion
   Taken together, these results suggested that sodium butyrate-induced autophagy was mediated by endoplasmic reticulum stress, and that preventing autophagy by blocking the endoplasmic reticulum stress response enhanced sodium butyrate-induced apoptosis. These results provide novel insights into the anti-tumor mechanisms of butyric acid.
C1 [Zhang, Jintao; Yi, Man; Zha, Longying; Li, Zhijia; Li, Cheng; Gong, Mingxing; Deng, Hong; Chu, Xinwei; Chen, Jiehua; Zhang, Zheqing; Mao, Limei; Sun, Suxia] Southern Med Univ, Guangdong Prov Key Lab Trop Dis Res, Dept Nutr & Food Hyg, Sch Publ Hlth, 1023 South Sha Tai Rd, Guangzhou 510515, Guangdong, Peoples R China.
   [Chen, Siqiang] Guangdong Entry Exit Inspect & Quarantine Bur, Dept Certificat Supervis, Guojian Bldg,66,Huacheng Ave, Guangzhou 510623, Guangdong, Peoples R China.
RP Sun, SX (corresponding author), Southern Med Univ, Guangdong Prov Key Lab Trop Dis Res, Dept Nutr & Food Hyg, Sch Publ Hlth, 1023 South Sha Tai Rd, Guangzhou 510515, Guangdong, Peoples R China.
EM suxiasun@hotmail.com
OI Sun, Suxia/0000-0002-1159-6191
FU National Natural Science Foundation of ChinaNational Natural Science
   Foundation of China (NSFC) [81202204]; Guangdong National Natural
   Science Foundation [S2012010009467]; Project for Excellent Young
   University Teacher
FX Financial support for this study was provided by National Natural
   Science Foundation of China (No. 81202204), Guangdong National Natural
   Science Foundation (No. S2012010009467), Project for Excellent Young
   University Teacher awarded to Southern Medical University.
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NR 50
TC 51
Z9 56
U1 3
U2 26
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 1160 BATTERY STREET, STE 100, SAN FRANCISCO, CA 94111 USA
SN 1932-6203
J9 PLOS ONE
JI PLoS One
PD JAN 19
PY 2016
VL 11
IS 1
AR e0147218
DI 10.1371/journal.pone.0147218
PG 25
WC Multidisciplinary Sciences
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Science & Technology - Other Topics
GA DB5BP
UT WOS:000368528400125
PM 26784903
OA Green Published, Green Submitted, gold
DA 2022-04-25
ER

PT J
AU Xu, GQ
   Yang, M
   Wang, QL
   Zhao, LF
   Zhu, SJ
   Zhu, LX
   Xu, TR
   Cao, RX
   Li, C
   Liu, QY
   Xiong, W
   Su, Y
   Dong, J
AF Xu, Guoqiang
   Yang, Mei
   Wang, Qiaoli
   Zhao, Liufang
   Zhu, Sijin
   Zhu, Lixiu
   Xu, Tianrui
   Cao, Ruixue
   Li, Cheng
   Liu, Qiuyan
   Xiong, Wei
   Su, Yan
   Dong, Jian
TI A Novel Prognostic Prediction Model for Colorectal Cancer Based on Nine
   Autophagy-Related Long Noncoding RNAs
SO FRONTIERS IN ONCOLOGY
LA English
DT Article
DE colorectal cancer; autophagy; long noncoding RNAs; risk score;
   prognostic prediction model
ID CELL-PROLIFERATION; KNOCKDOWN; PCAT6; METASTASIS; PROGRESSION;
   STATISTICS; EXPRESSION; MIGRATION; INVASION; TUMOR
AB Introduction Colorectal cancer (CRC) is the most common gastrointestinal cancer and has a low overall survival rate. Tumor-node-metastasis staging alone is insufficient to predict patient prognosis. Autophagy and long noncoding RNAs play important roles in regulating the biological behavior of CRC. Therefore, establishing an autophagy-related lncRNA (ARlncRNA)-based bioinformatics model is important for predicting survival and facilitating clinical treatment.
   Methods CRC data were retrieved from The Cancer Genome Atlas. The database was randomly divided into train set and validation set; then, univariate and multivariate Cox regression analyses were performed to screen prognosis-related ARlncRNAs for prediction model construction. Interactive network and Sankey diagrams of ARlncRNAs and messenger RNAs were plotted. We analyzed the survival rate of high- and low-risk patients and plotted survival curves and determined whether the risk score was an independent predictor of CRC. Receiver operating characteristic curves were used to evaluate model sensitivity and specificity. Then, the expression level of lncRNA was detected by quantitative real-time polymerase chain reaction, and the location of lncRNA was observed by fluorescence in situ hybridization. Additionally, the protein expression was detected by Western blot.
   Results A prognostic prediction model of CRC was built based on nine ARlncRNAs (NKILA, LINC00174, AC008760.1, LINC02041, PCAT6, AC156455.1, LINC01503, LINC00957, and CD27-AS1). The 5-year overall survival rate was significantly lower in the high-risk group than in the low-risk group among train set, validation set, and all patients (all p < 0.001). The model had high sensitivity and accuracy in predicting the 1-year overall survival rate (area under the curve = 0.717). The prediction model risk score was an independent predictor of CRC. LINC00174 and NKILA were expressed in the nucleus and cytoplasm of normal colonic epithelial cell line NCM460 and colorectal cancer cell lines HT29. Additionally, LINC00174 and NKILA were overexpressed in HT29 compared with NCM460. After autophagy activation, LINCC00174 expression was significantly downregulated both in NCM460 and HT29, while NKILA expression was significantly increased.
   Conclusion The new ARlncRNA-based model predicts CRC patient prognosis and provides new research ideas regarding potential mechanisms regulating the biological behavior of CRC. ARlncRNAs may play important roles in personalized cancer treatment.
C1 [Xu, Guoqiang; Wang, Qiaoli; Zhu, Sijin; Zhu, Lixiu; Xu, Tianrui; Cao, Ruixue; Li, Cheng; Xiong, Wei] Kunming Med Univ, Yunnan Canc Hosp, Dept Radiotherapy, Affiliated Hosp 3, Kunming, Yunnan, Peoples R China.
   [Yang, Mei] Kunming Med Univ, Yunnan Canc Hosp, Cadre Med Dept, Affiliated Hosp 3, Kunming, Yunnan, Peoples R China.
   [Zhao, Liufang] Kunming Med Univ, Yunnan Canc Hosp, Dept Head & Neck Surg 1, Affiliated Hosp 3, Kunming, Yunnan, Peoples R China.
   [Liu, Qiuyan] Panzhihua Univ, Panzhihua Integrated Tradit Chinese & Western Med, Dept Oncol, Affiliated Hosp, Panzhihua, Peoples R China.
   [Su, Yan] Kunming Med Univ, Yunnan Canc Hosp, Dept Grad Student Management, Affiliated Hosp 3, Kunming, Yunnan, Peoples R China.
   [Dong, Jian] Kunming Med Univ, Yunnan Canc Hosp, Dept Med Oncol, Affiliated Hosp 3, Kunming, Yunnan, Peoples R China.
RP Xiong, W (corresponding author), Kunming Med Univ, Yunnan Canc Hosp, Dept Radiotherapy, Affiliated Hosp 3, Kunming, Yunnan, Peoples R China.; Su, Y (corresponding author), Kunming Med Univ, Yunnan Canc Hosp, Dept Grad Student Management, Affiliated Hosp 3, Kunming, Yunnan, Peoples R China.; Dong, J (corresponding author), Kunming Med Univ, Yunnan Canc Hosp, Dept Med Oncol, Affiliated Hosp 3, Kunming, Yunnan, Peoples R China.
EM panda_wei_wei@163.com; 1023445466@qq.com; ynszlyydj@163.com
RI Guoqiang, Xu/ABC-7298-2021; Zhao, Liufang/AFP-5716-2022
OI Guoqiang, Xu/0000-0003-3708-4167; Zhao, Liufang/0000-0003-3283-052X
FU Kunming Medical University
FX Funding This study was supported by Ten Thousand Plan Youth Talent
   Project in Yunnan Province and Innovation Fund project of Graduate
   Student in Kunming Medical University (2021S242).
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NR 47
TC 0
Z9 0
U1 1
U2 1
PU FRONTIERS MEDIA SA
PI LAUSANNE
PA AVENUE DU TRIBUNAL FEDERAL 34, LAUSANNE, CH-1015, SWITZERLAND
SN 2234-943X
J9 FRONT ONCOL
JI Front. Oncol.
PD OCT 8
PY 2021
VL 11
AR 613949
DI 10.3389/fonc.2021.613949
PG 15
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA WM2WM
UT WOS:000710950900001
PM 34692467
OA Green Published, gold
DA 2022-04-25
ER

PT J
AU Hu, WH
   Yang, WC
   Liu, PF
   Liu, TT
   Morgan, P
   Tsai, WL
   Pan, HW
   Lee, CH
   Shu, CW
AF Hu, Wan-Hsiang
   Yang, Wen-Chi
   Liu, Pei-Feng
   Liu, Ting-Ting
   Morgan, Paul
   Tsai, Wei-Lun
   Pan, Hung-Wei
   Lee, Cheng-Hsin
   Shu, Chih-Wen
TI Clinicopathological Association of Autophagy Related 5 Protein with
   Prognosis of Colorectal Cancer
SO DIAGNOSTICS
LA English
DT Article
DE autophagy; ATG5; prognosis; colorectal cancer
ID EXPRESSION
AB Gene mutation and pathogenesis bacteria are highly associated with colorectal cancer (CRC) development and progression. Autophagy is a self-clearance pathway to degrade abnormal proteins and infected bacteria in cells. Autophagy plays a dual role in cancer development. Among the autophagy-related (ATG) proteins, ATG5 is the key component required for the core machinery of autophagy. However, the role of ATG5 in CRC malignancy remains unclear. Herein, we found that a high ATG5 protein level was correlated with poor overall survival (OS) and disease-free survival (DFS) of 118 patients with CRC. After stratification with demographic and clinicopathologic factors, a high ATG5 protein level was significantly correlated with unfavorable overall survival in female and elder (>60 year) CRC patients and tumor tissues with poor differentiation, late T stages (III + IV), whereas the ATG5 protein level was positively associated with the overall survival in CRC patients without lymph node invasion and radiation therapy. In contrast, a high ATG5 protein level was significantly associated with worse DFS in CRC patients with early stage of AJCC and no radiation therapy. In addition, colorectal cancer cells stably harboring small interfering RNA (siRNA) against ATG5 diminished the tumorsphere formation and sensitized cancer cells to chemotherapeutic agents. Taken together, our results suggest that ATG5 might be a prognostic biomarker for CRC and a potential therapeutic target for CRC patients.
C1 [Hu, Wan-Hsiang] Kaohsiung Chang Gung Mem Hosp, Dept Colorectal Surg, Kaohsiung 83341, Taiwan.
   [Hu, Wan-Hsiang; Liu, Ting-Ting] Chang Gung Univ, Coll Med, Kaohsiung 83341, Taiwan.
   [Hu, Wan-Hsiang] Chang Gung Univ, Grad Inst Clin Med Sci, Coll Med, Kaohsiung 83341, Taiwan.
   [Yang, Wen-Chi] E DA Hosp, Div Hematol & Med Oncol, Dept Internal Med, Kaohsiung 82445, Taiwan.
   [Yang, Wen-Chi; Morgan, Paul; Pan, Hung-Wei] I Shou Univ, Sch Med Int Students, Kaohsiung 82445, Taiwan.
   [Liu, Pei-Feng; Lee, Cheng-Hsin; Shu, Chih-Wen] Kaohsiung Med Univ, Dept Biomed Sci & Environm Biol, Kaohsiung 80708, Taiwan.
   [Liu, Pei-Feng] Kaohsiung Med Univ Hosp, Dept Med Res, Kaohsiung 80708, Taiwan.
   [Liu, Ting-Ting] I Shou Univ, Dept Med Lab Sci, Kaohsiung 82445, Taiwan.
   [Liu, Ting-Ting] Kaohsiung Chang Gung Mem Hosp, Dept Pathol, Kaohsiung 83341, Taiwan.
   [Tsai, Wei-Lun] Kaohsiung Vet Gen Hosp, Dept Internal Med, Kaohsiung 81362, Taiwan.
   [Tsai, Wei-Lun] Natl Yang Ming Univ, Sch Med, Taipei 11221, Taiwan.
   [Shu, Chih-Wen] Natl Sun Yat Sen Univ, Inst Biopharmaceut Sci, Kaohsiung 80424, Taiwan.
RP Shu, CW (corresponding author), Kaohsiung Med Univ, Dept Biomed Sci & Environm Biol, Kaohsiung 80708, Taiwan.; Shu, CW (corresponding author), Natl Sun Yat Sen Univ, Inst Biopharmaceut Sci, Kaohsiung 80424, Taiwan.
EM gary.hu0805@gmail.com; wenchi890079@gmail.com; pfliu908203@gmail.com;
   liutt107@cgmh.org.tw; buddymorgan@gmail.com; wltsai@vghks.gov.tw;
   d89444001@gmail.com; angioadsc@gmail.com; cwshu@g-mail.nsysu.edu.tw
OI Morgan, Paul/0000-0002-3231-0738; Yang, Wen-Chi/0000-0001-7062-5194;
   Shu, Chih-Wen/0000-0002-7774-0002; Liu, Pei-Feng/0000-0002-7849-8940
FU Ministry of Science and Technology MOSTMinistry of Science and
   Technology, China [108-2320-B-110008-MY3, 108-2320-B-075B-003];
   Kaohsiung Chang Gung Memorial HospitalChang Gung Memorial Hospital
   [CMRPG8G1001]; E-Da hospital [EDAHP110041]
FX The work was supported by the Ministry of Science and Technology MOST
   (108-2320-B-110008-MY3 and 108-2320-B-075B-003), Kaohsiung Chang Gung
   Memorial Hospital (CMRPG8G1001) and E-Da hospital (EDAHP110041).
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NR 31
TC 1
Z9 1
U1 0
U2 0
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 2075-4418
J9 DIAGNOSTICS
JI Diagnostics
PD MAY
PY 2021
VL 11
IS 5
AR 782
DI 10.3390/diagnostics11050782
PG 13
WC Medicine, General & Internal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC General & Internal Medicine
GA SH0CM
UT WOS:000653806100001
PM 33926066
OA gold, Green Published
DA 2022-04-25
ER

PT J
AU Dashti, F
   Mirazimi, SMA
   Rabiei, N
   Fathazam, R
   Rabiei, N
   Piroozmand, H
   Vosough, M
   Rahimian, N
   Hamblin, MR
   Mirzaei, H
AF Dashti, Fatemeh
   Mirazimi, Seyed Mohammad Ali
   Rabiei, Nikta
   Fathazam, Reza
   Rabiei, Negin
   Piroozmand, Haleh
   Vosough, Massoud
   Rahimian, Neda
   Hamblin, Michael R.
   Mirzaei, Hamed
TI The role of non-coding RNAs in chemotherapy for gastrointestinal cancers
SO MOLECULAR THERAPY-NUCLEIC ACIDS
LA English
DT Review
ID HEPATOCELLULAR-CARCINOMA CELLS; HUMAN GASTRIC-CANCER; INCREASES
   DRUG-RESISTANCE; EPITHELIAL-MESENCHYMAL TRANSITION; DIFFERENTIAL
   MICRORNA EXPRESSION; REGULATES CISPLATIN-RESISTANCE; MODULATES
   MULTIDRUG-RESISTANCE; SENSITIZES COLORECTAL-CANCER; SUPPRESSES
   TUMOR-GROWTH; PANCREATIC-CANCER
AB Gastrointestinal (GI) cancers, including colorectal, gastric, hepatic, esophageal, and pancreatic tumors, are responsible for large numbers of deaths around the world. Chemotherapy is the most common approach used to treat advanced GI cancer. However, chemoresistance has emerged as a critical challenge that prevents successful tumor elimination, leading to metastasis and recurrence. Chemoresistance mechanisms are complex, and many factors and pathways are involved. Among these factors, non-coding RNAs (ncRNAs) are critical regulators of GI tumor development and subsequently can induce resistance to chemotherapy. This occurs because ncRNAs can target multiple signaling pathways, affect downstream genes, and modulate proliferation, apoptosis, tumor cell migration, and autophagy. ncRNAs can also induce cancer stem cell features and affect the epithelial-mesenchymal transition. Thus, ncRNAs could possibly act as new targets in chemotherapy combinations to treat GI cancer and to predict treatment response.
C1 [Dashti, Fatemeh; Mirazimi, Seyed Mohammad Ali] Kashan Univ Med Sci, Sch Med, Kashan, Iran.
   [Dashti, Fatemeh; Mirazimi, Seyed Mohammad Ali] Kashan Univ Med Sci, Student Res Comm, Kashan, Iran.
   [Rabiei, Nikta; Fathazam, Reza; Rabiei, Negin] Shiraz Univ Med Sci, Sch Med, Shiraz, Iran.
   [Piroozmand, Haleh] Islamic Azad Univ, Fac Vet Sci, Sci & Res Branch, Tehran, Iran.
   [Vosough, Massoud] ACECR, Royan Inst Stem Cell Biol & Technol, Cell Sci Res Ctr, Dept Regenerat Med, Tehran, Iran.
   [Rahimian, Neda] Iran Univ Med Sci IUMS, Endocrine Res Ctr, Inst Endocrinol & Metab, Tehran, Iran.
   [Hamblin, Michael R.] Univ Johannesburg, Fac Hlth Sci, Laser Res Ctr, ZA-2028 Doornfontein, South Africa.
   [Hamblin, Michael R.] Iran Univ Med Sci, Radiat Biol Res Ctr, Tehran, Iran.
   [Mirzaei, Hamed] Kashan Univ Med Sci, Res Ctr Biochem & Nutr Metab Dis, Inst Basic Sci, Kashan, Iran.
RP Rahimian, N (corresponding author), Iran Univ Med Sci IUMS, Endocrine Res Ctr, Inst Endocrinol & Metab, Tehran, Iran.; Hamblin, MR (corresponding author), Univ Johannesburg, Fac Hlth Sci, Laser Res Ctr, ZA-2028 Doornfontein, South Africa.; Mirzaei, H (corresponding author), Kashan Univ Med Sci, Res Ctr Biochem & Nutr Metab Dis, Inst Basic Sci, Kashan, Iran.
EM rahimian.n@iums.ac.ir; hamblin.lab@gmail.com; mirzaei-h@kaums.ac.ir
RI Rahimian, Neda/AAJ-8068-2020; Hamblin, Michael R/H-2758-2019
OI Rahimian, Neda/0000-0003-2432-5099; Hamblin, Michael
   R/0000-0001-6431-4605; mirzaei, hamed/0000-0002-9399-8281; Rabiei,
   Nikta/0000-0002-4646-1262
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NR 499
TC 5
Z9 5
U1 9
U2 9
PU CELL PRESS
PI CAMBRIDGE
PA 50 HAMPSHIRE ST, FLOOR 5, CAMBRIDGE, MA 02139 USA
SN 2162-2531
J9 MOL THER-NUCL ACIDS
JI Mol. Ther.-Nucl. Acids
PD DEC 3
PY 2021
VL 26
BP 892
EP 926
DI 10.1016/j.omtn.2021.10.004
EA OCT 2021
PG 35
WC Medicine, Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Research & Experimental Medicine
GA XO4TH
UT WOS:000730179100013
PM 34760336
OA Green Published, gold
DA 2022-04-25
ER

PT J
AU Schiavano, GF
   De Santi, M
   Brandi, G
   Fanelli, M
   Bucchini, A
   Giamperi, L
   Giomaro, G
AF Schiavano, Giuditta Fiorella
   De Santi, Mauro
   Brandi, Giorgio
   Fanelli, Mirco
   Bucchini, Anahi
   Giamperi, Laura
   Giomaro, Giovanna
TI Inhibition of Breast Cancer Cell Proliferation and In Vitro
   Tumorigenesis by a New Red Apple Cultivar
SO PLOS ONE
LA English
DT Article
ID ANTIPROLIFERATIVE ACTIVITY; ANTIOXIDANT ACTIVITY; MAMMARY-TUMORS;
   FLAVONOIDS; COLON; VEGETABLES; APOPTOSIS; FRUIT; JUICE; CHEMOPREVENTION
AB Purpose
   The aim of this study was to evaluate the antiproliferative activity in breast cancer cells and the inhibition of tumorigenesis in pre-neoplastic cells of a new apple cultivar with reddish pulp, called the Pelingo apple.
   Methods
   The antiproliferative activity was evaluated in MCF-7 and MDA-MB-231 human breast cancer cells. The inhibition of tumorigenesis was performed in JB6 promotion-sensitive (P+) cells.
   Results
   Results showed that Pelingo apple juice is characterized by a very high polyphenol content and strongly inhibited breast cancer cell proliferation. Its antiproliferative activity was found to be higher than the other five apple juices tested. Pelingo juice induced cell accumulation in the G2/M phase of the cell cycle and autophagy through overexpression of p21, inhibition of extracellular signal-regulated kinases 1/2 (ERK1/2) activity and an increase in lipidated microtubule-associated protein-1 light chain-3 beta (LC3B). Remarkably, Pelingo juice inhibited the 12-o-tetra-decanoyl-phorbol-13-acetate (TPA)-induced tumorigenesis of JB6 P+ cells, suppressing colony formation in semi-solid medium and TPA-induced ERK1/2 phosphorylation.
   Conclusions
   Our data indicate that the Pelingo apple is rich in food components that can markedly inhibit in vitro tumorigenesis and growth of human breast cancer cells and could provide natural bioactive non-nutrient compounds, with potential chemopreventive activity.
C1 [Schiavano, Giuditta Fiorella; De Santi, Mauro; Brandi, Giorgio; Fanelli, Mirco] Univ Urbino Carlo Bo, Dept Biomol Sci, Urbino, PU, Italy.
   [Bucchini, Anahi; Giamperi, Laura; Giomaro, Giovanna] Univ Urbino Carlo Bo, Dept Earth Life & Environm Sci, Urbino, PU, Italy.
RP Schiavano, GF (corresponding author), Univ Urbino Carlo Bo, Dept Biomol Sci, Urbino, PU, Italy.
EM giuditta.schiavano@uniurb.it
RI Fanelli, Mirco/F-2665-2011; De Santi, Mauro/F-5401-2013
OI Fanelli, Mirco/0000-0002-9649-8661; De Santi, Mauro/0000-0003-2983-8344;
   Schiavano, Giuditta Fiorella/0000-0002-1427-3486; Bucchini, Anahi Elena
   Ada/0000-0003-3100-9262; Brandi, Giorgio/0000-0003-1380-6137
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NR 56
TC 22
Z9 23
U1 1
U2 10
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 1160 BATTERY STREET, STE 100, SAN FRANCISCO, CA 94111 USA
SN 1932-6203
J9 PLOS ONE
JI PLoS One
PD AUG 18
PY 2015
VL 10
IS 8
AR e0135840
DI 10.1371/journal.pone.0135840
PG 17
WC Multidisciplinary Sciences
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Science & Technology - Other Topics
GA CP1VY
UT WOS:000359666100073
PM 26284516
OA Green Published, gold, Green Submitted
DA 2022-04-25
ER

PT J
AU Chou, TF
   Li, KL
   Frankowski, KJ
   Schoenen, FJ
   Deshaies, RJ
AF Chou, Tsui-Fen
   Li, Kelin
   Frankowski, Kevin J.
   Schoenen, Frank J.
   Deshaies, Raymond J.
TI Structure-Activity Relationship Study Reveals ML240 and ML241 as Potent
   and Selective Inhibitors of p97 ATPase
SO CHEMMEDCHEM
LA English
DT Article
DE AAA ATPase; autophagy; cancer; structure-activity relationships;
   ubiquitin proteasome
ID AAA-ATPASE; PROTEIN VCP; UBIQUITIN; CDC48/P97; COMPLEX; MEDIATE;
   P97/VCP; DOMAIN; LINKS; ER
AB To discover more potent p97 inhibitors, we carried out a structureactivity relationship study of the quinazoline scaffold previously identified from our HTS campaigns. Two improved inhibitors, ML240 and ML241, inhibit p97 ATPase with IC50 values of 100 nM. Both compounds inhibited degradation of a p97-dependent but not a p97-independent proteasome substrate in a dual-reporter cell line. They also impaired the endoplasmic-reticulum-associated degradation (ERAD) pathway. Unexpectedly, ML240 potently stimulated accumulation of LC3-II within minutes, inhibited cancer cell growth, and rapidly mobilized the executioner caspases 3 and 7, whereas ML241 did not. The behavior of ML240 suggests that disruption of the protein homeostasis function of p97 leads to more rapid activation of apoptosis than is observed with a proteasome inhibitor. Further characterization revealed that ML240 has broad antiproliferative activity toward the NCI-60 panel of cancer cell lines, but slightly lower activity toward normal cells. ML240 also synergizes with the proteasome inhibitor MG132 to kill multiple colon cancer cell lines. Meanwhile, both probes have low off-target activity toward a panel of protein kinases and central nervous system targets. Our results nominate ML240 as a promising starting point for the development of a novel agent for the chemotherapy of cancer, and provide a rationale for developing pathway-specific p97 inhibitors.
C1 [Chou, Tsui-Fen; Deshaies, Raymond J.] CALTECH, Div Biol, Pasadena, CA 91125 USA.
   [Chou, Tsui-Fen; Deshaies, Raymond J.] CALTECH, Howard Hughes Med Inst, Pasadena, CA 91125 USA.
   [Li, Kelin; Frankowski, Kevin J.; Schoenen, Frank J.] Univ Kansas, Specialized Chem Ctr, Struct Biol Ctr, Lawrence, KS 66047 USA.
   [Chou, Tsui-Fen] Harbor UCLA Med Ctr, Dept Pediat, Div Med Genet, Torrance, CA 90502 USA.
   [Chou, Tsui-Fen] Los Angeles Biomed Res Inst, Torrance, CA 90502 USA.
RP Chou, TF (corresponding author), CALTECH, Div Biol, 1200 E Calif Blvd, Pasadena, CA 91125 USA.
EM tsuifenchou@ucla.edu; deshaies@caltech.edu
RI Deshaies, Raymond/B-8354-2014
OI Deshaies, Raymond/0000-0002-3671-9354; Schoenen,
   Frank/0000-0003-2711-1117
FU National Institute of Mental Health's Psychoactive Drug Screening
   ProgramUnited States Department of Health & Human ServicesNational
   Institutes of Health (NIH) - USANIH National Institute of Mental Health
   (NIMH) [HHSN-271-2008-00025-C]; NIH Molecular Libraries Probe Production
   Centers Network [5U54HG005031]; Howard Hughes Medical InstituteHoward
   Hughes Medical Institute; NATIONAL HUMAN GENOME RESEARCH INSTITUTEUnited
   States Department of Health & Human ServicesNational Institutes of
   Health (NIH) - USANIH National Human Genome Research Institute (NHGRI)
   [U54HG005031] Funding Source: NIH RePORTER
FX We thank B. E. Nordin and M. P. Patricelli (ActivX Biosciences La Jolla,
   CA, USA) for analyzing the ACJI-47 positive control free of charge in
   the kinase profiling experiments. K<INF>i</INF> determinations and
   receptor binding profiles were generously provided by the National
   Institute of Mental Health's Psychoactive Drug Screening Program,
   Contract no. HHSN-271-2008-00025-C (NIMH PDSP). The NIMH PDSP is
   Directed by Bryan L. Roth, MD PhD (University of North Carolina, Chapel
   Hill, NC, USA) and Project Officer Jamie Driscol (NIMH, Bethesda MD,
   USA). The NCI 60-cell-line screen was performed by the Developmental
   Therapeutics Program at the NCI. We thank Jeffrey Aube (University of
   Kansas, Lawrence, KS, USA) for helpful discussions, P. Porubsky
   (University of Kansas) for compound management, Ben Neuenswander
   (University of Kansas) for compound purification and high-resolution
   mass determination, Justin Douglas and Sarah Neuenswander (University of
   Kansas) for NMR assistance, R. Weinberg (Massachusetts Institute of
   Technology, Cambridge, MA, USA) via H. Chang (Stanford University, CA,
   USA) for providing PHMLEB and PHMLER cells, K. S. Osthoff (Eberhard
   Karls University, Tubingen, Germany) via G. M. Cohen (University of
   Leicester, UK) for caspase 9-/- cells, G. Salvesen (Sanford-Burnham
   Medical Research Institute) for caspase 8-/- cells, and H. Park, R.
   Oania, and D. Shimoda for technical assistance. This work was supported
   by a grant from the NIH Molecular Libraries Probe Production Centers
   Network to Jeffrey Aube (PI) (5U54HG005031). R.J.D. and T.-F.C. were
   supported by the Howard Hughes Medical Institute, of which R.J.D. is an
   Investigator.
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NR 36
TC 94
Z9 94
U1 1
U2 24
PU WILEY-V C H VERLAG GMBH
PI WEINHEIM
PA POSTFACH 101161, 69451 WEINHEIM, GERMANY
SN 1860-7179
EI 1860-7187
J9 CHEMMEDCHEM
JI ChemMedChem
PD FEB
PY 2013
VL 8
IS 2
BP 297
EP 312
DI 10.1002/cmdc.201200520
PG 16
WC Chemistry, Medicinal; Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA 079LU
UT WOS:000314172700013
PM 23316025
OA Green Accepted, Green Submitted, Green Published
DA 2022-04-25
ER

PT J
AU Lokireddy, S
   Wijesoma, IW
   Bonala, S
   Wei, M
   Sze, SK
   McFarlane, C
   Kambadur, R
   Sharma, M
AF Lokireddy, Sudarsanareddy
   Wijesoma, Isuru Wijerupage
   Bonala, Sabeera
   Wei, Meng
   Sze, Siu Kwan
   McFarlane, Craig
   Kambadur, Ravi
   Sharma, Mridula
TI RETRACTED: Myostatin is a novel tumoral factor that induces cancer
   cachexia (Retracted article. See vol. 473, pg. 1111, 2016)
SO BIOCHEMICAL JOURNAL
LA English
DT Article; Retracted Publication
DE activin receptor type II B; autophagy-lysosome system; myostatin;
   nuclear factor kappa B (NF-kappa B); reactive oxygen species (ROS);
   skeletal muscle wasting; tumoral factor; ubiquitin-proteasome system
ID SKELETAL-MUSCLE HYPERTROPHY; MITOCHONDRIAL E3; PATHWAYS; ATROPHY;
   DIFFERENTIATION; ACTIVATION; MECHANISMS; PROTEINS; DYNAMICS; COMPLEX
AB Humoral and tumoral factors collectively promote cancer-induced skeletal muscle wasting by increasing protein degradation. Although several humoral proteins, namely TNF alpha (tumour necrosis factor alpha) and IL (interleukin)-6, have been shown to induce skeletal muscle wasting, there is a lack of information regarding the tumoral factors that contribute to the atrophy of muscle during cancer cachexia. Therefore, in the present study, we have characterized the secretome of C26 colon cancer cells to identify the tumoral factors involved in cancer-induced skeletal muscle wasting. In the present study, we show that myostatin, a procachectic TGF beta (transforming growth factor beta) superfamily member, is abundantly secreted by C26 cells. Consistent with myostatin signalling during cachexia, treating differentiated C2C12 myotubes with C26 CM (conditioned medium) resulted in myotubular atrophy due to the up-regulation of muscle-specific E3 ligases, atrogin-1 and MuRF1 (muscle RING-finger protein 1), and enhanced activity of the ubiquitin proteasome pathway. Furthermore, the C26 CM also activated ActRIIB (activin receptor type II B)/Smad and NF-kappa B (nuclear factor kappa B) signalling, and reduced the activity of the IGF-I (insulin-like growth factor 1)/P13K (phosphoinositide 3-kinase)/Akt pathway, three salient molecular features of myostatin action in skeletal muscles. Antagonists to myostatin prevented C26 CM-induced wasting in muscle cell cultures, further confirming that tumoral myostatin may be a key contributor in the pathogenesis of cancer cachexia. Finally, we show that treatment with C26 CM induced the autophagy-lysosome pathway and reduced the number of mitochondria in myotubes. These two previously unreported observations were recapitulated in skeletal muscles collected from C26 tumour-bearing mice.
C1 [Sharma, Mridula] Natl Univ Singapore, Yong Loo Lin Sch Med, Dept Biochem, Singapore 117595, Singapore.
   [Lokireddy, Sudarsanareddy; Wijesoma, Isuru Wijerupage; Bonala, Sabeera; Wei, Meng; Sze, Siu Kwan; Kambadur, Ravi] Nanyang Technol Univ, Sch Biol Sci, Singapore, Singapore.
   [McFarlane, Craig; Kambadur, Ravi] ASTAR, Singapore Inst Clin Sci, Singapore, Singapore.
RP Sharma, M (corresponding author), Natl Univ Singapore, Yong Loo Lin Sch Med, Dept Biochem, Singapore 117595, Singapore.
EM bchmridu@nus.edu.sg
RI Sze, Siu Kwan/AAO-3342-2020
OI Sze, Siu Kwan/0000-0002-5652-1687
FU NICHD (National Institute of Child Health and Human Development)United
   States Department of Health & Human ServicesNational Institutes of
   Health (NIH) - USANIH Eunice Kennedy Shriver National Institute of Child
   Health & Human Development (NICHD); MOE (Ministry of Education),
   SingaporeMinistry of Education, Singapore [T208B3211]; BMRC (Biomedical
   Research Council), SingaporeAgency for Science Technology & Research
   (ASTAR) [07/1/21/19/521]
FX We thank Esther Latres (Regeneron Pharmaceuticals, Tarrytown, NJ,
   U.S.A.) for providing the anti-atrogin-1 and anti-MuRF1 antibodies used
   in the present study. The MF20 and T14 monoclonal antibodies developed
   by Donald A. Fischman and Frank E. Stockdale respectively were obtained
   from the Developmental Studies Hybridoma Bank developed under the
   auspices of the NICHD (National Institute of Child Health and Human
   Development) and maintained by Department of Biology, The University of
   Iowa, Iowa City, IA, U.S.A. Finally, we thank Addgene (Cambridge, MA,
   U.S.A.) for providing the reporter vectors [FoxO3 (Dr Michael Greenberg,
   #1789), PGC-1 alpha (Dr Bruce Spiegelman, #8887) and 4X SBE (Dr Bert
   Vogelstein, #16495)].; This work was supported by the MOE (Ministry of
   Education), Singapore [grant number T208B3211] and BMRC (Biomedical
   Research Council), Singapore [grant number 07/1/21/19/521].
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NR 46
TC 70
Z9 76
U1 0
U2 27
PU PORTLAND PRESS LTD
PI LONDON
PA CHARLES DARWIN HOUSE, 12 ROGER STREET, LONDON WC1N 2JU, ENGLAND
SN 0264-6021
EI 1470-8728
J9 BIOCHEM J
JI Biochem. J.
PD AUG 15
PY 2012
VL 446
BP 23
EP 36
DI 10.1042/BJ20112024
PN 1
PG 14
WC Biochemistry & Molecular Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology
GA 990JH
UT WOS:000307626300003
PM 22621320
OA hybrid, Green Published
DA 2022-04-25
ER

PT J
AU Lembo-Fazio, L
   Nigro, G
   Noel, G
   Rossi, G
   Chiara, F
   Tsilingiri, K
   Rescigno, M
   Rasola, A
   Bernardini, ML
AF Lembo-Fazio, L.
   Nigro, G.
   Noel, G.
   Rossi, G.
   Chiara, F.
   Tsilingiri, K.
   Rescigno, M.
   Rasola, A.
   Bernardini, M. L.
TI Gadd45 alpha activity is the principal effector of Shigella
   mitochondria-dependent epithelial cell death in vitro and ex vivo
SO CELL DEATH & DISEASE
LA English
DT Article
DE apoptosis; mitochondria; Shigella; infection; Gadd45 alpha
ID MONOCYTE-DERIVED MACROPHAGES; GROWTH-ARREST; CANCER-CELL; APOPTOSIS;
   FLEXNERI; NECROSIS; MULTIPLICATION; INFECTION; AUTOPHAGY; RESPONSES
AB Modulation of death is a pathogen strategy to establish residence and promote survival in host cells and tissues. Shigella spp. are human pathogens that invade colonic mucosa, where they provoke lesions caused by their ability to manipulate the host cell responses. Shigella spp. induce various types of cell death in different cell populations. However, they are equally able to protect host cells from death. Here, we have investigated on the molecular mechanisms and cell effectors governing the balance between survival and death in epithelial cells infected with Shigella. To explore these aspects, we have exploited both, the HeLa cell invasion assay and a novel ex vivo human colon organ culture model of infection that mimics natural conditions of shigellosis. Our results definitely show that Shigella induces a rapid intrinsic apoptosis of infected cells, via mitochondrial depolarization and the ensuing caspase-9 activation. Moreover, for the first time we identify the eukaryotic stress-response factor growth arrest and DNA damage 45 alpha as a key player in the induction of the apoptotic process elicited by Shigella in epithelial cells, revealing an unexplored role of this molecule in the course of infections sustained by invasive pathogens. Cell Death and Disease ( 2011) 2, e122; doi: 10.1038/cddis.2011.4; published online 24 February 2011
C1 [Bernardini, M. L.] Univ Roma La Sapienza, Inst Pasteur, Fdn Cenci Bolognetti, Dipartimento Biol & Biotecnol Charles Darwin, I-00185 Rome, Italy.
   [Rossi, G.] Univ Camerino, Dipartimento Sci Vet, Matelica, Macerata, Italy.
   [Chiara, F.; Rasola, A.] Univ Padua, Dipartimento Sci Biomed, Padua, Italy.
   [Chiara, F.] Univ Padua, Dipartimento Med Ambientale & Sanita Pubbl, Padua, Italy.
   [Tsilingiri, K.; Rescigno, M.] Inst Oncol, Dept Expt Oncol European, Milan, Italy.
RP Bernardini, ML (corresponding author), Univ Roma La Sapienza, Inst Pasteur, Fdn Cenci Bolognetti, Dipartimento Biol & Biotecnol Charles Darwin, Via Dei Sardi 70, I-00185 Rome, Italy.
EM marialina.bernardini@uniroma1.it
RI Rescigno, Maria/J-9704-2012
OI Rescigno, Maria/0000-0002-6464-509X; chiara,
   federica/0000-0003-2396-3080; BERNARDINI, Maria/0000-0002-4305-7694;
   Lembo Fazio, Luigi/0000-0001-5684-9191; Rasola,
   Andrea/0000-0003-4522-3008
FU Italian 'Ministero dell'Istruzione, Universita e Ricerca'Ministry of
   Education, Universities and Research (MIUR); Luigi Lembo-Fazio;
   Marie-Curie fellowshipEuropean Commission; cross-talk network
FX This work was partially supported by grants from the Italian 'Ministero
   dell'Istruzione, Universita e Ricerca' (PRIN 2009). Luigi Lembo-Fazio,
   Giulia Nigro and Gaelle Noel were fellows of the 'Istituto
   Pasteur-Fondazione Cenci Bolognetti'. Katerina Tsilingiri is a recipient
   of a Marie-Curie fellowship within the cross-talk network.
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NR 40
TC 19
Z9 19
U1 0
U2 3
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 2041-4889
J9 CELL DEATH DIS
JI Cell Death Dis.
PD FEB
PY 2011
VL 2
AR e122
DI 10.1038/cddis.2011.4
PG 12
WC Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Cell Biology
GA 726CH
UT WOS:000287695600005
PM 21368893
OA Green Published, gold
DA 2022-04-25
ER

PT J
AU Zhang, HY
   Lei, YL
   Yuan, P
   Li, LJ
   Luo, C
   Gao, R
   Tian, J
   Feng, ZH
   Nice, EC
   Sun, J
AF Zhang, Haiyuan
   Lei, Yunlong
   Yuan, Ping
   Li, Lingjun
   Luo, Chao
   Gao, Rui
   Tian, Jun
   Feng, Zuohua
   Nice, Edouard C.
   Sun, Jun
TI ROS-Mediated Autophagy Induced by Dysregulation of Lipid Metabolism
   Plays a Protective Role in Colorectal Cancer Cells Treated with Gambogic
   Acid
SO PLOS ONE
LA English
DT Article
ID MALIGNANT GLIOMA-CELLS; INDUCED APOPTOSIS; TUMOR PROGRESSION; OXIDATIVE
   STRESS; REDOX REGULATION; KAPPA-B; OXYGEN; DEATH; ACTIVATION; INDUCTION
AB Gambogic acid (GA), the main active component of gamboge resin, has potent antitumor activity both in vivo and in vitro. However, the underlying molecular mechanisms remain unclear. In this study, we found that GA could initiate autophagy in colorectal cancer cells, and inhibition of the autophagy process accelerated the effect of proliferative inhibition and apoptotic cell death induced by GA, implying a protective role of autophagy. Two-dimensional electrophoresis-based proteomics showed that GA treatment altered the expression of multiple proteins involved in redox signaling and lipid metabolism. Functional studies revealed that GA-induced dysregulation of lipid metabolism could activate 5-lipoxygenase (5-LOX), resulting in intracellular ROS accumulation, followed by inhibition of Akt-mTOR signaling and autophagy initiation. Finally, results using a xenograft model suggested ROS-induced autophagy protect against the antitumor effect of GA. Taken together, these data showed new biological activities of GA against colorectal cancer underlying the protective role of ROS-induced autophagy. This study will provide valuable insights for future studies regarding the anticancer mechanisms of GA.
C1 [Zhang, Haiyuan; Yuan, Ping; Li, Lingjun; Luo, Chao; Gao, Rui; Tian, Jun; Feng, Zuohua; Sun, Jun] Huazhong Univ Sci & Technol, Tongji Med Coll, Dept Biochem & Mol Biol, Wuhan 430074, Peoples R China.
   [Lei, Yunlong] Chongqing Med Univ, Dept Biochem & Mol Biol, Chongqing, Peoples R China.
   [Lei, Yunlong] Chongqing Med Univ, Mol Med & Canc Res Ctr, Chongqing, Peoples R China.
   [Nice, Edouard C.] Monash Univ, Dept Biochem & Mol Biol, Clayton, Vic, Australia.
RP Sun, J (corresponding author), Huazhong Univ Sci & Technol, Tongji Med Coll, Dept Biochem & Mol Biol, Wuhan 430074, Peoples R China.
EM sun_jun99@163.com
OI Lei, Yunlong/0000-0002-7918-0221
FU National Natural Science Foundation of ChinaNational Natural Science
   Foundation of China (NSFC) [30672480]; National High Technology Research
   and Development Program of China (863 Program)National High Technology
   Research and Development Program of China [2012AA020201]; National 973
   Basic Research Program of ChinaNational Basic Research Program of China
   [2013CB911300]; Education Department of Hubei province science and
   technology research projects of outstanding young talent project
   [Q20091207]
FX This work was supported by grants from National Natural Science
   Foundation of China (Grant number: 30672480), National High Technology
   Research and Development Program of China (863 Program; No.
   2012AA020201), the National 973 Basic Research Program of China
   (2013CB911300) and the Education Department of Hubei province science
   and technology research projects of outstanding young talent
   project(Q20091207). The funders had no role in study design, data
   collection and analysis, decision to publish, or preparation of the
   manuscript.
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NR 91
TC 37
Z9 40
U1 4
U2 33
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 1160 BATTERY STREET, STE 100, SAN FRANCISCO, CA 94111 USA
SN 1932-6203
J9 PLOS ONE
JI PLoS One
PD MAY 8
PY 2014
VL 9
IS 5
AR e96418
DI 10.1371/journal.pone.0096418
PG 14
WC Multidisciplinary Sciences
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Science & Technology - Other Topics
GA AK1XT
UT WOS:000338213300035
PM 24810758
OA Green Submitted, Green Published, gold
DA 2022-04-25
ER

PT J
AU Duan, P
   Hu, CH
   Quan, C
   Yu, TT
   Zhou, W
   Yuan, M
   Shi, YQ
   Yang, KD
AF Duan, Peng
   Hu, Chunhui
   Quan, Chao
   Yu, Tingting
   Zhou, Wei
   Yuan, Meng
   Shi, Yuqin
   Yang, Kedi
TI 4-Nonylphenol induces apoptosis, autophagy and necrosis in Sertoli
   cells: Involvement of ROS-mediated AMPK/AKT-mTOR and JNK pathways
SO TOXICOLOGY
LA English
DT Article
DE 4-Nonylphenol; Sertoli cells; Apoptosis; Autophagy; ROS; AMPK/Akt/JNK
   signalling
ID ACTIVATED PROTEIN-KINASE; BPA-INDUCED APOPTOSIS; COLON-CANCER CELLS;
   SIGNALING PATHWAY; CYCLE ARREST; AKT/MTOR PATHWAY; DOWN-REGULATION;
   STEM-CELLS; TM4 CELLS; IN-VITRO
AB The xenoestrogen 4-nonylphenol (NP) induces reproductive dysfunction of male rats, but the fundamental mechanism of this phenomenon is largely unexplored. Sertoli cells (SCs) are pivotal for spermatogenesis and male fertility. The involvement of autophagy in NP-induced apoptotic and necrotic death of SCs was investigated. In this study, 24-h exposure of SCs to 20-30 mu M NP decreased cell viability, caused G2/M arrest, triggered Delta Psi m loss, increased ROS production and induced caspase-dependent apoptsis, necrosis as well as autophagosome formation. NP-induced autophagy was confirmed by monodansylcadaverine-staining and LC3-I/LC3-II conversion. Furthermore, NP up-regulated the (Thr)172p- AMPK/AMPK and (Thr183/185)p-JNK/JNK ratios. This was followed by the down-regulation of Ser(473)p-Akt/Akt, (Thr1462)p-TSC2/TSC2, (ser2448)p-mTOR/mTOR, (Thr389)p-p70S6K/p70S6K and (Thr37/45)p-4EBP1/4EBP1. Intriguingly, NP-induced apoptosis, autophagy and necrosis could be inhibited through blocking ROS generation by N-acetylcysteine. Autophagy inhibitor 3-MA enhanced NP-induced apoptosis and necrosis. Moreover, The activation of AMPK/mTOR/p70s6k/4EBP1 and JNK signalling pathways induced by NP could be efficiently reversed by pretreatment of N-acetylcysteine or 3-MA. Collectively, our findings provide the first evidence that NP promotes apoptosis, autophagy and necrosis simultaneously in SCs and that this process may involve ROS-dependent JNK- and Akt/AMPK/mTOR pathways. Modulation of autophagy induced by NP may serve as a survival mechanism against apoptosis and necrosis. (C) 2016 Elsevier Ireland Ltd. All rights reserved.
C1 [Duan, Peng; Quan, Chao; Yu, Tingting; Zhou, Wei; Yuan, Meng; Yang, Kedi] Huazhong Univ Sci & Technol, Tongji Med Coll, Dept Occupat & Environm Hlth, MOE Minist Educ,Key Lab Environm & Hlth, Wuhan 430030, Peoples R China.
   [Hu, Chunhui] Hubei Univ Med, Dept Lab Med, Taihe Hosp, Shiyan 442000, Hubei, Peoples R China.
   [Shi, Yuqin] Wuhan Univ Sci & Technol, Coll Med, Sch Publ Hlth, Dept Epidemiol & Hlth Stat, Wuhan 430030, Peoples R China.
RP Yang, KD (corresponding author), Huazhong Univ Sci & Technol, Tongji Med Coll, Dept Occupat & Environm Hlth, 13 Hangkong Rd, Wuhan 430030, Hubei Province, Peoples R China.
EM yangkd@mails.tjmu.edu.cn
FU National Natural Science Foundation of ChinaNational Natural Science
   Foundation of China (NSFC) [81372960, 81172623]
FX This work is supported by grants from The National Natural Science
   Foundation of China (grant number: 81372960, 81172623).
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NR 62
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Z9 93
U1 3
U2 86
PU ELSEVIER IRELAND LTD
PI CLARE
PA ELSEVIER HOUSE, BROOKVALE PLAZA, EAST PARK SHANNON, CO, CLARE, 00000,
   IRELAND
SN 0300-483X
J9 TOXICOLOGY
JI Toxicology
PD FEB 3
PY 2016
VL 341
BP 28
EP 40
DI 10.1016/j.tox.2016.01.004
PG 13
WC Pharmacology & Pharmacy; Toxicology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy; Toxicology
GA DG1QY
UT WOS:000371843800003
PM 26804764
DA 2022-04-25
ER

PT J
AU Wang, YY
   Qin, C
   Yang, G
   Zhao, BB
   Wang, WB
AF Wang, Yuanyang
   Qin, Cheng
   Yang, Gang
   Zhao, Bangbo
   Wang, Weibin
TI The role of autophagy in pancreatic cancer progression
SO BIOCHIMICA ET BIOPHYSICA ACTA-REVIEWS ON CANCER
LA English
DT Review
DE Pancreatic cancer; Autophagy; Epithelial-mesenchymal transition; Glucose
   metabolism; Immunotherapy; Chemoresistance
ID EPITHELIAL-MESENCHYMAL TRANSITION; DUCTAL ADENOCARCINOMA;
   HEPATOCELLULAR-CARCINOMA; GEMCITABINE RESISTANCE; COLORECTAL-CANCER;
   STELLATE CELLS; GROWTH; INHIBITION; INVASION; SURVIVAL
AB Patients with pancreatic cancer have an abysmal survival rate. The poor prognosis of pancreatic cancer is due to the difficulty of making an early diagnosis, high rate of metastasis, and frequent chemoresistance. In recent years, as a self-regulatory procedure within cells, the effect and mechanism of autophagy have been explored. Dysregulated autophagy serves as a double-edged sword in cancer development in which autophagy inhibits cancer initiation but promotes cancer progression. After tumor formation, activation of autophagy can induce epithelialmesenchymal transition, regulate metabolism, specifically glutamine usage and the glycolytic process, and mediate drug resistance in pancreatic cancer. Multiple genes, RNA molecules, proteins, and certain drugs exert antitumor effects by inhibiting autophagy-mediated drug resistance. Several clinical trials have combined autophagy inhibitors with chemotherapeutic drugs in pancreatic cancer treatment, some of which have shown promising results. In conclusion, autophagy plays a vital role in pancreatic cancer progression and deserves further study.
C1 [Wang, Yuanyang; Qin, Cheng; Yang, Gang; Zhao, Bangbo; Wang, Weibin] Chinese Acad Med Sci, Peking Union Med Coll, Peking Union Med Coll Hosp, Dept Gen Surg,State Key Lab Complex Severe & Rare, Beijing 100730, Peoples R China.
RP Wang, WB (corresponding author), Chinese Acad Med Sci, Peking Union Med Coll, Peking Union Med Coll Hosp, Dept Gen Surg,State Key Lab Complex Severe & Rare, Beijing 100730, Peoples R China.
EM pumc_wangyuanyang@student.pumc.edu.cn; wwb_xh@163.com
FU National Natural Science Foundation of ChinaNational Natural Science
   Foundation of China (NSFC) [81773215]; Chinese Academy of Medical
   Sciences [2019XK320002]
FX WWB received support from the National Natural Science Foundation of
   China (No.81773215) and the Chinese Academy of Medical Sciences
   (No.2019XK320002).
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NR 122
TC 2
Z9 2
U1 13
U2 22
PU ELSEVIER
PI AMSTERDAM
PA RADARWEG 29, 1043 NX AMSTERDAM, NETHERLANDS
SN 0304-419X
EI 1879-2561
J9 BBA-REV CANCER
JI Biochim. Biophys. Acta-Rev. Cancer
PD DEC
PY 2021
VL 1876
IS 2
AR 188592
DI 10.1016/j.bbcan.2021.188592
EA JUL 2021
PG 11
WC Biochemistry & Molecular Biology; Biophysics; Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Biophysics; Oncology
GA US0WQ
UT WOS:000697158300007
PM 34274449
DA 2022-04-25
ER

PT J
AU Lin, ZY
   Yun, QZ
   Wu, L
   Zhang, TW
   Yao, TZ
AF Lin, Zhu Yue
   Yun, Qu Zhen
   Wu, Liu
   Zhang, Tian Wen
   Yao, Tang Ze
TI Pharmacological basis and new insights of deguelin concerning its
   anticancer effects
SO PHARMACOLOGICAL RESEARCH
LA English
DT Article
DE Deguelin; Anticancer; Apoptosis; PI3K/Akt signaling pathway; NF-kappa B
   signaling pathway; Wnt signaling pathway
ID TO-MESENCHYMAL TRANSITION; COLON-CANCER CELLS; LUNG-CANCER; BIOLOGICAL
   EVALUATION; HSP90 ACTIVITY; AKT INHIBITOR; TUMOR-GROWTH; APOPTOSIS;
   METASTASIS; MIGRATION
AB Deguelin is a rotenoid of the flavonoid family, which can be extracted from Lonchocarpus, Derris, or Tephrosia. It possesses the inhibition of cancer cell proliferation by inducing apoptosis through regulating the phosphoinositide 3-kinase/protein kinase B (PI3K/Akt) signaling pathway, the NF-kappa B signaling pathway, the Wnt signaling pathway, the adenosine 5 '-monophosphate (AMP)-activated protein kinase (AMPK) signaling pathway and epidermal growth factor receptor (EGFR) signaling, activating the p38 mitogen-activated protein kinase (MAPK) pathway, repression of Bmi1, targeting cyclooxygenase-2 (COX-2), targeting galectin-1, promotion of glycogen synthase kinase-3 beta (GSK3 beta)/FBW7-mediated Mcl-1 destabilization and targeting mitochondria via downregulating Hexokinases II-mediated glycolysis, PUMA-mediation, which are some crucial molecules which modulate closely cancer cell growth and metastasis. Deguelin inhibits tumor cell propagation and malignant transformation through targeting angiogenesis, targeting lymphangiogenesis, targeting focal adhesion kinase (FAK), inhibiting the CtsZ/FAK signaling pathway, targeting epithelial-mesenchymal transition (EMT), the NF-kappa B signaling pathway, regulating NIMA-related kinase 2 (NEK2). In addition, deguelin possesses other biological activities, such as targeting cell cycle arrest, modulation of autophagy, inhibition of hedgehog pathway, inducing differentiation of mutated NPM1 acute myeloid leukemia etc. Therefore, deguelin is a promising chemopreventive agent for cancer therapy.
C1 [Lin, Zhu Yue; Wu, Liu; Zhang, Tian Wen; Yao, Tang Ze] Dalian Med Univ, Pharmacol Dept, 9 West Sect,South Rd Lvshun, Dalian 116044, Liaoning, Peoples R China.
   [Yun, Qu Zhen; Wu, Liu; Zhang, Tian Wen] Dalian Med Univ, Pathophysiol Dept, Dalian 116044, Liaoning, Peoples R China.
RP Yao, TZ (corresponding author), Dalian Med Univ, Pharmacol Dept, 9 West Sect,South Rd Lvshun, Dalian 116044, Liaoning, Peoples R China.
EM tangzeyao411@dmu.edu.com
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NR 81
TC 0
Z9 0
U1 7
U2 7
PU ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD
PI LONDON
PA 24-28 OVAL RD, LONDON NW1 7DX, ENGLAND
SN 1043-6618
EI 1096-1186
J9 PHARMACOL RES
JI Pharmacol. Res.
PD DEC
PY 2021
VL 174
AR 105935
DI 10.1016/j.phrs.2021.105935
EA OCT 2021
PG 13
WC Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA XG4GQ
UT WOS:000724713300003
PM 34644595
DA 2022-04-25
ER

PT J
AU Huang, KT
   Kuo, IY
   Tsai, MC
   Wu, CH
   Hsu, LW
   Chen, LY
   Kung, CP
   Cheng, YF
   Goto, S
   Chou, YW
   Chen, CL
   Lin, CC
   Chen, KD
AF Huang, Kuang-Tzu
   Kuo, I-Ying
   Tsai, Ming-Chao
   Wu, Chun-Hsien
   Hsu, Li-Wen
   Chen, Li-Yu
   Kung, Chao-Pin
   Cheng, Yu-Fan
   Goto, Shigeru
   Chou, Yu-Wei
   Chen, Chao-Long
   Lin, Chih-Che
   Chen, Kuang-Den
TI Factor VII-Induced MicroRNA-135a Inhibits Autophagy and Is Associated
   with Poor Prognosis in Hepatocellular Carcinoma
SO MOLECULAR THERAPY-NUCLEIC ACIDS
LA English
DT Article
ID PROTEASE-ACTIVATED RECEPTOR-2; CELL-PROLIFERATION; BETA-CATENIN;
   COLON-CANCER; EXPRESSION; LIVER; PHOSPHORYLATION; TRANSFORMATION;
   PROGRESSION; SUPPRESSOR
AB Hepatocellular carcinoma (HCC) is one of the most common and aggressive malignancies worldwide. Treatment outcomes remain poor mainly due to lack of good diagnostic/prognostic markers and limited therapeutic strategies. We previously characterized aberrant activation of the TF/FVII/PAR2 pathway, which subsequently results in decreased autophagy, as a crucial event in malignant progression of HCC.
   Here, we identified miR-135a as a highly upregulated miRNA in HCC in response to TF/FVII/PAR2 activation. Analyzing 103 HCC patient specimens, we confirmed that miR-135a was frequently elevated in HCC tissues with higher FVII expression compared to adjacent non-cancerous counterparts. Increased miR-135a levels in HCC were also associated with tumor staging, recurrence, microvascular invasion, and decreased disease-free survival. We subsequently identified Atg14, a key component that regulates the formation of auto-phagosome as a direct target of miR-135a. Ectopic expression of miR-135a suppressed Atg14 levels and inhibited the autophagic processes. Our results indicate strong positive correlations between miR-135a levels and malignant behaviors in HCC patients and also suggest novel functions of miR-135a in regulation of autophagy, which could be useful as a potential target for prognostic and therapeutic uses.
C1 [Huang, Kuang-Tzu; Kung, Chao-Pin; Chen, Chao-Long; Chen, Kuang-Den] Kaohsiung Chang Gung Mem Hosp, Inst Translat Res Biomed, 123 Da Pi Rd, Kaohsiung 83301, Taiwan.
   [Huang, Kuang-Tzu; Kuo, I-Ying; Wu, Chun-Hsien; Hsu, Li-Wen; Chen, Li-Yu; Kung, Chao-Pin; Chen, Chao-Long; Lin, Chih-Che; Chen, Kuang-Den] Kaohsiung Chang Gung Mem Hosp, Dept Surg, Liver Transplantat Ctr, 123 Da Pi Rd, Kaohsiung 83301, Taiwan.
   [Tsai, Ming-Chao] Kaohsiung Chang Gung Mem Hosp, Dept Internal Med, Div Hepatogastroenterol, Kaohsiung 83301, Taiwan.
   [Cheng, Yu-Fan] Kaohsiung Chang Gung Mem Hosp, Dept Diagnost Radiol, Kaohsiung 83301, Taiwan.
   [Goto, Shigeru] Fukuoka Inst Occupat Hlth, Fukuoka 8150081, Japan.
   [Chou, Yu-Wei] Kaohsiung Chang Gung Mem Hosp, Tissue Bank, Kaohsiung 83301, Taiwan.
   [Chou, Yu-Wei] Kaohsiung Chang Gung Mem Hosp, BioBank, Kaohsiung 83301, Taiwan.
RP Chen, KD (corresponding author), Kaohsiung Chang Gung Mem Hosp, Inst Translat Res Biomed, 123 Da Pi Rd, Kaohsiung 83301, Taiwan.; Lin, CC; Chen, KD (corresponding author), Kaohsiung Chang Gung Mem Hosp, Dept Surg, Liver Transplantat Ctr, 123 Da Pi Rd, Kaohsiung 83301, Taiwan.
EM immunologylin@gmail.com; dennis8857@gmail.com
RI Tsai, Ming Chao/ABA-9806-2020; Kuo, I-Ying/AAE-4741-2020
OI , Ming-Chao/0000-0002-3613-2051
FU Ministry of Science and Technology of TaiwanMinistry of Science and
   Technology, Taiwan [MOST 104-2314-B-182A-018, MOST
   105-2314-B-182A-037-MY2, MOST 104-2314-B-182A-089-MY3]; Chang Gung
   Memorial HospitalChang Gung Memorial Hospital [CMRPG8C1151, CMRPG8D1032,
   CMRPG8D1033, CMRPG8D0561, CMRPG8D0751, CMRPG8D1022, CMRPG8D1023,
   CMRPG8A1203, CMRPG8E1651, CMRPG8C0952, CMRPG8D1012]; Tissue Bank Core
   Lab at Kaohsiung Chang Gung Memorial HospitalChang Gung Memorial
   Hospital [CLRPG8B0033, CLRPG8E0161, CMRPG8D0062]
FX This work was supported by grants from the following sources: Ministry
   of Science and Technology of Taiwan (MOST 104-2314-B-182A-018 and MOST
   105-2314-B-182A-037-MY2 to C.-L.C. and MOST 104-2314-B-182A-089-MY3 to
   Y.-F.C.) and Chang Gung Memorial Hospital (CMRPG8C1151, CMRPG8D1032, and
   CMRPG8D1033 to K.-T.H.; CMRPG8D0561, CMRPG8D0751, CMRPG8D1022, and
   CMRPG8D1023 to K.-D.C.; CMRPG8A1203 and CMRPG8E1651 to C.-C.L.; and
   CMRPG8C0952 and CMRPG8D1012 to C.-L.C.). We also thank the Tissue Bank
   Core Lab at Kaohsiung Chang Gung Memorial Hospital (CLRPG8B0033,
   CLRPG8E0161, and CMRPG8D0062 to Y.-W.C.) for excellent technical
   support.
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NR 48
TC 15
Z9 17
U1 1
U2 2
PU CELL PRESS
PI CAMBRIDGE
PA 50 HAMPSHIRE ST, FLOOR 5, CAMBRIDGE, MA 02139 USA
SN 2162-2531
J9 MOL THER-NUCL ACIDS
JI Mol. Ther.-Nucl. Acids
PD DEC 15
PY 2017
VL 9
BP 274
EP 283
DI 10.1016/j.omtn.2017.10.002
PG 10
WC Medicine, Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Research & Experimental Medicine
GA FQ6SJ
UT WOS:000418494000026
PM 29246306
OA Green Published, gold
DA 2022-04-25
ER

PT J
AU Thoresen, SB
   Pedersen, NM
   Liestol, K
   Stenmark, H
AF Thoresen, Sigrid B.
   Pedersen, Nina Marie
   Liestol, Knut
   Stenmark, Harald
TI A phosphatidylinositol 3-kinase class III sub-complex containing VPS15,
   VPS34, Beclin 1, UVRAG and BIF-1 regulates cytokinesis and degradative
   endocytic traffic
SO EXPERIMENTAL CELL RESEARCH
LA English
DT Article
DE Endocytosis; Cytokinesis; Autophagy; PI 3-kinase; Tumor suppressor
ID TUMOR-SUPPRESSOR; EARLY ENDOSOMES; MICROSATELLITE INSTABILITY; PROMOTES
   TUMORIGENESIS; MEMBRANE CURVATURE; AUTOPHAGY GENE; COLON-CANCER;
   PROTEINS; CELLS; ESCRT
AB The mammalian class III phosphatidylinositol 3-kinase (PI3K-III) complex regulates fundamental cellular functions, including growth factor receptor degradation, cytokinesis and autophagy. Recent studies suggest the existence of distinct PI3K-III sub-complexes that can potentially confer functional specificity. While a substantial body of work has focused on the roles of individual PI3K-III subunits in autophagy, functional studies on their contribution to endocytic receptor downregulation and cytokinesis are limited. We therefore sought to elucidate the specific nature of the PI3K-III complexes involved in these two processes. High-content microscopy-based assays combined with siRNA-mediated depletion of individual subunits indicated that a specific sub-complex containing VPS15, VP534, Beclin 1, UVRAG and BIF-1 regulates both receptor degradation and cytokinesis, whereas ATG14L, a PI3K-III subunit involved in autophagy, is not required. The unanticipated role of UVRAG and BIF-1 in cytokinesis was supported by a strong localisation of these proteins to the midbody. Importantly, while the tumour suppressive functions of Beclin 1, UVRAG and BIF-1 have previously been ascribed to their roles in autophagy, these results open the possibility that they may also contribute to tumour suppression via downregulation of mitogenic signalling by growth factor receptors or preclusion of aneuploidy by ensuring faithful completion of cell division. (C) 2010 Elsevier Inc. All rights reserved.
C1 [Thoresen, Sigrid B.; Pedersen, Nina Marie; Liestol, Knut; Stenmark, Harald] Univ Oslo, Ctr Canc Biomed, Fac Med, N-0310 Oslo, Norway.
   [Thoresen, Sigrid B.; Pedersen, Nina Marie; Stenmark, Harald] Oslo Univ Hosp, Dept Biochem, Inst Canc Res, Norwegian Radium Hosp, N-0310 Oslo, Norway.
RP Stenmark, H (corresponding author), Univ Oslo, Ctr Canc Biomed, Fac Med, N-0310 Oslo, Norway.
EM sigrid.thoresen@rr-research.no; Nina.Marie.Pedersen@rr-research.no;
   knut@ifi.uio.no; stenmark@ulrik.uio.no
RI Stenmark, Harald/B-8868-2008
FU South-Eastern Norway Health Authority; Research Council of
   NorwayResearch Council of Norway; European Research CouncilEuropean
   Research Council (ERC)European Commission; Norwegian Cancer
   SocietyNorwegian Cancer Society
FX The authors thank Prof. T. Yoshimori and Dr. N. Mizushima for providing
   anti-ATG14L antibodies. The work presented in this study was supported
   by funds from the South-Eastern Norway Health Authority, the Research
   Council of Norway, the European Research Council, and the Norwegian
   Cancer Society.
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NR 48
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U1 0
U2 13
PU ELSEVIER INC
PI SAN DIEGO
PA 525 B STREET, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 0014-4827
EI 1090-2422
J9 EXP CELL RES
JI Exp. Cell Res.
PD DEC 10
PY 2010
VL 316
IS 20
BP 3368
EP 3378
DI 10.1016/j.yexcr.2010.07.008
PG 11
WC Oncology; Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Cell Biology
GA 684CC
UT WOS:000284523600005
PM 20643123
OA Green Submitted
DA 2022-04-25
ER

PT J
AU Lv, C
   Zeng, HW
   Wang, JX
   Yuan, X
   Zhang, C
   Fang, T
   Yang, PM
   Wu, T
   Zhou, YD
   Nagle, DG
   Zhang, WD
AF Lv, Chao
   Zeng, Hua-Wu
   Wang, Jin-Xin
   Yuan, Xing
   Zhang, Chuang
   Fang, Ting
   Yang, Pei-Ming
   Wu, Tong
   Zhou, Yu-Dong
   Nagle, Dale G.
   Zhang, Wei-Dong
TI The antitumor natural product tanshinone IIA inhibits protein kinase C
   and acts synergistically with 17-AAG
SO CELL DEATH & DISEASE
LA English
DT Article
ID DRUG TARGET ENGAGEMENT; PROSTATE-CANCER CELLS; THERMAL SHIFT ASSAY;
   BREAST-CANCER; IN-VIVO; PKC ISOFORMS; PI3K/AKT/MTOR PATHWAY; MOLECULAR
   TARGETS; CONNECTIVITY MAP; COLON-CARCINOMA
AB Tanshinone IIA (Tan IIA), the primary bioactive compound derived from the traditional Chinese medicine (TCM) Salvia miltiorrhiza Bunge, has been reported to possess antitumor activity. However, its antitumor mechanisms are not fully understood. To resolve the potential antitumor mechanism(s) of Tan IIA, its gene expression profiles from our database was analyzed by connectivity map (CMAP) and the CMAP-based mechanistic predictions were confirmed/validated in further studies. Specifically, Tan IIA inhibited total protein kinase C (PKC) activity and selectively suppressed the expression of cytosolic and plasma membrane PKC isoforms zeta and epsilon. The Ras/MAPK pathway that is closely regulated by the PKC signaling is also inhibited by Tan IIA. While Tan IIA did not inhibit heat shock protein 90 (Hsp90), it synergistically enhanced the antitumor efficacy of the Hsp90 inhibitors 17-AAG and ganetespib in human breast cancer MCF-7 cells. In addition, Tan IIA significantly inhibited PI3K/Akt/mTOR signaling, and induced both cell cycle arrest and autophagy. Collectively, these studies provide new insights into the molecular mechanisms responsible for antitumor activity of Tan IIA.
C1 [Lv, Chao; Yang, Pei-Ming; Wu, Tong; Zhang, Wei-Dong] China State Inst Pharmaceut Ind, Shanghai Inst Pharmaceut Ind, Shanghai 201203, Peoples R China.
   [Zeng, Hua-Wu; Wang, Jin-Xin; Yuan, Xing; Zhang, Wei-Dong] Second Mil Med Univ, Sch Pharm, Shanghai 200433, Peoples R China.
   [Zhang, Chuang] Zhengzhou Univ, Sch Pharmaceut Sci, Zhengzhou 450001, Henan, Peoples R China.
   [Fang, Ting] Fujian Univ Tradit Chinese Med, Sch Pharm, Fuzhou 350108, Fujian, Peoples R China.
   [Zhou, Yu-Dong; Nagle, Dale G.] Shanghai Univ Tradit Chinese Med, Inst Interdisciplinary Integrat Biomed Res, Shanghai 201203, Peoples R China.
   [Zhou, Yu-Dong] Univ Mississippi, Dept Chem & Biochem, Coll Liberal Arts, University, MS 38677 USA.
   [Nagle, Dale G.] Univ Mississippi, Sch Pharm, Dept Biomol Sci, University, MS 38677 USA.
   [Nagle, Dale G.] Univ Mississippi, Sch Pharm, Pharmaceut Sci Res Inst, University, MS 38677 USA.
RP Zhang, WD (corresponding author), China State Inst Pharmaceut Ind, Shanghai Inst Pharmaceut Ind, Shanghai 201203, Peoples R China.; Zhang, WD (corresponding author), Second Mil Med Univ, Sch Pharm, Shanghai 200433, Peoples R China.
EM wdzhangy@hotmail.com
OI Nagle, Dale/0000-0001-7883-2673
FU Professor of Chang Jiang Scholars Program, NSFC [81230090, 81520108030,
   21472238, 81602980]; Shanghai Engineering Research Center for the
   Preparation of Bioactive Natural Products [16DZ2280200]; Scientific
   Foundation of Shanghai China [12401900801, 13401900103, 13401900101];
   National Major Project of China [2011ZX09307002-03]; NIHUnited States
   Department of Health & Human ServicesNational Institutes of Health (NIH)
   - USA [CA199016]; NATIONAL CANCER INSTITUTEUnited States Department of
   Health & Human ServicesNational Institutes of Health (NIH) - USANIH
   National Cancer Institute (NCI) [R15CA199016] Funding Source: NIH
   RePORTER
FX The work was supported by Professor of Chang Jiang Scholars Program,
   NSFC (81230090, 81520108030, 21472238, 81602980), Shanghai Engineering
   Research Center for the Preparation of Bioactive Natural Products
   (16DZ2280200), the Scientific Foundation of Shanghai China (12401900801,
   13401900103, 13401900101), National Major Project of China
   (2011ZX09307002-03), Y.D.Z is in part supported by NIH grant CA199016.
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NR 54
TC 33
Z9 38
U1 13
U2 29
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 2041-4889
J9 CELL DEATH DIS
JI Cell Death Dis.
PD FEB 7
PY 2018
VL 9
AR 165
DI 10.1038/s41419-017-0247-5
PG 13
WC Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Cell Biology
GA FZ2IN
UT WOS:000427401400007
PM 29416003
OA Green Published, gold
DA 2022-04-25
ER

PT J
AU Jara, JA
   Lopez-Munoz, R
AF Jara, J. A.
   Lopez-Munoz, R.
TI Metformin and cancer: Between the bioenergetic disturbances and the
   antifolate activity
SO PHARMACOLOGICAL RESEARCH
LA English
DT Review
DE Cancer; Chemotherapy; Mitochondria; Metformin; Complex I; Folate cycle;
   Nucleotides
ID MESENCHYMAL TRANSITION EMT; TYPE-2 DIABETES-MELLITUS; ACTIVATED
   PROTEIN-KINASE; CELL-CYCLE ARREST; BREAST-CANCER; MAMMALIAN TARGET;
   VITAMIN-B-12 DEFICIENCY; HOMOCYSTEINE LEVELS; COLON-CANCER; STEM-CELLS
AB For decades, metformin has been the first-line drug for the treatment of type II diabetes mellitus, and it thus is the most widely prescribed antihyperglycemic drug. Retrospective studies associate the use of metformin with a reduction in cancer incidence and cancer-related death. However, despite extensive research about the molecular effects of metformin in cancer cells, its mode of action remains controversial. In this review, we summarize the current molecular evidence in an effort to elucidate metformin's mode of action against cancer cells. Some authors describe that metformin acts directly on mitochondria, inhibiting complex I and restricting the cell's ability to cope with energetic stress. Furthermore, as the drug interrupts the tricarboxylic acid cycle, metformin-induced alteration of mitochondrial function leads to a compensatory increase in lactate and glycolytic ATP. It has also been reported that cell cycle arrest, autophagy, apoptosis and cell death induction is mediated by the activation of AMPK and Redd1 proteins, thus inhibiting the mTOR pathway. Additionally, unbiased metabolomics studies have provided strong evidence to support that metformin alters the methionine and folate cycles, with a concomitant decrease in nucleotide synthesis. Indeed, purines such as thymidine or hypoxanthine restore the proliferation of tumor cells treated with metformin in vitro. Consequently, some authors prefer to refer to metformin as an "antimetabolite drug" rather than a "mitochondrial toxin". Finally, we also review the current controversy concerning the relationship between the experimental conditions of in vitro-reported effects and the plasma concentrations achieved by chronic treatment with metformin. (c) 2015 Elsevier Ltd. All rights reserved.
C1 [Jara, J. A.] Univ Chile, Fac Odontol, ICOD, Unidad Farmacol & Farmacogenet, Santiago, Chile.
   [Lopez-Munoz, R.] Univ Austral Chile, Fac Ciencias Vet, Inst Farmacol & Morfofisiol, Valdivia, Chile.
RP Lopez-Munoz, R (corresponding author), Univ Austral Chile, Fac Ciencias Vet, Inst Farmacol & Morfofisiol, Campus Isla Teja S-N,POB 5090000, Valdivia, Chile.
EM rodrigo.lopez@uach.cl
RI Jara, Jose/K-1936-2014; Lopez-Muñoz, Rodrigo/I-1097-2013
OI Lopez-Muñoz, Rodrigo/0000-0003-1825-8563
FU Vicerrectoria de Investigacion, Universidad de Chile [156]; Consejo
   Nacional de Investigaciones Cientificas y Tecnologicas-CONICYT, Chile
   [791220004]; Direccion de Investigacion, Universidad Austral de Chile
   [S-2015-05]
FX JAJ is supported by the grants U-INICIA #156 (Vicerrectoria de
   Investigacion, Universidad de Chile) and "Proyecto de Insercion en la
   Academia" #791220004 (Consejo Nacional de Investigaciones Cientificas y
   Tecnologicas-CONICYT, Chile). RLM is supported by the grant DID-UACh
   #S-2015-05 (Direccion de Investigacion, Universidad Austral de Chile).
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NR 78
TC 33
Z9 36
U1 2
U2 46
PU ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD
PI LONDON
PA 24-28 OVAL RD, LONDON NW1 7DX, ENGLAND
SN 1043-6618
J9 PHARMACOL RES
JI Pharmacol. Res.
PD NOV
PY 2015
VL 101
SI SI
BP 102
EP 108
DI 10.1016/j.phrs.2015.06.014
PG 7
WC Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA CV4TF
UT WOS:000364258700012
PM 26277279
DA 2022-04-25
ER

PT J
AU Yan, YM
   Jiang, K
   Liu, P
   Zhang, XB
   Dong, X
   Gao, JC
   Liu, QT
   Barr, MP
   Zhang, Q
   Hou, XK
   Meng, SS
   Gong, P
AF Yan, Yumei
   Jiang, Ke
   Liu, Peng
   Zhang, Xianbin
   Dong, Xin
   Gao, Jingchun
   Liu, Quentin
   Barr, Martin P.
   Zhang, Quan
   Hou, Xiukun
   Meng, Songshu
   Gong, Peng
TI Bafilomycin A1 induces caspase-independent cell death in hepatocellular
   carcinoma cells via targeting of autophagy and MAPK pathways
SO SCIENTIFIC REPORTS
LA English
DT Article
ID VACUOLAR H+-ATPASE; COLON-CANCER CELLS; CYCLIN D1; INHIBITION;
   APOPTOSIS; GROWTH; LINE
AB Hepatocellular carcinoma (HCC) is refractory to chemotherapies, necessitating novel effective agents. The lysosome inhibitor Bafilomycin A1 (BafA1) at high concentrations displays cytotoxicity in a variety of cancers. Here we show that BafA1 at nanomolar concentrations suppresses HCC cell growth in both 2 dimensional (2D) and 3D cultures. BafA1 induced cell cycle arrest in the G1 phase and triggered Cyclin D1 turnover in HCC cells in a dual-specificity tyrosine phosphorylation-regulated kinase 1B (DYRK1B) dependent manner. Notably, BafA1 induced caspase-independent cell death in HCC cells by impairing autophagy flux as demonstrated by elevated LC3 conversion and p62/SQSTM1 levels. Moreover, genetic ablation of LC3 significantly attenuated BafA1-induced cytotoxicity of HCC cells. We further demonstrate that pharmacological down-regulation or genetic depletion of p38 MAPK decreased BafA1-induced cell death via abolishment of BafA1-induced upregulation of Puma. Notably, knockdown of Puma impaired BafA1-induced HCC cell death, and overexpression of Puma enhanced BafA1-mediated HCC cell death, suggesting a role for Puma in BafA1-mediated cytotoxicity. Interestingly, pharmacological inhibition of JNK with SP600125 enhanced BafA1-mediated cytotoxicity both in vitro and in xenografts derived from HCC cells. Taken together, our data suggest that BafA1 may offer potential as an effective therapy for HCC.
C1 [Yan, Yumei; Liu, Peng; Zhang, Xianbin; Dong, Xin; Gao, Jingchun; Gong, Peng] Dalian Med Univ, Affiliated Hosp 1, Dept Hepatobiliary Surg, 222 Zhongshan Rd, Dalian 116021, Peoples R China.
   [Yan, Yumei; Hou, Xiukun] Dalian Med Univ, Dept Ultrasound 1, Affiliated Hosp 1, 222 Zhongshan Rd, Dalian 116021, Peoples R China.
   [Jiang, Ke; Liu, Quentin; Meng, Songshu] Dalian Med Univ, Ctr Canc, Inst Canc Stem Cell, 9 Lvshun Rd South, Dalian 116044, Peoples R China.
   [Barr, Martin P.] St James Hosp, Trinity Ctr Hlth Sci, Trinity Translat Med Inst, Thorac Oncol Res Grp, Dublin, Ireland.
   [Barr, Martin P.] Trinity Coll Dublin, Dublin, Ireland.
   [Zhang, Quan] Yangzhou Univ, Coll Vet Med, Yangzhou 225009, Jiangsu, Peoples R China.
   [Yan, Yumei; Gong, Peng] Dalian Key Lab Hepatobiliary Pancreat Dis Prevent, Dalian 116021, Peoples R China.
   [Yan, Yumei] Dalian Med Univ, Grad Sch, 9 Lvshun Rd South, Dalian 116044, Peoples R China.
RP Gong, P (corresponding author), Dalian Med Univ, Affiliated Hosp 1, Dept Hepatobiliary Surg, 222 Zhongshan Rd, Dalian 116021, Peoples R China.; Hou, XK (corresponding author), Dalian Med Univ, Dept Ultrasound 1, Affiliated Hosp 1, 222 Zhongshan Rd, Dalian 116021, Peoples R China.; Meng, SS (corresponding author), Dalian Med Univ, Ctr Canc, Inst Canc Stem Cell, 9 Lvshun Rd South, Dalian 116044, Peoples R China.; Gong, P (corresponding author), Dalian Key Lab Hepatobiliary Pancreat Dis Prevent, Dalian 116021, Peoples R China.
EM xiukunhou28@sina.com; ssmeng@dmu.edu.cn; gongpengdalian@163.com
OI Barr, Martin/0000-0001-5202-9655; Zhang, Xianbin/0000-0002-0948-6698
FU National Science Foundation of ChinaNational Natural Science Foundation
   of China (NSFC) [81572707, 81473504, 81502674]; Liaoning Provincial
   Science and Technology Plan Project [201202051]; Program for Liaoning
   Excellent Talents in University [LR2015018]
FX We thank Tamotsu Yoshimori (Osaka University, Osaka, Japan) for the
   GFP-mRFP-LC3 plasmid. This work was supported by grants from the
   National Science Foundation of China (81572707 to SM, 81473504 to PG,
   81502674 to KJ) and Liaoning Provincial Science and Technology Plan
   Project (201202051 to XH). Program for Liaoning Excellent Talents in
   University (LR2015018 to PG).
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NR 21
TC 47
Z9 48
U1 2
U2 27
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 2045-2322
J9 SCI REP-UK
JI Sci Rep
PD NOV 15
PY 2016
VL 6
AR 37052
DI 10.1038/srep37052
PG 13
WC Multidisciplinary Sciences
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Science & Technology - Other Topics
GA EB8NQ
UT WOS:000387648200003
PM 27845389
OA Green Published, gold
DA 2022-04-25
ER

PT J
AU Yang, L
   Liu, YQ
   Wang, M
   Qian, YY
   Dai, XJ
   Zhu, YD
   Chen, J
   Guo, SY
   Hisamitsu, T
AF Yang, Lin
   Liu, Yanqing
   Wang, Mei
   Qian, Yayun
   Dai, Xiaojun
   Zhu, Yaodong
   Chen, Jue
   Guo, Shiyu
   Hisamitsu, Tadashi
TI Celastrus orbiculatus extract triggers apoptosis and autophagy via
   PI3K/Akt/mTOR inhibition in human colorectal cancer cells
SO ONCOLOGY LETTERS
LA English
DT Article
DE Celastrus orbiculatus extract; autophagy; apoptosis
ID SIGNALING PATHWAY; MAMMALIAN TARGET; SELF-DIGESTION; BCL-2 FAMILY;
   IN-VITRO; DISEASE; DEATH; ANGIOGENESIS; CONSTITUENTS; MECHANISMS
AB Celastrus orbiculatus is used as a folk medicine in China for the treatment of numerous diseases. The ethyl acetate extract of Celastrus orbiculatus (COE) also displays a wide range of anti-cancer activities in the laboratory. However, the effectiveness of COE-induced autophagy and its mechanism of action in colorectal cancer cells have not been investigated thus far. The present study analyzed the effect of COE on HT-29 cell viability, apoptosis and autophagy using MTT assay, flow cytometry, transmission electron microscopy and western blotting. Additionally, the autophagy inhibitor 3-methyladenine and the autophagy inducer rapamycin were used to further explore the effects of COE-induced autophagy in HT-29 cells. The present study also examined whether the phosphatidylinositol-4,5-bisphosphate 3-kinase (PI3K)/Akt/mechanistic target of rapamycin (mTOR)/p70 ribosomal protein S6 kinase (p70S6K) signaling pathway was involved in the regulation of COE-induced autophagy. The results revealed that COE inhibited HT-29 cell proliferation and decreased cell survival in a time- and dose-dependent manner, and that COE possessed the ability to induce both apoptosis and autophagy in HT-29 cells. Furthermore, autophagy and apoptosis induced by COE synergized to inhibit colorectal cancer growth. In addition, COE treatment decreased the phosphorylation of Akt and its downstream effectors mTOR and p70S6K. Taken together, these results demonstrate that both autophagy and apoptosis were activated during COE treatment of HT-29 cells, and that COE-induced autophagy decreases the viability of HT-29 cells via a mechanism that may depend on the PI3K/Akt/mTOR/p70S6K signaling pathway. Furthermore, compounds that induce autophagy administered in combination with COE may be an attractive strategy for enhancing the anti-tumor potency of COE in colorectal cancer.
C1 [Yang, Lin; Liu, Yanqing; Wang, Mei; Qian, Yayun; Dai, Xiaojun; Zhu, Yaodong; Chen, Jue] Yangzhou Univ, Inst Tradit Chinese Med & Western Med, Sch Med, 11 Huaihai Rd, Yangzhou 225009, Jiangsu, Peoples R China.
   [Yang, Lin; Liu, Yanqing; Qian, Yayun; Dai, Xiaojun; Zhu, Yaodong; Chen, Jue] Jiangsu Key Lab Integrated Tradit Chinese & Weste, Yangzhou 225001, Jiangsu, Peoples R China.
   [Yang, Lin; Liu, Yanqing; Qian, Yayun; Dai, Xiaojun; Zhu, Yaodong; Chen, Jue] Jiangsu Coinnovat Ctr Prevent & Control Important, Yangzhou 225009, Jiangsu, Peoples R China.
   [Wang, Mei] Yangzhou Univ, Dept Gastroenterol, Peoples Hosp Yangzhou 1, Sch Clin 2, Yangzhou 225000, Jiangsu, Peoples R China.
   [Guo, Shiyu; Hisamitsu, Tadashi] Showa Univ, Sch Med, Dept Physiol, Tokyo 1428555, Japan.
RP Liu, YQ (corresponding author), Yangzhou Univ, Inst Tradit Chinese Med & Western Med, Sch Med, 11 Huaihai Rd, Yangzhou 225009, Jiangsu, Peoples R China.
EM liuyanqing2014@163.com
FU National Natural Science Foundation of China (Beijing, China)National
   Natural Science Foundation of China (NSFC) [81403232, 81274141,
   81450051]; Natural Science Foundation of Jiangsu Province of China
   (Nanjing, China) [BK 2012686, SBK 2014021480]
FX The present study was financially supported by grants from the National
   Natural Science Foundation of China (Beijing, China; grant nos.
   81403232, 81274141 and 81450051) and the Natural Science Foundation of
   Jiangsu Province of China (Nanjing, China; grant nos. BK 2012686 and SBK
   2014021480).
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NR 39
TC 33
Z9 42
U1 0
U2 13
PU SPANDIDOS PUBL LTD
PI ATHENS
PA POB 18179, ATHENS, 116 10, GREECE
SN 1792-1074
EI 1792-1082
J9 ONCOL LETT
JI Oncol. Lett.
PD NOV
PY 2016
VL 12
IS 5
BP 3771
EP 3778
DI 10.3892/ol.2016.5213
PG 8
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA ED4RR
UT WOS:000388838900108
PM 27895729
OA Green Submitted, Green Published, gold
DA 2022-04-25
ER

PT J
AU Pan, TH
   Liu, JW
   Xu, S
   Yu, Q
   Wang, HP
   Sun, HX
   Wu, J
   Zhu, Y
   Zhou, JW
   Zhu, YL
AF Pan, Tianhui
   Liu, Jingwen
   Xu, Song
   Yu, Qiao
   Wang, Hongping
   Sun, Hongxiang
   Wu, Jia
   Zhu, Yue
   Zhou, Jianwei
   Zhu, Yongliang
TI ANKRD22, a novel tumor microenvironment-induced mitochondrial protein
   promotes metabolic reprogramming of colorectal cancer cells
SO THERANOSTICS
LA English
DT Article
DE Colorectal cancer; Tumor microenvironment; Cancer-initiating cells;
   ANKRD22; Metabolic reprogramming
ID STEM-CELLS; GLYCOLYSIS; PLURIPOTENCY; PLASTICITY; CARCINOMA; MARKERS
AB Background: The leading cause of poor prognosis in colorectal cancer (CRC) is the presence of colorectal cancer-initiating cells (CCICs). The interplay between the tumor microenvironment (TME) and CRC cells induces reacquisition of initiating cell characteristics, but the underlying mechanisms remain elusive.
   Methods: Candidate molecules were screened by global differential cDNA expression profiles of CCICs, which were enriched from patient-derived tumor xenograft models. Luciferase reporters and chromatin immunoprecipitation assays were used to explore the mechanism of TME factors regulating the transcription of ANKRD22. The effects of Ankyrin repeat domain-containing protein 22 (ANKRD22) on energy metabolism were monitored by extracellular flux and C-13-based metabolic flux analysis. Mass spectrometry was used to identify the interacting partners of ANKRD22. Morphological changes of CCICs overexpressing ANKRD22 were observed by electron microscopy. The effects of ANKRD22 on mitochondrial lipid metabolism were analyzed by lipidomics.
   Results: We identified a novel nucleus-encoded mitochondrial membrane protein, ANKRD22, which was upregulated in CCICs. We found that ANKRD22 was induced by the p38/MAX pathway activated by different TME stimuli. As a key transcription factor, MAX promoted the transcription of ANKRD22. Expression of ANKRD22 promoted glycolysis associated with a decrease in ATP/ADP and an increase in AMP/ATP levels, which were related to its interaction with pyruvate dehydrogenase kinase isoform 1 (PDK1) and multiple subunits of ATP synthase. Further, in CCICs, ANKRD22 cooperated with the lipid transport protein, Extended Synaptotagmin-1 (E-Syt1), to transport excess lipids into mitochondria and reduced the number of mitochondria in an autophagy-independent manner, thus meeting the metabolic requirements of CCICs.
   Conclusion: ANKRD22 induced by TME promotes the metabolic reprogramming of CRC cells. Our study has identified ANKRD22/E-Syt1 as a potential target for eradicating CCICs.
C1 [Pan, Tianhui; Liu, Jingwen; Xu, Song; Yu, Qiao; Wang, Hongping; Wu, Jia; Zhu, Yongliang] Zhejiang Univ, Sch Med, Affiliated Hosp 2, Lab Gastroenterol Dept, Hangzhou 310009, Zhejiang, Peoples R China.
   [Zhou, Jianwei] Zhejiang Univ, Sch Med, Affiliated Hosp 2, Dept Gynecol, Hangzhou 310009, Zhejiang, Peoples R China.
   [Sun, Hongxiang] Zhejiang Univ, Coll Anim Sci, Lab Nat Drug, Hangzhou 310058, Zhejiang, Peoples R China.
   [Zhu, Yongliang] Key Lab Tumor Microenviroment & Immune Therapy Zh, Hangzhou 310009, Zhejiang, Peoples R China.
   [Zhu, Yue] Wenzhou Med Univ, Coll Stormotologry, Wenzhou 325035, Zhejiang, Peoples R China.
RP Zhu, YL (corresponding author), Zhejiang Univ, Sch Med, Affiliated Hosp 2, Lab Gastroenterol Dept, Hangzhou 310009, Zhejiang, Peoples R China.; Zhou, JW (corresponding author), Zhejiang Univ, Sch Med, Affiliated Hosp 2, Dept Gynecol, Hangzhou 310009, Zhejiang, Peoples R China.
EM 2195045@zju.edu.cn; ylzhu@zju.edu.cn
FU National Science of Foundation Committee of China [81672898, 81472723,
   81602584, 81700455]
FX We thank Ms. Dong Qi at Cancer Institute of Zhejiang University for her
   excellent skills in Confocal microscopy. This work was supported by
   grants from the National Science of Foundation Committee of China
   (81672898, 81472723, 81602584 and 81700455).
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NR 53
TC 13
Z9 13
U1 4
U2 14
PU IVYSPRING INT PUBL
PI LAKE HAVEN
PA PO BOX 4546, LAKE HAVEN, NSW 2263, AUSTRALIA
SN 1838-7640
J9 THERANOSTICS
JI Theranostics
PY 2020
VL 10
IS 2
BP 516
EP 536
DI 10.7150/thno.37472
PG 21
WC Medicine, Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Research & Experimental Medicine
GA JQ3UN
UT WOS:000498874200004
PM 31903135
OA gold, Green Published
DA 2022-04-25
ER

PT J
AU Yang, J
   Jiang, H
   Wang, CY
   Yang, B
   Zhao, LJ
   Hu, DL
   Qiu, GH
   Dong, XL
   Xiao, B
AF Yang, Jie
   Jiang, Hai
   Wang, Chunyu
   Yang, Bo
   Zhao, Lijun
   Hu, Dongling
   Qiu, Guihua
   Dong, Xiaolin
   Xiao, Bin
TI Oridonin triggers apoptosis in colorectal carcinoma cells and
   suppression of microRNA-32 expression augments oridonin-mediated
   apoptotic effects
SO BIOMEDICINE & PHARMACOTHERAPY
LA English
DT Article
DE Oridonin; Colorectal carcinoma cells; Apoptosis; MicroRNA-32; Caspase-3;
   Caspase-9
ID CANCER-CELLS; GLUTATHIONE DEPLETION; MITOCHONDRIAL PATHWAY;
   GROWTH-INHIBITION; UP-REGULATION; PROLIFERATION; LINE; STATISTICS;
   MECHANISM; AUTOPHAGY
AB Oridonin, a bioactive diterpenoid isolated from Rabdosia rubescens, has been found to exhibit various anti-tumor effects. In this work, to investigate its pharmacological effects on human colorectal carcinoma HCT-116 and LoVo cells, cell proliferation and apoptosis were respectively evaluated by 3-[4,5-dimethylthiazol-2-yl]-2, 5-diphenyltetrazolium bromide (MTT) assay, annexin V-FITC, and propidium iodide (PI) staining. Western blotting was used to detect the expression levels of Bim, Bax, Bcl-2, cytosolic cytochrome c, procaspase-9, cleaved caspase-9, procaspase-3, and caspase-3 proteins. Caspase-Glo-9 and Caspase-Glo-3 assays were applied to determine caspase-9 and caspase-3 activity. MicroRNA-32 (miR-32) expression level was detected by real-time quantitative reverse transcription-polymerase chain reaction (qRT-PCR). The in vivo anti-tumor effects of oridonin were evaluated using cell lines HCT-116 and LoVo xenograft model. The results indicated that oridonin effectively inhibited cell proliferation and induced apoptosis in HCT-116 and LoVo cells in a concentration-dependent manner. Oridonin treatment upregulated the expression levels of Bim, Bax, cytosolic cytochrome c, cleaved caspase-9 and cleaved caspase-3 proteins, downregulated the expression levels of Bcl-2, procaspase-9 and procaspase-3 proteins, and meanwhile obviously activated caspase-9 and caspase-3 in a dose-dependent manner in HCT-116 and LoVo cells. The results of qRT-PCR demonstrated that oridonin treatment significantly decreased miR-32 expression, and furthermore, suppression of miR-32 expression by miR-32 inhibitors augmented oridonin-mediated inhibitory and apoptotic effects in HCT-116 and LoVo cells. In vivo results indicated that oridonin administration through intraperitoneal injection suppressed tumor growth in nude mice. Therefore, these findings suggest that oridonin maybe is a potential candidate for colorectal cancer treatment. (C) 2015 Elsevier Masson SAS. All rights reserved.
C1 [Yang, Jie; Zhao, Lijun; Hu, Dongling; Qiu, Guihua; Dong, Xiaolin] Hubei Univ Med, Renmin Hosp, Dept Med Care Ctr, Shiyan 442000, Hubei Province, Peoples R China.
   [Jiang, Hai] Hubei Univ Med, Renmin Hosp, Dept Cardiothorac Surg, Shiyan 442000, Hubei Province, Peoples R China.
   [Wang, Chunyu; Yang, Bo; Xiao, Bin] Hubei Univ Med, Renmin Hosp, Ultrason Imaging Div, Shiyan 442000, Hubei Province, Peoples R China.
RP Xiao, B (corresponding author), Hubei Univ Med, Renmin Hosp, Ultrason Imaging Div, Shiyan 442000, Hubei Province, Peoples R China.
EM xiao_bin168@126.com
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NR 47
TC 21
Z9 22
U1 2
U2 16
PU ELSEVIER FRANCE-EDITIONS SCIENTIFIQUES MEDICALES ELSEVIER
PI PARIS
PA 23 RUE LINOIS, 75724 PARIS, FRANCE
SN 0753-3322
EI 1950-6007
J9 BIOMED PHARMACOTHER
JI Biomed. Pharmacother.
PD MAY
PY 2015
VL 72
BP 125
EP 134
DI 10.1016/j.biopha.2015.04.016
PG 10
WC Medicine, Research & Experimental; Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Research & Experimental Medicine; Pharmacology & Pharmacy
GA CJ7JF
UT WOS:000355670400020
PM 26054686
DA 2022-04-25
ER

PT J
AU Kaistha, BP
   Lorenz, H
   Schmidt, H
   Sipos, B
   Pawlak, M
   Gierke, B
   Kreider, R
   Lankat-Buttgereit, B
   Sauer, M
   Fiedler, L
   Krattenmacher, A
   Geisel, B
   Kraus, JM
   Frese, KK
   Kelkenberg, S
   Giese, NA
   Kestler, HA
   Gress, TM
   Buchholz, M
AF Kaistha, Brajesh P.
   Lorenz, Holger
   Schmidt, Harald
   Sipos, Bence
   Pawlak, Michael
   Gierke, Berthold
   Kreider, Ramona
   Lankat-Buttgereit, Brigitte
   Sauer, Melanie
   Fiedler, Lisa
   Krattenmacher, Anja
   Geisel, Bettina
   Kraus, Johann M.
   Frese, Kristopher K.
   Kelkenberg, Sabine
   Giese, Nathalia A.
   Kestler, Hans A.
   Gress, Thomas M.
   Buchholz, Malte
TI PLAC8 Localizes to the Inner Plasma Membrane of Pancreatic Cancer Cells
   and Regulates Cell Growth and Disease Progression through Critical
   Cell-Cycle Regulatory Pathways
SO CANCER RESEARCH
LA English
DT Article
ID FLUORESCENCE PROTEASE PROTECTION; SUBCELLULAR-LOCALIZATION; LIVING
   CELLS; COLON-CANCER; EXPRESSION; ONZIN; MICE; DIFFERENTIATION;
   MICROARRAY; APOPTOSIS
AB Pancreatic ductal adenocarcinoma (PDAC) carries the most dismal prognosis of all solid tumors and is generally strongly resistant to currently available chemo- and/or radiotherapy regimens, including targeted molecular therapies. Therefore, unraveling the molecular mechanisms underlying the aggressive behavior of pancreatic cancer is a necessary prerequisite for the development of novel therapeutic approaches. We previously identified the protein placenta-specific 8 (PLAC8, onzin) in a genome-wide search for target genes associated with pancreatic tumor progression and demonstrated that PLAC8 is strongly ectopically expressed in advanced preneoplastic lesions and invasive human PDAC. However, the molecular function of PLAC8 remained unclear, and accumulating evidence suggested its role is highly strate that in contrast to other cellular systems, PLAC8 protein localizes to the inner face of the plasma membrane in pancreatic cancer cells, where it interacts with specific membranous structures in a temporally and spatially stable manner. Inhibition of PLAC8 expression strongly inhibited pancreatic cancer cell growth by attenuating cell-cycle progression, which was associated with transcriptional and/or posttranslational modification of the central cell-cycle regulators CDKN1A, retinoblastoma protein, and cyclin D1 (CCND1), but did not impact autophagy. Moreover, Plac8 deficiency significantly inhibited tumor formation in genetically engineered mouse models of pancreatic cancer. Together, our findings establish PLAC8 as a central mediator of tumor progression in PDAC and as a promising candidate gene for diagnostic and therapeutic targeting. (C)2015 AACR.
C1 [Kaistha, Brajesh P.; Schmidt, Harald; Kreider, Ramona; Lankat-Buttgereit, Brigitte; Sauer, Melanie; Fiedler, Lisa; Krattenmacher, Anja; Geisel, Bettina; Gress, Thomas M.; Buchholz, Malte] Univ Marburg, Clin Gastroenterol Endocrinol Metab & Infectiol, D-35043 Marburg, Germany.
   [Lorenz, Holger] Univ Heidelberg ZMBH, Zentrum Mol Biol, Cent Imaging Facil, Heidelberg, Germany.
   [Sipos, Bence] Univ Clin Tubingen, Dept Pathol, Tubingen, Germany.
   [Pawlak, Michael; Gierke, Berthold] Univ Tubingen, NMI Nat & Med Sci Inst, Dept Biochem & Prot Profiling, Reutlingen, Germany.
   [Kraus, Johann M.; Kestler, Hans A.] Univ Ulm, Med Syst Biol, D-89069 Ulm, Germany.
   [Frese, Kristopher K.] Univ Toronto, Princess Margaret Hosp, Toronto, ON, Canada.
   [Kelkenberg, Sabine] CeGaT GmbH, Tubingen, Germany.
   [Giese, Nathalia A.] Univ Clin Heidelberg, Dept Surg, Heidelberg, Germany.
RP Buchholz, M (corresponding author), Univ Marburg, Zentrum Tumor & Immunbiol, Hans Meerwein Str 3, D-35043 Marburg, Germany.
EM malte.buchholz@staff.uni-marburg.de
RI Kestler, Hans A./D-5799-2012; Sauer, Markus/C-4378-2017
OI Kestler, Hans A./0000-0002-4759-5254; Sauer, Markus/0000-0002-1692-3219;
   Kaistha, Brajesh Pratap/0000-0002-4071-6260; Gress,
   Thomas/0000-0002-9333-5461
FU German Research Foundation (DFG)German Research Foundation (DFG) [Bu
   1536/3-1]; Heidelberger Pancobank (BMBF) [01GS08114]; BMBF grantFederal
   Ministry of Education & Research (BMBF) [01EY1101]; EU FP7 grant
   [602783]
FX This work was funded in part by the German Research Foundation (DFG;
   grant Bu 1536/3-1), Heidelberger Pancobank (BMBF grant 01GS08114), BMBF
   grant 01EY1101, and EU FP7 grant no. 602783 (large-scale integrated
   project "CAM-PaC").
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NR 38
TC 41
Z9 45
U1 0
U2 14
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD JAN 1
PY 2016
VL 76
IS 1
BP 96
EP 107
DI 10.1158/0008-5472.CAN-15-0216
PG 12
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA DA1KE
UT WOS:000367553900014
PM 26669866
DA 2022-04-25
ER

PT J
AU Fernandes, LG
   Tobias, GC
   Paixao, AO
   Dourado, PM
   Voltarelli, VA
   Brum, PC
AF Fernandes, L. G.
   Tobias, G. C.
   Paixao, A. O.
   Dourado, P. M.
   Voltarelli, V. A.
   Brum, P. C.
TI Exercise training delays cardiac remodeling in a mouse model of cancer
   cachexia
SO LIFE SCIENCES
LA English
DT Article
DE Aerobic exercise training; Cancer cachexia; Cardiac damage; Fibrosis;
   Inflammation; Necrosis
ID QUALITY-OF-LIFE; HEART-FAILURE; SYMPATHETIC HYPERACTIVITY; DYSFUNCTION;
   CAPACITY; MECHANISMS; BENEFITS; IMPACT; CELLS
AB Aims: We aimed to investigate the impact of cancer cachexia and previous aerobic exercise training (AET) on cardiac function and structure in tumor bearing mice.
   Main methods: Colon adenocarcinoma cells 26 (CT26) were subcutaneously injected in BALB/c mice to establish robust cancer cachexia model. AET was performed on a treadmill during 45 days, 60 min/5 days per week. Cardiac function was evaluated by echocardiography and cardiac morphology was assessed by light microscopy. The protein expression levels of mitochondrial complex were analyzed by Western blotting. The mRNA levels of genes related to cardiac remodeling and autophagy were analyzed by quantitative Real-Time PCR.
   Key findings: Our data confirms CT26 tumor bearing mice as a well-characterized and robust model of cancer cachexia. CT26 mice exhibited cardiac remodeling and dysfunction characterized by cardiac atrophy and impaired left ventricle ejection fraction paralleled by cardiac necrosis, inflammation and fibrosis. AET partially reversed the left ventricle ejection fraction and led to significant anti-cardiac remodeling effect associated reduced necrosis, inflammation and cardiac collagen deposition in CT26 mice. Reduced TGF-beta 1 mRNA levels, increased mitochondrial complex IV protein levels and partial recovery of BNIP3 mRNA levels in cardiac tissue were associated with the cardiac effects of AET in CT26 mice. Thus, we suggest AET as a powerful regulator of key pathways involved in cardiac tissue homeostasis in cancer cachexia.
   Significance: Our study provides a robust model of cancer cachexia, as well as highlights the potential and integrative effects of AET as a preventive strategy for reducing cardiac damage in cancer cachexia.
C1 [Fernandes, L. G.] Univ Sao Paulo, Med Sch, Dept Expt Pathophysiol, Sao Paulo, Brazil.
   [Fernandes, L. G.; Tobias, G. C.; Paixao, A. O.; Voltarelli, V. A.; Brum, P. C.] Univ Sao Paulo, Sch Phys Educ & Sport, Sao Paulo, Brazil.
   [Dourado, P. M.] Univ Sao Paulo, Clin Hosp, Fac Med, Heart Inst, Sao Paulo, Brazil.
RP Brum, PC (corresponding author), Univ Sao Paulo, Escola Educ Fis & Esporte, Dept Biodinam Movimento Corpo Humano, Av Prof Mello Moraes,65 Butanta, BR-05508900 Sao Paulo, SP, Brazil.
EM pcbrum@usp.br
RI Brum, Patricia C/E-6605-2011; Voltarelli, Vanessa Azevedo/AAB-8897-2021;
   Voltarelli, Vanessa Azevedo/J-3419-2015
OI Brum, Patricia C/0000-0002-4750-6506; Voltarelli, Vanessa
   Azevedo/0000-0003-0087-646X; Voltarelli, Vanessa
   Azevedo/0000-0003-0087-646X; Reis, AlessanRSS/0000-0001-8486-7469;
   Paixao, Ailma/0000-0003-2805-7319
FU Fundacao de Amparo a Pesquisa do Estado de Sao Paulo, Sao Paulo - SP
   (FAPESP)Fundacao de Amparo a Pesquisa do Estado de Sao Paulo (FAPESP)
   [2016/22835-5, 2014/25830-9, 2015/22814-5]; Conselho Nacional de
   Pesquisa e Desenvolvimento - Brasil (CNPq)Conselho Nacional de
   Desenvolvimento Cientifico e Tecnologico (CNPQ) [BPQ-306261/2016-2]
FX This work was supported by Fundacao de Amparo a Pesquisa do Estado de
   Sao Paulo, Sao Paulo - SP (FAPESP #2016/22835-5, #2014/25830-9,
   #2015/22814-5), PCB holds financial support from Conselho Nacional de
   Pesquisa e Desenvolvimento - Brasil (CNPq, BPQ-306261/2016-2).
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NR 57
TC 4
Z9 4
U1 1
U2 7
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0024-3205
EI 1879-0631
J9 LIFE SCI
JI Life Sci.
PD NOV 1
PY 2020
VL 260
AR 118392
DI 10.1016/j.lfs.2020.118392
PG 12
WC Medicine, Research & Experimental; Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Research & Experimental Medicine; Pharmacology & Pharmacy
GA OH5FK
UT WOS:000582605800040
PM 32898523
DA 2022-04-25
ER

PT J
AU Yang, Y
   Wen, FB
   Dang, LF
   Fan, YX
   Liu, DL
   Wu, K
   Zhao, S
AF Yang Yang
   Wen Fengbiao
   Dang Lifeng
   Fan Yuxia
   Liu Donglei
   Wu Kai
   Zhao Song
TI Insulin enhances apoptosis induced by cisplatin in human esophageal
   squamous cell carcinoma EC9706 cells related to inhibition of autophagy
SO CHINESE MEDICAL JOURNAL
LA English
DT Article
DE esophageal squamous cell carcinoma; insulin; chemotherapy sensitivity;
   autophagy; apoptosis; PI3K/Akt/mTOR signalling pathway
ID CANCER-THERAPY; COLON-CANCER; 5-FLUOROURACIL; TEMOZOLOMIDE; EXPRESSION;
   RESISTANCE; GROWTH; TUMORS
AB Background Chemoresistance is common among patients with esophageal squamous cell carcinoma (ESCC). We investigated the effect and mechanism of insulin on enhancing anticancer functions of cisplatin in human esophageal cancer cell line EC9706.
   Methods The viability of EC9706 cells exposed to cisplatin was assessed using MTT assay. The times T1, when the number of living cells reached a plateau and T2, when the number of living cells reached a new plateau after the addition of insulin were found. T1 and T2 plateau cells were stained by Annexin V-FITC/PI and monodansylcadaverin (MDC). Fluorescent microscopy was used to observe the expression of apoptosis and autophagy intuitively. Apoptotic ratio and fluorescent intensity were analysed by flow cytometry (FCM) quantitatively. Western blotting analysis was used to estimate the protein expression levels of AKT, mTOR, PI3K, PTEN, autophage related indicator LC3-II and autophage related protein Beclin1 changes that occurred in the course of treatment.
   Results A larger number of typical autophagosomes were detected in EC9706 cells exposed to cisplatin. Insulin can increase the apoptosis induced by cisplatin. Apoptotic ratio of T1 plateau cells ((32.6 +/- 4.3)%) is significantly less than T2 plateau ((47.5 +/- 5.6)%). MDC fluorescent intensity at T1 plateau (104.9 +/- 1 3.2) was significantly higher than intensity at T2 plateau (82.6 +/- 10.3). After cotreatment with insulin, the expression level of LC3-II, Beclin1 and PTEN in T2 plateau cells were significantly downregulated, but AKT, mTOR and PI3K expressions significantly upregulated compared with T1 plateau.
   Conclusions Insulin could enhance cisplatin-induced apoptosis in human esophageal squamous cell carcinoma EC9706 cells related to inhibition of autophagy. The activation of PI3K/Akt/mTOR signaling pathway induced by insulin resulted in the suppression of autophagy in EC9706 cells, which may be attributed to the anticancer effects of cisplatin.
C1 [Yang Yang; Wen Fengbiao; Liu Donglei; Wu Kai; Zhao Song] Zhengzhou Univ, Dept Thorac Surg, Affiliated Hosp 1, Zhengzhou 450052, Henan, Peoples R China.
   [Dang Lifeng] Zhengzhou Univ, Phys Examinat Ctr, Affiliated Hosp 1, Zhengzhou 450052, Henan, Peoples R China.
   [Fan Yuxia] Zhengzhou Univ, Dept Thyroid Surg, Affiliated Hosp 1, Zhengzhou 450052, Henan, Peoples R China.
   Zhengzhou Univ, Open Key Clin Med Expt Lab, Inst Henan Prov, Inst Mol Canc Surg, Zhengzhou 450052, Henan, Peoples R China.
   Key Thorac Tumour Expt Lab Zhengzhou, Zhengzhou 450052, Henan, Peoples R China.
RP Zhao, S (corresponding author), Zhengzhou Univ, Dept Thorac Surg, Affiliated Hosp 1, 1 Jianshe East Rd, Zhengzhou 450052, Henan, Peoples R China.
EM zhaosong@zzu.edu.cn
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NR 26
TC 10
Z9 13
U1 0
U2 14
PU CHINESE MEDICAL ASSOC
PI BEIJING
PA 42 DONGSI XIDAJIE, BEIJING 100710, PEOPLES R CHINA
SN 0366-6999
J9 CHINESE MED J-PEKING
JI Chin. Med. J.
PD JAN 20
PY 2014
VL 127
IS 2
BP 353
EP 358
DI 10.3760/cma.j.issn.0366-6999.20130996
PG 6
WC Medicine, General & Internal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC General & Internal Medicine
GA 302LV
UT WOS:000330606900025
PM 24438628
DA 2022-04-25
ER

PT J
AU Kim, MJ
   Kang, YJ
   Sung, B
   Jang, JY
   Ahn, YR
   Oh, HJ
   Choi, H
   Choi, I
   Im, E
   Moon, HR
   Chung, HY
   Kim, ND
AF Kim, Min Jeong
   Kang, Young Jung
   Sung, Bokyung
   Jang, Jung Yoon
   Ahn, Yu Ra
   Oh, Hye Jin
   Choi, Heejeong
   Choi, Inkyu
   Im, Eunok
   Moon, Hyung Ryong
   Chung, Hae Young
   Kim, Nam Deuk
TI Novel SIRT Inhibitor, MHY2256, Induces Cell Cycle Arrest, Apoptosis, and
   Autophagic Cell Death in HCT116 Human Colorectal Cancer Cells
SO BIOMOLECULES & THERAPEUTICS
LA English
DT Article
DE SIRT inhibitor; MHY2256; Colorectal cancer cells; Cell cycle arrest;
   Apoptosis; Autophagy
ID DISCOVERY; D1
AB We examined the anticancer effects of a novel sirtuin inhibitor, MHY2256, on HCT116 human colorectal cancer cells to investigate its underlying molecular mechanisms. MHY2256 significantly suppressed the activity of sirtuin 1 and expression levels of sirtuin 1/2 and stimulated acetylation of forkhead box O1, which is a target protein of sirtuin 1. Treatment with MHY2256 inhibited the growth of the HCT116 (TP53 wild-type), HT-29 (TP53 mutant), and DLD-1 (TP53 mutant) human colorectal cancer cell lines. In addition, MHY2256 induced G0/G1 phase arrest of the cell cycle progression, which was accompanied by the reduction of cyclin D1 and cyclin E and the decrease of cyclin-dependent kinase 2, cyclin-dependent kinase 4, cyclin-dependent kinase 6, phosphorylated retinoblastoma protein, and E2F transcription factor 1. Apoptosis induction was shown by DNA fragmentation and increase in late apoptosis, which were detected using flow cytometric analysis. MHY2256 downregulated expression levels of procaspase-8, -9, and -3 and led to subsequent poly(ADP-ribose) polymerase cleavage. MHY2256-induced apoptosis was involved in the activation of caspase-8, -9, and -3 and was prevented by pretreatment with Z-VAD-FMK, a pan-caspase inhibitor. Furthermore, the autophagic effects of MHY2256 were observed as cytoplasmic vacuolation, green fluorescent protein-light-chain 3 punctate dots, accumulation of acidic vesicular organelles, and upregulated expression level of light-chain 3-II. Taken together, these results suggest that MHY2256 could be a potential novel sirtuin inhibitor for the chemoprevention or treatment of colorectal cancer or both.
C1 [Kim, Min Jeong; Kang, Young Jung; Sung, Bokyung; Jang, Jung Yoon; Ahn, Yu Ra; Oh, Hye Jin; Choi, Heejeong; Choi, Inkyu; Im, Eunok; Moon, Hyung Ryong; Chung, Hae Young; Kim, Nam Deuk] Pusan Natl Univ, Coll Pharm, Div Pharm, Busan 46241, South Korea.
RP Kim, ND (corresponding author), Pusan Natl Univ, Coll Pharm, Div Pharm, Busan 46241, South Korea.
EM nadkim@pusan.ac.kr
RI Sung, Bokyung/AAX-5697-2021
OI Kim, Nam Deuk/0000-0001-9033-9865
FU Pusan National UniversityPusan National University
FX This work was supported by a 2-Year Research Grant of Pusan National
   University.
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NR 28
TC 7
Z9 7
U1 0
U2 3
PU KOREAN SOC APPLIED PHARMACOLOGY
PI SEOUL
PA RM 805, KOREAN FEDERATION SCIENCE & TECHNOLOGY B/D, 635-4 YEOKSAM-DONG,
   KANGNAM-GU, SEOUL, 135-703, SOUTH KOREA
SN 1976-9148
EI 2005-4483
J9 BIOMOL THER
JI Biomol. Ther.
PD NOV
PY 2020
VL 28
IS 6
BP 561
EP 568
DI 10.4062/biomolther.2020.153
PG 8
WC Biochemistry & Molecular Biology; Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Pharmacology & Pharmacy
GA QC5YT
UT WOS:000614912400009
PM 33073770
OA Green Published
DA 2022-04-25
ER

PT J
AU Sun, XP
   Veeraraghavan, VP
   Surapaneni, KM
   Hussain, S
   Mathanmohun, M
   Alharbi, SA
   Aladresi, AAM
   Chinnathambi, A
AF Sun, Xiaopeng
   Veeraraghavan, Vishnu Priya
   Surapaneni, Krishna Mohan
   Hussain, Sardar
   Mathanmohun, Maghimaa
   Alharbi, Sulaiman Ali
   Aladresi, Aref Ali Mohammed
   Chinnathambi, Arunachalam
TI Eugenol-piperine loaded polyhydroxy butyrate/polyethylene glycol
   nanocomposite-induced apoptosis and cell death in nasopharyngeal cancer
   (C666-1) cells through the inhibition of the PI3K/AKT/mTOR signaling
   pathway
SO JOURNAL OF BIOCHEMICAL AND MOLECULAR TOXICOLOGY
LA English
DT Article
DE apoptosis; C666-1 cells; eugenol; nasopharyngeal cancer; piperine;
   polyhydroxy butyrate
ID HERBS; NANOPARTICLES; NANOCARRIERS; ENHANCEMENT; ANTICANCER; AUTOPHAGY;
   DELIVERY; CARRIERS; DESIGN; FLUID
AB Nasopharyngeal cancer is a malignancy developing from the nasopharynx epithelium due to smoking and nitrosamine-containing foods. Nasopharyngeal cancer is highly endemic to Southeast Asia. Eugenol and piperine have shown many anticancer activities on numerous cancer types, like colon, lung, liver, and breast cancer. In this study, we amalgamated eugenol and piperine loaded with a polyhydroxy butyrate/polyethylene glycol nanocomposite (Eu-Pi/PHB-PEG-NC) for better anticancer results against nasopharyngeal cancer (C666-1) cells. In the current study, nasopharyngeal cancer cell lines C666-1 were utilized to appraise the cytotoxic potential of Eug-Pip-PEG-NC on cell propagation, programmed cell death, and relocation. Eu-Pi/PHB-PEG-NC inhibits cellular proliferation on C666-1 cells in a dose-dependent manner, and when compared with 20 mu g/ml, 15 mu g/ml of loaded mixture evidently restrained the passage aptitude of C666-1 cells, this was attended with a downregulated expression of mitochondrial membrane potential. Treatment with 15 mu g/ml Eu-Pi/PHB-PEG-NC suggestively amplified cell apoptosis in the C666-1 cells. Furthermore, its cleaved caspase-3, 8, and 9 and Bax gene expression was augmented and Bcl-2 gene expression was diminished after Eu-Pi/PHB-PEG-NC treatment. Additionally, our data established that the collective effect of Eu-Pi/PHB-PEG-NC loaded micelles inhibited the expansion of C666-1 cells augmented apoptosis connected with the intrusion of PI3K/Akt/mTOR signaling pathway.
C1 [Sun, Xiaopeng] Xi An Jiao Tong Univ, Fac Med, Dept Surg, Xian, Peoples R China.
   [Sun, Xiaopeng] Xian Med Coll, Dept Otolaryngol, Affiliated Hosp 2, Xian, Peoples R China.
   [Veeraraghavan, Vishnu Priya] Saveetha Univ, Saveetha Inst Med & Tech Sci, Saveetha Dent Coll, Dept Biochem, Chennai, Tamil Nadu, India.
   [Surapaneni, Krishna Mohan] Panimalar Med Coll Hosp & Res Inst, Dept Biochem, Chennai, Tamil Nadu, India.
   [Surapaneni, Krishna Mohan] Panimalar Med Coll Hosp & Res Inst, Dept Clin Skills, Chennai, Tamil Nadu, India.
   [Surapaneni, Krishna Mohan] Panimalar Med Coll Hosp & Res Inst, Dept Simulat, Chennai, Tamil Nadu, India.
   [Hussain, Sardar] Govt Sci Coll, Dept Biotechnol, Chitradurga, Karnataka, India.
   [Mathanmohun, Maghimaa] Muthayammal Coll Arts & Sci, Dept MicroBiol, Rasipuram, Namakkal, Tamilnadu, India.
   [Alharbi, Sulaiman Ali; Aladresi, Aref Ali Mohammed; Chinnathambi, Arunachalam] King Saud Univ, Coll Sci, Dept Bot & Microbiol, Riyadh 11451, Saudi Arabia.
RP Chinnathambi, A (corresponding author), King Saud Univ, Coll Sci, Dept Bot & Microbiol, Riyadh 11451, Saudi Arabia.
EM carunachalam@ksu.edu.sa
RI Krishna Mohan, Surapaneni/K-4865-2013; Mathanmohun,
   Maghimaa/AAY-6310-2020
OI Krishna Mohan, Surapaneni/0000-0002-5204-5708; Mathanmohun,
   Maghimaa/0000-0002-9043-435X
FU Deanship of Scientific Research at King Saud UniversityKing Saud
   University [RG-1435-081]
FX The authors would like to extend their sincere appreciation to the
   Deanship of Scientific Research at King Saud University for its funding
   of this study through the Research Group Number (RG-1435-081).
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NR 57
TC 2
Z9 2
U1 3
U2 7
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1095-6670
EI 1099-0461
J9 J BIOCHEM MOL TOXIC
JI J. Biochem. Mol. Toxicol.
PD APR
PY 2021
VL 35
IS 4
AR e22700
DI 10.1002/jbt.22700
EA JAN 2021
PG 12
WC Biochemistry & Molecular Biology; Toxicology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Toxicology
GA RN7IY
UT WOS:000605996000001
PM 33421271
DA 2022-04-25
ER

PT J
AU Wang, J
   Liang, D
   Zhang, XP
   He, CF
   Cao, L
   Zhang, SQ
   Xiao, X
   Li, SJ
   Cao, YX
AF Wang, Jin
   Liang, Dong
   Zhang, Xue-Pei
   He, Chen-Fei
   Cao, Lei
   Zhang, San-Qi
   Xiao, Xue
   Li, Shui-Jie
   Cao, Yong-Xiao
TI Novel PI3K/Akt/mTOR signaling inhibitor, W922, prevents colorectal
   cancer growth via the regulation of autophagy
SO INTERNATIONAL JOURNAL OF ONCOLOGY
LA English
DT Article
DE W922; PI3K; Akt; mTOR inhibitor; colorectal cancer; cell cycle arrest;
   autophagy
ID CELL-CYCLE; TARGETS; VS-5584; TUMOR
AB W922, a novel PI3K/Akt/mTOR pathway inhibitor, exhibits efficient anti-tumor effects on HCT116, MCF-7 and A549 human cancer cells compared with other synthesized compounds. The present study aimed to investigate its anti-tumor effects on colorectal cancer cells. A total, of seven different colorectal cell lines were selected to test the anti-proliferation profile of W922, and HCT116 was found to be the most sensitive cell line to the drug treatment. W922 inhibited HCT116 cell viability and cell proliferation in vitro in concentration- and time-dependent manners. Furthermore, W922 suppressed the tumor growth in a xenograft mouse model and exhibited low toxicity. The proteomic alterations in W922-treated HCT116 cells were found to be associated with cell cycle arrest, negative regulation of signal transduction and lysosome-related processes. W922 caused cell cycle arrest of HCT116 cells in G(0)-G(1) phase, but only triggered slight apoptosis. In addition, the PI3K/Akt/mTOR signaling proteins were dephosphorylated upon W922 treatment. It has been reported that inhibition of mTOR is relevant to autophagy, and the present results also indicated that W922 was involved in autophagy induction. An autophagy inhibitor, chloroquine, was used to co-treat HCT116 cells with W922, and it was identified that the cell cycle arrest was impaired. Moreover, co-treatment of W922 and chloroquine led to a significant population of apoptotic cells, thus providing a promising therapeutic strategy for colorectal cancer.
C1 [Wang, Jin; Liang, Dong; Cao, Lei; Xiao, Xue; Cao, Yong-Xiao] Xi An Jiao Tong Univ, Hlth Sci Ctr, Sch Basic Med Sci, Dept Pharmacol, 76 West Yanta Rd, Xian 710061, Shaanxi, Peoples R China.
   [Zhang, Xue-Pei] Chinese Acad Sci, Shanghai Inst Organ Chem, Ctr Excellence Mol Synth, State Key Lab Bioorgan & Nat Prod Chem, Shanghai 200032, Peoples R China.
   [He, Chen-Fei; Li, Shui-Jie] Karolinska Inst, Dept Microbiol Tumor & Cell Biol, 9 Biomed Solnavagen, S-17165 Stockholm, Sweden.
   [Zhang, San-Qi] Xi An Jiao Tong Univ, Sch Pharm, Dept Pharmaceut Chem, Xian 710061, Shaanxi, Peoples R China.
RP Cao, YX (corresponding author), Xi An Jiao Tong Univ, Hlth Sci Ctr, Sch Basic Med Sci, Dept Pharmacol, 76 West Yanta Rd, Xian 710061, Shaanxi, Peoples R China.; Li, SJ (corresponding author), Karolinska Inst, Dept Microbiol Tumor & Cell Biol, 9 Biomed Solnavagen, S-17165 Stockholm, Sweden.
EM shuijie.li@ki.se; yxy@mail.xjtu.edu.cn
FU National Natural Science Foundation of ChinaNational Natural Science
   Foundation of China (NSFC) [81670001]; Natural Science Basic Research
   Project of Shaanxi Province [2018JQ8042]
FX This work was supported by the National Natural Science Foundation of
   China (grant no. 81670001) and Natural Science Basic Research Project of
   Shaanxi Province (grant no. 2018JQ8042).
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NR 40
TC 3
Z9 3
U1 3
U2 9
PU SPANDIDOS PUBL LTD
PI ATHENS
PA POB 18179, ATHENS, 116 10, GREECE
SN 1019-6439
EI 1791-2423
J9 INT J ONCOL
JI Int. J. Oncol.
PD JAN
PY 2021
VL 58
IS 1
BP 70
EP 82
DI 10.3892/ijo.2020.5151
PG 13
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA PE8RD
UT WOS:000598627700006
PM 33367926
OA Green Published, hybrid
DA 2022-04-25
ER

PT J
AU Choi, JH
   Cho, YS
   Ko, YH
   Hong, SU
   Park, JH
   Lee, MA
AF Choi, Ji Hye
   Cho, Young-Seok
   Ko, Yoon Ho
   Hong, Soon Uk
   Park, Jin Hee
   Lee, Myung Ah
TI Absence of Autophagy-Related Proteins Expression Is Associated with Poor
   Prognosis in Patients with Colorectal Adenocarcinoma
SO GASTROENTEROLOGY RESEARCH AND PRACTICE
LA English
DT Article
ID CANCER CELLS; BECLIN 1; TUMORIGENESIS; PATTERNS; LC3; INHIBITION; IMPACT
AB Background/Aim. Autophagy, a cellular degradation process, has paradoxical roles in tumorigenesis and the progression of human cancers. The aim of this study was to investigate the expression levels of autophagy-related proteins in colorectal cancer (CRC) and to evaluate their prognostic significance. Methods. This study is a retrospective review of immunohistochemical and clinicopathological data. All specimens evaluated were obtained from 263 patients with colorectal cancer who had undergone surgery between November 1996 and August 2007. The primary outcomes measured were the expression levels of three autophagy-related proteins (ATG5, BECN1/Beclin 1, and Microtubule-associated protein 1 light chain 3B (LC3B)) by immunohistochemistry and its association in clinicopathological parameters and patient survival. Results. The autophagy-related protein expression frequencies were 65.1% (151/232) for ATG5, 71.3% (174/244) for BECN1, and 74.7% (186/249) for LC3B for the 263 patients. Correlation between the expression of autophagy-related proteins was significant for all protein pairs. Multivariate analysis showed that negative LC3B expression and absence of autophagy-related proteins expression were independently associated with poor prognosis. Conclusion. Absence of autophagy-related proteins expression is associated with poor clinical outcome in CRC, suggesting that these proteins have potential uses as novel prognostic markers.
C1 [Choi, Ji Hye; Park, Jin Hee] Catholic Univ Korea, Coll Med, Dept Biomed Sci, Seoul 137701, South Korea.
   [Cho, Young-Seok; Ko, Yoon Ho] Catholic Univ Korea, Coll Med, Uijeongbu St Marys Hosp, Dept Internal Med, Uijongbu 480717, South Korea.
   [Hong, Soon Uk] Univ Ulsan, Coll Med, Asan Med Ctr, Dept Pathol, Seoul 138736, South Korea.
   [Lee, Myung Ah] Catholic Univ Korea, Coll Med, Seoul St Marys Hosp, Dept Internal Med, Seoul 137701, South Korea.
RP Cho, YS (corresponding author), Catholic Univ Korea, Coll Med, Uijeongbu St Marys Hosp, Dept Internal Med, Uijongbu 480717, South Korea.
EM yscho@catholic.ac.kr; koyoonho@catholic.ac.kr
FU Institute of Clinical Medicine Research, Uijeongbu St. Mary's Hospital,
   The Catholic University of Korea; Basic Science Research Program through
   the National Research Foundation of Korea; Ministry of Education,
   Science and TechnologyMinistry of Education, Science and Technology,
   Republic of Korea [NRF-2010-0023295]
FX This study was supported by a grant of the Institute of Clinical
   Medicine Research, Uijeongbu St. Mary's Hospital, The Catholic
   University of Korea (Y.-S. Cho & Y. H. Ko) and a grant of Basic Science
   Research Program through the National Research Foundation of Korea
   funded by the Ministry of Education, Science and Technology
   (NRF-2010-0023295) (Y.-S. Cho).
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NR 41
TC 31
Z9 32
U1 0
U2 2
PU HINDAWI LTD
PI LONDON
PA ADAM HOUSE, 3RD FLR, 1 FITZROY SQ, LONDON, W1T 5HF, ENGLAND
SN 1687-6121
EI 1687-630X
J9 GASTROENT RES PRACT
JI Gastroenterol. Res. Pract.
PY 2014
VL 2014
AR 179586
DI 10.1155/2014/179586
PG 10
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA AD0AG
UT WOS:000332895600001
PM 24723943
OA gold, Green Published, Green Submitted
DA 2022-04-25
ER

PT J
AU Huang, C
   He, CP
   Ruan, P
   Zhou, R
AF Huang, Chao
   He, Chunping
   Ruan, Peng
   Zhou, Rui
TI TSPYL5 activates endoplasmic reticulum stress to inhibit cell
   proliferation, migration and invasion in colorectal cancer
SO ONCOLOGY REPORTS
LA English
DT Article
DE colorectal cancer; TSPYL5; endoplasmic reticulum stress; apoptosis; cell
   proliferation
ID ABERRANT PROMOTER METHYLATION; PROTECTIVE AUTOPHAGY; LUNG-CANCER;
   GROWTH; GENE; EXPRESSION; RESISTANCE; APOPTOSIS; AXIS
AB Testis-specific protein Y-encoded-like 5 (TSPYL5), a member of the nucleosome assembly protein (NAP) superfamily, functions as a tumor suppressor in ovarian and lung cancer, yet its clinical significance and molecular mechanism in colorectal cancer (CRC) remain unclear. TSPYL5 expression was analyzed using the Gene Expression Profiling Interactive Analysis (GEPIA) database. CRC cell lines HCT116 and HT29 were forced to overexpress TSPYL5 by transfection with pcDNA3.1-TSPYL5. Cell proliferation, apoptosis, migration, and invasion were examined by EdU proliferation assays, flow cytometry, and Transwell assays, respectively. Endoplasmic reticulum stress (ERS) was examined by transmission electron microscopy. Western blot analyses were performed to assess the expression of ERS-associated proteins. GEPIA database analysis showed that CRC patients had lower levels of TSPYL5 expression in their tumor tissues when compared with their para-carcinoma tissues. In vitro experiments indicated that TSPYL5 overexpression significantly suppressed cell proliferation, migration, and invasion, and induced apoptosis and ERS in HCT116 and HT29 cells. Furthermore, the levels of caspase-1, caspase-3, Bax, ATF4, and CHOP protein expression were upregulated after TSPYL5 was overexpressed. In conclusion, our data suggest that TSPYL5 can activate an ERS response that suppresses the proliferation, migration, and invasion of tumor cells. This mechanism may represent a promising therapeutic strategy for CRC.
C1 [Huang, Chao; He, Chunping; Ruan, Peng; Zhou, Rui] Wuhan Univ, Renmin Hosp, Dept Gastroenterol, 99 Zhang Zhidong Rd, Wuhan 430060, Hubei, Peoples R China.
RP Huang, C (corresponding author), Wuhan Univ, Renmin Hosp, Dept Gastroenterol, 99 Zhang Zhidong Rd, Wuhan 430060, Hubei, Peoples R China.
EM rmh_huangchao@126.com
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NR 31
TC 2
Z9 2
U1 0
U2 1
PU SPANDIDOS PUBL LTD
PI ATHENS
PA POB 18179, ATHENS, 116 10, GREECE
SN 1021-335X
EI 1791-2431
J9 ONCOL REP
JI Oncol. Rep.
PD AUG
PY 2020
VL 44
IS 2
BP 449
EP 456
DI 10.3892/or.2020.7639
PG 8
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA NL1MT
UT WOS:000567188700004
PM 32627024
OA hybrid, Green Published
DA 2022-04-25
ER

PT J
AU Lee, AJX
   Roylance, R
   Sander, J
   Gorman, P
   Endesfelder, D
   Kschischo, M
   Jones, NP
   East, P
   Nicke, B
   Spassieva, S
   Obeid, LM
   Birkbak, NJ
   Szallasi, Z
   McKnight, NC
   Rowan, AJ
   Speirs, V
   Hanby, AM
   Downward, J
   Tooze, SA
   Swanton, C
AF Lee, Alvin J. X.
   Roylance, Rebecca
   Sander, Jil
   Gorman, Patricia
   Endesfelder, David
   Kschischo, Maik
   Jones, Neil P.
   East, Philip
   Nicke, Barbara
   Spassieva, Stefka
   Obeid, Lina M.
   Birkbak, Nicolai Juul
   Szallasi, Zoltan
   McKnight, Nicole C.
   Rowan, Andrew J.
   Speirs, Valerie
   Hanby, Andrew M.
   Downward, Julian
   Tooze, Sharon A.
   Swanton, Charles
TI CERT depletion predicts chemotherapy benefit and mediates cytotoxic and
   polyploid-specific cancer cell death through autophagy induction
SO JOURNAL OF PATHOLOGY
LA English
DT Article
DE CERT; autophagy; LAMP2; HER2; polyploidy; drug resistance
ID BREAST-CANCER; MITOTIC ARREST; CERAMIDE; SENSITIVITY; PACLITAXEL; GENES;
   ARRAY; SPHINGOLIPIDS; INTERFERENCE; METASTASIS
AB Chromosomal instability (CIN) has been implicated in multidrug resistance and the silencing of the ceramide transporter, CERT, promotes sensitization to diverse cytotoxics. An improved understanding of mechanisms governing multidrug sensitization might provide insight into pathways contributing to the death of CIN cancer cells. Using an integrative functional genomics approach, we find that CERT-specific multidrug sensitization is associated with enhanced autophagosomelysosome flux, resulting from the expression of LAMP2 following CERT silencing in colorectal and HER2+ breast cancer cell lines. Live cell microscopy analysis revealed that CERT depletion induces LAMP2-dependent death of polyploid cells following exit from mitosis in the presence of paclitaxel. We find that CERT is relatively over-expressed in HER2+ breast cancer and CERT protein expression acts as an independent prognostic variable and predictor of outcome in adjuvant chemotherapy-treated patients with primary breast cancer. These data suggest that the induction of LAMP2-dependent autophagic flux through CERT targeting may provide a rational approach to enhance multidrug sensitization and potentiate the death of polyploid cells following paclitaxel exposure to limit the acquisition of CIN and intra-tumour heterogeneity. Copyright (C) 2011 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.
C1 [Lee, Alvin J. X.; Sander, Jil; Endesfelder, David; East, Philip; Nicke, Barbara; McKnight, Nicole C.; Rowan, Andrew J.; Downward, Julian; Tooze, Sharon A.; Swanton, Charles] Canc Res UK London Res Inst, London WC2A 3LY, England.
   [Roylance, Rebecca; Gorman, Patricia] Queen Mary Univ London, Barts Canc Inst, London EC1M 6BQ, England.
   [Sander, Jil; Endesfelder, David; Kschischo, Maik] Univ Appl Sci Koblenz, D-53424 Remagen, Germany.
   [Jones, Neil P.] UCL, Wolfson Inst Biomed Res, London WC1E 6BT, England.
   [Spassieva, Stefka; Obeid, Lina M.] Med Univ S Carolina, Dept Med, Charleston, SC 29425 USA.
   [Obeid, Lina M.] Ralph H Johnson Vet Affairs Hosp, Div Gen Internal Med, Charleston, SC 29401 USA.
   [Birkbak, Nicolai Juul; Szallasi, Zoltan] Tech Univ Denmark, Ctr Biol Sequence Anal, DK-2800 Lyngby, Denmark.
   [Birkbak, Nicolai Juul] Harvard Univ, Sch Med, Dana Farber Canc Inst, Dept Canc Biol, Boston, MA 02115 USA.
   [Szallasi, Zoltan] Harvard Univ, Sch Med, Childrens Hosp, Harvard MIT Div Hlth Sci & Technol,Informat Progr, Boston, MA 02115 USA.
   [Speirs, Valerie; Hanby, Andrew M.] Univ Leeds, Leeds Inst Mol Med, Leeds LS9 7TF, W Yorkshire, England.
   [Swanton, Charles] UCL Canc Inst, London WC1E 6BT, England.
   [Swanton, Charles] Macmillan Canc Ctr, London WC1E 6BT, England.
RP Swanton, C (corresponding author), Canc Res UK London Res Inst, 44 Lincolns Inn Fields, London WC2A 3LY, England.
EM charles.swanton@cancer.org.uk
RI Speirs, Valerie/ABE-7377-2021; Lee, Alvin Jun Xing/A-1047-2017;
   Downward, Julian/A-3251-2012
OI Speirs, Valerie/0000-0002-0602-4666; Lee, Alvin Jun
   Xing/0000-0002-7427-9142; obeid, lina/0000-0002-0734-0847; Tooze,
   Sharon/0000-0002-2182-3116; Swanton, Charles/0000-0002-4299-3018;
   Howell, Michael/0000-0003-0912-0079; McKnight,
   Nicole/0000-0003-4269-3960; Downward, Julian/0000-0002-2331-4729; East,
   Philip/0000-0001-5801-5713; Szallasi, Zoltan/0000-0001-5395-7509;
   Birkbak, Nicolai/0000-0003-1613-9587
FU National Institute of HealthUnited States Department of Health & Human
   ServicesNational Institutes of Health (NIH) - USA [NCI SPORE P50 CA
   89393, R21LM008823-01A1]; Danish Council for Independent
   Research/Medical Sciences (FSS)Det Frie Forskningsrad (DFF)Danish
   Medical Research Council; Breast Cancer Research Foundation (BCRF);
   Medical Research CouncilUK Research & Innovation (UKRI)Medical Research
   Council UK (MRC)European Commission; CR-UKCancer Research UK; Cancer
   Research UKCancer Research UK [15680] Funding Source: researchfish;
   Medical Research CouncilUK Research & Innovation (UKRI)Medical Research
   Council UK (MRC)European Commission [G0701935] Funding Source:
   researchfish; NATIONAL CANCER INSTITUTEUnited States Department of
   Health & Human ServicesNational Institutes of Health (NIH) - USANIH
   National Cancer Institute (NCI) [P50CA089393, P01CA097132] Funding
   Source: NIH RePORTER; NATIONAL CENTER FOR RESEARCH RESOURCESUnited
   States Department of Health & Human ServicesNational Institutes of
   Health (NIH) - USANIH National Center for Research Resources (NCRR)
   [P20RR017677] Funding Source: NIH RePORTER; NATIONAL INSTITUTE ON
   AGINGUnited States Department of Health & Human ServicesNational
   Institutes of Health (NIH) - USANIH National Institute on Aging (NIA)
   [R01AG016583] Funding Source: NIH RePORTER; NATIONAL LIBRARY OF
   MEDICINEUnited States Department of Health & Human ServicesNational
   Institutes of Health (NIH) - USANIH National Library of Medicine (NLM)
   [R21LM008823] Funding Source: NIH RePORTER; Veterans AffairsUS
   Department of Veterans Affairs [I01BX000156] Funding Source: NIH
   RePORTER; MRCUK Research & Innovation (UKRI)Medical Research Council UK
   (MRC) [G0701935] Funding Source: UKRI
FX We thank the following: Sarah McClelland, Jasmin Zohren and Rebecca
   Burrell for help with manuscript preparation; Hannah Armer and Lucy
   Collinson from the EM facility at Cancer Research UK (CR-UK) LRI and
   Niamh Murphy for help with the breast cancer TMA cohort. CS is funded by
   the Medical Research Council and CR-UK. AL, NM, AR, JD and ST are funded
   by CR-UK. ZS is funded by the National Institute of Health (Grant Nos
   NCI SPORE P50 CA 89393 and R21LM008823-01A1), the Danish Council for
   Independent Research/Medical Sciences (FSS) and the Breast Cancer
   Research Foundation (BCRF).
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NR 48
TC 37
Z9 37
U1 0
U2 2
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0022-3417
EI 1096-9896
J9 J PATHOL
JI J. Pathol.
PD FEB
PY 2012
VL 226
IS 3
BP 482
EP 494
DI 10.1002/path.2998
PG 13
WC Oncology; Pathology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Pathology
GA 877DY
UT WOS:000299158400011
PM 21953249
OA Green Published
DA 2022-04-25
ER

PT J
AU Wang, ZZ
   Jin, JJ
AF Wang, Zhaozhi
   Jin, Jianjun
TI LncRNA SLCO4A1-AS1 promotes colorectal cancer cell proliferation by
   enhancing autophagy via miR-508-3p/PARD3 axis
SO AGING-US
LA English
DT Article
DE colorectal cancer (CRC); SLCO4A1-AS1; PARD3; miR-508-3p; autophagy
ID LONG NONCODING RNAS; DOWN-REGULATION; STATISTICS; CARCINOMA; INVASION
AB Aberrant expressions of various long non-coding RNAs (lncRNAs) have been involved in the progression and pathogenesis of various carcinomas. However, the expression and biological function of SLCO4A1-AS1 in colorectal cancer (CRC) remain poorly understood. Gain-and loss-of-function assays were applied to determine the roles of SLCO4A1-AS1 in autophagy and CRC progression. qRT-PCR and in situ hybridization (ISH) results showed that SLCO4A1-AS1 was positively associated with PARD3 expression in CRC tissues. In vitro and in vivo studies revealed that SLCO4A1-AS1 knockdown repressed cytoprotective autophagy as assayed by transmission electron microscopy (TEM), and inhibited cell proliferation by directly targeting partition-defective 3 (PARD3). Mechanistically, SLCO4A1-AS1 acted as a sponge of miR-508-3p, leading to upregulation of PARD3 and promotion of CRC cell proliferation. The current study demonstrates that the SLCO4A1-AS1/miR-5083p/PARD3/autophagy pathway play a critical role in CRC cell proliferation, and might provide novel targets for developing therapeutic strategies for CRC.
C1 [Wang, Zhaozhi; Jin, Jianjun] Henan Univ Sci & Technol, Affiliated Hosp 1, Dept Gastrointestinal Med, Luoyang 471003, Henan, Peoples R China.
   [Wang, Zhaozhi; Jin, Jianjun] Henan Univ Sci & Technol, Coll Clin Med, Luoyang 471003, Henan, Peoples R China.
RP Wang, ZZ (corresponding author), Henan Univ Sci & Technol, Affiliated Hosp 1, Dept Gastrointestinal Med, Luoyang 471003, Henan, Peoples R China.; Wang, ZZ (corresponding author), Henan Univ Sci & Technol, Coll Clin Med, Luoyang 471003, Henan, Peoples R China.
EM wangzhaozhiroy@163.com
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NR 26
TC 22
Z9 23
U1 1
U2 3
PU IMPACT JOURNALS LLC
PI ORCHARD PARK
PA 6666 E QUAKER ST, STE 1, ORCHARD PARK, NY 14127 USA
SN 1945-4589
J9 AGING-US
JI Aging-US
PD JUL 31
PY 2019
VL 11
IS 14
BP 4876
EP 4889
DI 10.18632/aging.102081
PG 14
WC Cell Biology; Geriatrics & Gerontology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Cell Biology; Geriatrics & Gerontology
GA IO1KN
UT WOS:000479140500010
PM 31308265
OA Green Published, gold
DA 2022-04-25
ER

PT J
AU Germani, A
   Matrone, A
   Grossi, V
   Peserico, A
   Sanese, P
   Liuzzi, M
   Palermo, R
   Murzilli, S
   Campese, AF
   Ingravallo, G
   Canettieri, G
   Tezil, T
   Simone, C
AF Germani, Aldo
   Matrone, Antonio
   Grossi, Valentina
   Peserico, Alessia
   Sanese, Paola
   Liuzzi, Micaela
   Palermo, Rocco
   Murzilli, Stefania
   Campese, Antonio Francesco
   Ingravallo, Giuseppe
   Canettieri, Gianluca
   Tezil, Tugsan
   Simone, Cristiano
TI Targeted therapy against chemoresistant colorectal cancers: Inhibition
   of p38 alpha modulates the effect of cisplatin in vitro and in vivo
   through the tumor suppressor FoxO3A
SO CANCER LETTERS
LA English
DT Article
DE Dual therapy; p38 MAPK; Chemoresistance; Colorectal cancer; Cell death
ID ACTIVATED PROTEIN-KINASES; P38 MAPK; OVARIAN-CANCER; AMPK-FOXO3A AXIS;
   CELL-DEATH; RESISTANCE; CARCINOMA; AUTOPHAGY; COPPER; ERK
AB Chemoresistance is a major obstacle to effective therapy against colorectal cancer (CRC) and may lead to deadly consequences. The metabolism of CRC cells depends highly on the p38 MAPK pathway, whose involvement in maintaining a chemoresistant behavior is currently being investigated. Our previous studies revealed that p38 alpha is the main p38 isoform in CRC cells. Here we show that p38 alpha pharmacological inhibition combined with cisplatin administration decreases colony formation and viability of cancer cells and strongly increases Bax-dependent apoptotic cell death by activating the tumor suppressor protein FoxO3A. Our results indicate that FoxO3A activation up-regulates transcription of its target genes (p21, PTEN, Bim and GADD45), which forces both chemosensitive and chemoresistant CRC cells to undergo apoptosis. Additionally, we found that FoxO3A is required for apoptotic cell death induction, as confirmed by RNA interference experiments. In animal models xenografted with chemoresistant HT29 cells, we further confirmed that the p38-targeted dual therapy strategy produced an increase in apoptosis in cancer tissue leading to tumor regression. Our study uncovers a major role for the p38FoxO3A axis in chemoresistance, thereby suggesting a new therapeutic approach for CRC treatment; moreover, our results indicate that Bax status may be used as a predictive biomarker. (C) 2013 Elsevier Ireland Ltd. All rights reserved.
C1 [Germani, Aldo; Matrone, Antonio; Peserico, Alessia; Sanese, Paola; Tezil, Tugsan; Simone, Cristiano] Consorzio Mario Negri Sud, DTP, Lab Signal Dependent Transcript, I-66030 Santa Maria Imbaro, Ch, Italy.
   [Grossi, Valentina] IRCCS S de Bellis, Canc Genet Lab, I-70013 Castellana Grotte, Italy.
   [Liuzzi, Micaela; Ingravallo, Giuseppe] Univ Bari, DETO, Div Anat Pathol, I-70124 Bari, Italy.
   [Palermo, Rocco; Campese, Antonio Francesco; Canettieri, Gianluca] Ist Italiano Tecnol, Ctr Life Nano Sci Sapienza, Rome, Italy.
   [Murzilli, Stefania] Consorzio Mario Negri Sud, DTP, Anim Care Facil, I-66030 Santa Maria Imbaro, Ch, Italy.
   [Simone, Cristiano] Univ Bari, DIMO, Div Med Genet, I-70124 Bari, Italy.
RP Tezil, T (corresponding author), Consorzio Mario Negri Sud, DTP, Lab Signal Dependent Transcript, Via Nazl 8-A, I-66030 Santa Maria Imbaro, Ch, Italy.
EM teziltugsan@sabanciuniv.edu; cristiano.simone@uniba.it
RI Tezil, Tugsan/A-3909-2013; GROSSI, Valentina/O-6546-2019; Ingravallo,
   Giuseppe/Q-1477-2016; tezil, tugsan/P-4053-2019; Grossi,
   Valentina/K-9821-2016; Campese, Antonio/A-9783-2015; INGRAVALLO,
   Giuseppe/N-2466-2019; Palermo, Rocco/I-5140-2016; Sanese,
   Paola/AAC-1991-2019; Simone, Cristiano/K-3452-2018
OI Tezil, Tugsan/0000-0003-0796-3718; GROSSI,
   Valentina/0000-0003-3843-1618; Ingravallo, Giuseppe/0000-0002-4792-3545;
   Grossi, Valentina/0000-0003-3843-1618; INGRAVALLO,
   Giuseppe/0000-0002-4792-3545; Palermo, Rocco/0000-0003-0134-9370;
   Simone, Cristiano/0000-0002-2628-7658; Sanese,
   Paola/0000-0001-8872-7498; CANETTIERI, Gianluca/0000-0001-6694-2613;
   Peserico, Alessia/0000-0003-2025-2419
FU Italian Foundation for Cancer Research (FIRC) fellowshipsFondazione AIRC
   per la ricerca sul cancro; Italian Association for Cancer Research
   (AIRC)Fondazione AIRC per la ricerca sul cancro [IG10177]; Italian Fund
   for Basic Research (FIRB)
FX We thank Dr Francesco Paolo Joni for his helpful discussion during the
   preparation of the manuscript and editorial assistance. T.T. and A.P.
   are supported by Italian Foundation for Cancer Research (FIRC)
   fellowships. This study was partially supported by an 'Investigator
   Grant 2010' (IG10177) (to C.S.) from the Italian Association for Cancer
   Research (AIRC) and the Italian Fund for Basic Research (FIRB).
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NR 39
TC 37
Z9 39
U1 0
U2 14
PU ELSEVIER IRELAND LTD
PI CLARE
PA ELSEVIER HOUSE, BROOKVALE PLAZA, EAST PARK SHANNON, CO, CLARE, 00000,
   IRELAND
SN 0304-3835
EI 1872-7980
J9 CANCER LETT
JI Cancer Lett.
PD MAR 1
PY 2014
VL 344
IS 1
BP 110
EP 118
DI 10.1016/j.canlet.2013.10.035
PG 9
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA AB3KC
UT WOS:000331688700013
PM 24215867
DA 2022-04-25
ER

PT J
AU Xia, F
   Liu, PQ
   Li, M
AF Xia, Fan
   Liu, Peiqing
   Li, Min
TI The regulatory factors and pathological roles of autophagy-related
   protein 4 in diverse diseases: Recent research advances
SO MEDICINAL RESEARCH REVIEWS
LA English
DT Review
DE ATG4; autophagy; disease; inhibitor; regulatory factor
ID HEPATOCELLULAR-CARCINOMA; UP-REGULATION; COLORECTAL-CANCER;
   DOWN-REGULATION; LUNG-CANCER; ISCHEMIA/REPERFUSION INJURY; ATG8-PE
   DECONJUGATION; SUPPRESSES AUTOPHAGY; ATTENUATES AUTOPHAGY; CONJUGATION
   SYSTEMS
AB Macroautophagy (autophagy) is an evolutionarily conserved and dynamic degradation/recycling pathway in which portions of the cytoplasm, such as dysfunctional proteins and surplus organelles, are engulfed by double-membrane bound vesicles through a lysosome-dependent process. As the only proteolytic enzyme of the core mammalian autophagy proteins, autophagy-related protein 4 (ATG4) primes newly synthesized pro-light chain 3 (LC3) to form LC3-I that attaches to phosphatidylethanolamine and delipidates LC3-PE to LC3-I for recycling. Besides autophagy, ATG4 has been shown to be involved in regulating various biological and pathological processes. The roles of ATG4 in cancer therapy, a methodology for ATG4 activity detection, and the discovery of chemical modulators have been well-reviewed. However, a comprehensive summary on how ATG4 is regulated by multiple factors and, thereby, how ATG4 influences autophagy or other pathways remains lacking. In this paper, we summarize multiple processes and molecules that regulate the activity of ATG4, such as micro-RNAs, posttranslational modifications, and small molecules. Additionally, we focus on the relationship between ATG4 and diverse diseases, including cancer, neurodegeneration, microbial infection, and other diseases. It provides insight regarding potential ATG4-targeted therapeutic opportunities, which could be beneficial for future studies and human health.
C1 [Xia, Fan; Liu, Peiqing; Li, Min] Sun Yat Sen Univ, Natl & Local United Engn Lab Druggabil & New Drug, Guangdong Prov Key Lab Chiral Mol & Drug Discover, Sch Pharmaceut Sci,Dept Pharmacol & Toxicol, Guangzhou 510006, Guangdong, Peoples R China.
RP Liu, PQ; Li, M (corresponding author), Sun Yat Sen Univ, Natl & Local United Engn Lab Druggabil & New Drug, Guangdong Prov Key Lab Chiral Mol & Drug Discover, Sch Pharmaceut Sci,Dept Pharmacol & Toxicol, Guangzhou 510006, Guangdong, Peoples R China.
EM liupq@mail.sysu.edu.cn; limin65@mail.sysu.edu.cn
OI li, min/0000-0002-5657-8675
FU National Natural Science Foundation of ChinaNational Natural Science
   Foundation of China (NSFC) [31970699, 31671437]; Guangdong Basic and
   Applied Basic Research Foundation [2019A1515011030]; Guangdong
   Provincial Key Laboratory of Construction Foundation [2019B030301005];
   Key-Area Research and Development Program of Guangdong Province
   [2020B1111110003]; National Major Special Projects for the Creation and
   Manufacture of New Drugs [2019ZX09301104]
FX This study was supported by the National Natural Science Foundation of
   China (31970699 and 31671437), the Guangdong Basic and Applied Basic
   Research Foundation (2019A1515011030), the Guangdong Provincial Key
   Laboratory of Construction Foundation (2019B030301005), the Key-Area
   Research and Development Program of Guangdong Province
   (2020B1111110003), and the National Major Special Projects for the
   Creation and Manufacture of New Drugs (2019ZX09301104).
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NR 202
TC 5
Z9 5
U1 6
U2 16
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0198-6325
EI 1098-1128
J9 MED RES REV
JI Med. Res. Rev.
PD MAY
PY 2021
VL 41
IS 3
BP 1644
EP 1675
DI 10.1002/med.21772
EA DEC 2020
PG 32
WC Chemistry, Medicinal; Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA RM3PS
UT WOS:000598258200001
PM 33314291
DA 2022-04-25
ER

PT J
AU Qiu, GL
   Li, XQ
   Che, XM
   Wei, C
   He, SC
   Lu, J
   Jia, ZL
   Pang, K
   Fan, L
AF Qiu, Guanglin
   Li, Xuqi
   Che, Xiangming
   Wei, Chao
   He, Shicai
   Lu, Jing
   Jia, Zongliang
   Pang, Ke
   Fan, Lin
TI SIRT1 is a regulator of autophagy: Implications in gastric cancer
   progression and treatment
SO FEBS LETTERS
LA English
DT Review
DE Gastric cancer; Silent mating type information regulation 1; Autophagy;
   Tumor suppressor; Tumor promoter
ID HISTONE DEACETYLASE EXPRESSION; RAPAMYCIN-INDUCED AUTOPHAGY; CELL
   CARCINOMA PATIENTS; HELICOBACTER-PYLORI; COLORECTAL-CANCER;
   POOR-PROGNOSIS; CLINICOPATHOLOGICAL SIGNIFICANCE; VACUOLATING CYTOTOXIN;
   UP-REGULATION; DNA-DAMAGE
AB Silent mating type information regulation 1 (SIRT1) is implicated in tumorigenesis through its effect on autophagy. In gastric cancer (GC), SIRT1 is a marker for prognosis and is involved in cell invasion, proliferation, epithelial-mesenchymal transition (EMT) and drug resistance. Autophagy can function as a cell-survival mechanism or lead to cell death during the genesis and treatment of GC. This functionality is determined by factors including the stage of the tumor, cellular context and stress levels. Interestingly, SIRT1 can regulate autophagy through the deacetylation of autophagy-related genes (ATGs) and mediators of autophagy. Taken together, these findings support the need for continued research efforts to understand the mechanisms mediating the development of gastric cancer and unveil new strategies to eradicate this disease. (C) 2015 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved.
C1 [Qiu, Guanglin; Li, Xuqi; Che, Xiangming; He, Shicai; Lu, Jing; Jia, Zongliang; Fan, Lin] Xi An Jiao Tong Univ, Dept Gen Surg, Affiliated Hosp 1, Coll Med, Xian 710061, Shaanxi Provinc, Peoples R China.
   [Wei, Chao] Xian Hlth Sch, Xian 710054, Shaanxi Provinc, Peoples R China.
   [Pang, Ke] Shaanxi Friendship Hosp, Xian 710068, Shaanxi Provinc, Peoples R China.
RP Fan, L (corresponding author), Xi An Jiao Tong Univ, Dept Gen Surg, Affiliated Hosp 1, Coll Med, 277 Yanta West Rd, Xian 710061, Shaanxi Provinc, Peoples R China.
EM linnet@mail.xjtu.edu.cn
RI Li, Xuqi/B-3090-2014
OI Li, Xuqi/0000-0002-2497-020X
FU National Natural Science Foundation of ChinaNational Natural Science
   Foundation of China (NSFC) [81270150]; International Cooperation Project
   of Science and Technology Research of Shaanxi Province [2012KW-41]
FX This study was supported by grants from the National Natural Science
   Foundation of China (No. 81270150) and the International Cooperation
   Project of Science and Technology Research of Shaanxi Province (No.
   2012KW-41).
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NR 135
TC 45
Z9 50
U1 2
U2 27
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1873-3468
J9 FEBS LETT
JI FEBS Lett.
PD JUL 22
PY 2015
VL 589
IS 16
BP 2034
EP 2042
DI 10.1016/j.febslet.2015.05.042
PG 9
WC Biochemistry & Molecular Biology; Biophysics; Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Biophysics; Cell Biology
GA CN9XT
UT WOS:000358805100002
PM 26049033
OA Bronze
DA 2022-04-25
ER

PT J
AU Bortolami, M
   Comparato, A
   Benna, C
   Errico, A
   Maretto, I
   Pucciarelli, S
   Cillo, U
   Farinati, F
AF Bortolami, Marina
   Comparato, Alessandra
   Benna, Clara
   Errico, Andrea
   Maretto, Isacco
   Pucciarelli, Salvatore
   Cillo, Umberto
   Farinati, Fabio
TI Gene and protein expression of mTOR and LC3 in hepatocellular carcinoma,
   colorectal liver metastasis and "normal" liver tissues
SO PLOS ONE
LA English
DT Article
ID HEPATITIS-B-VIRUS; MAMMALIAN TARGET; AUTOPHAGY; CANCER; PHOSPHORYLATION;
   INFLAMMATION; RESISTANCE; MICRORNAS; PATHWAY; MICE
AB The physiological role of autophagy in the progression of liver diseases is still debated. To understand the clinical relevance of autophagy in primary e secondary hepatic tumors, we analyzed the expression of mTOR (mammalian target of rapamycin), a key regulator of autophagy; Raptor (regulatory-associated protein of mTOR); ULK1 (Unc-51 like kinase 1) determinant in the autophagy initiation; LC3 (microtubule-associated protein 1A/1B-light chain 3), a specific marker of autophagosomes; and p62, a selective autophagy receptor. Samples from subjects with chronic hepatitis (n.58), cirrhosis (n.12), hepatocellular carcinoma (HCC, n.56), metastases (n.48) from colorectal cancer and hyperplasia or gallbladder stones (n.7), the latter considered as controls, were examined. Gene expression analysis was carried out in n.213 tissues by absolute q-PCR, while protein expression by Western Blot in n.191 lysates, including tumoral, surrounding tumoral and normal tissues. Nonparametric statistical tests were used for comparing expression levels in the above-mentioned groups. Subgroup analysis was performed considering viral infection and chemotherapy treatment. The mTOR transcriptional level was significantly lower in metastases compared to HCC (P = 0.0001). p-mTOR(Ser2448) and LC3II/LC3I protein levels were significantly higher in metastases compared to HCC (P = 0.008 and P<0.0001, respectively). ULK(Ser757) levels were significantly higher in HCC compared to metastases (P = 0.0002) while the HCV- and HBV- related HCC showed the highest p62 levels. Chemotherapy induced a down-regulation of the p-mTOR(Ser2448) in metastases and in non-tumor surrounding tissues in treated patients compared to untreated (P = 0.001 and P = 0.005, respectively). Conclusions: the different expression of proteins considered, owning their interaction and diverse tissue microenvironment, indicate an impairment of the autophagy flux in primary liver tumors that is critical for the promotion of tumorigenesis process and a coexistence of autophagy inhibition and activation mechanisms in secondary liver tumors. Differences in mTOR and LC3 transcripts emerged in tumor-free tissues, therefore particular attention should be considered in selecting the control group.
C1 [Bortolami, Marina; Comparato, Alessandra; Errico, Andrea; Farinati, Fabio] Univ Padua, Dept Surg Oncol & Gastroenterol, DISCOG, Sch Med,Gastroenterol Unit, Padua, Italy.
   [Benna, Clara; Maretto, Isacco; Pucciarelli, Salvatore; Cillo, Umberto] Univ Padua, Dept Surg Oncol & Gastroenterol, DISCOG, Sch Med,Surg Unit, Padua, Italy.
RP Bortolami, M (corresponding author), Univ Padua, Dept Surg Oncol & Gastroenterol, DISCOG, Sch Med,Gastroenterol Unit, Padua, Italy.
EM marina.bortolami@unipd.it
RI benna, clara/K-1083-2018; PUCCIARELLI, SALVATORE/J-5050-2018
OI FARINATI, FABIO/0000-0002-2944-1374; PUCCIARELLI,
   SALVATORE/0000-0001-5289-9925
FU University of Padova [BIRD175781]
FX MB: 2017-prot. BIRD175781 University of Padova The funders had no role
   in study design, data collection and analysis, decision to publish, or
   preparation of the manuscript.
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NR 64
TC 1
Z9 1
U1 1
U2 3
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 1160 BATTERY STREET, STE 100, SAN FRANCISCO, CA 94111 USA
SN 1932-6203
J9 PLOS ONE
JI PLoS One
PD DEC 23
PY 2020
VL 15
IS 12
AR e0244356
DI 10.1371/journal.pone.0244356
PG 24
WC Multidisciplinary Sciences
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Science & Technology - Other Topics
GA PL4CI
UT WOS:000603071600001
PM 33362215
OA Green Published, gold
DA 2022-04-25
ER

PT J
AU Liu, JT
   Fan, LL
   Wang, H
   Sun, GP
AF Liu, Jiatao
   Fan, Lulu
   Wang, Hua
   Sun, Guoping
TI Autophagy, a double-edged sword in anti-angiogenesis therapy
SO MEDICAL ONCOLOGY
LA English
DT Review
DE Autophagy; Anti-angiogenesis; Hypoxia
ID HYPOXIA-INDUCIBLE FACTOR-1-ALPHA; METASTATIC COLORECTAL-CANCER;
   PLATINUM-BASED CHEMOTHERAPY; HEPATOCELLULAR-CARCINOMA; CELL-DEATH;
   ANTIANGIOGENIC THERAPY; DRUG-RESISTANCE; LUNG-CANCER; CISPLATIN
   RESISTANCE; TUMOR ANGIOGENESIS
AB Autophagy is a highly conservative cell behavior to keep the intracellular homeostasis and is frequently activated when cells encounter disgusting conditions, such as nutrition or growth factor deprive, hypoxia and cytotoxic agents. However, the precise role of autophagy under various conditions may be opposite, differ from protect cells survival to promote cells death, and the mechanism of this conditional-dependent role is still unclear. Anti-angiogenesis agents, such as bevacizumab, sorafenib and sunitinib, could reduce tumor microvascular density and increase tumor hypoxia, thus up-regulating autophagy activation of tumor cells, but the function of autophagy induced by anti-angiogenesis agents is still divergent and is considered to play a cytoprotective role in most cases. In this review, we mainly discuss the relationship between anti-angiogenesis therapy-induced hypoxia and autophagy, and pay special attention on the exact role of anti-angiogenesis agents induced autophagy in the process of anti-angiogenesis treatment.
C1 [Liu, Jiatao; Fan, Lulu; Wang, Hua; Sun, Guoping] Anhui Med Univ, Affiliated Hosp 1, Dept Oncol, Hefei 230022, Anhui, Peoples R China.
   [Liu, Jiatao] Anhui Med Univ, Affiliated Hosp 1, Dept Pharm, Hefei 230022, Anhui, Peoples R China.
RP Sun, GP (corresponding author), Anhui Med Univ, Affiliated Hosp 1, Dept Oncol, 218 Jixi Rd, Hefei 230022, Anhui, Peoples R China.
EM sungp@ahmu.edu.cn
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NR 124
TC 53
Z9 55
U1 2
U2 31
PU HUMANA PRESS INC
PI TOTOWA
PA 999 RIVERVIEW DRIVE SUITE 208, TOTOWA, NJ 07512 USA
SN 1357-0560
EI 1559-131X
J9 MED ONCOL
JI Med. Oncol.
PD JAN
PY 2016
VL 33
IS 1
AR 10
DI 10.1007/s12032-015-0721-9
PG 13
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA DA0WL
UT WOS:000367518200010
PM 26715036
DA 2022-04-25
ER

PT J
AU Gil, J
   Karpinski, P
   Sasiadek, MM
AF Gil, Justyna
   Karpinski, Pawel
   Sasiadek, Maria M.
TI Transcriptomic Profiling for the Autophagy Pathway in Colorectal Cancer
SO INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
LA English
DT Article
DE autophagy; gene expression; colorectal cancer
ID CONSENSUS MOLECULAR SUBTYPES; EXPRESSION; TUMORIGENESIS; MUTATIONS;
   UNDERLIE; PROTEINS
AB The role of autophagy in colorectal cancer (CRC) pathogenesis appears to be crucial. Autophagy acts both as a tumor suppressor, by removing redundant cellular material, and a tumor-promoting factor, by providing access to components necessary for growth, metabolism, and proliferation. To date, little is known about the expression of genes that play a basal role in the autophagy in CRC. In this study, we aimed to compare the expression levels of 46 genes involved in the autophagy pathway between tumor-adjacent and tumor tissue, employing large RNA sequencing (RNA-seq) and microarray datasets. Additionally, we verified our results using data on 38 CRC cell lines. Gene set enrichment analysis revealed a significant deregulation of autophagy-related gene sets in CRC. The unsupervised clustering of tumors using the mRNA levels of autophagy-related genes revealed the existence of two major clusters: microsatellite instability (MSI)-enriched and -depleted. In cluster 1 (MSI-depleted), ATG9B and LAMP1 genes were the most prominently expressed, whereas cluster 2 (MSI-enriched) was characterized by DRAM1 upregulation. CRC cell lines were also clustered according to MSI-enriched/-depleted subgroups. The moderate deregulation of autophagy-related genes in cancer tissue, as compared to adjacent tissue, suggests a prominent field cancerization or early disruption of autophagy. Genes differentiating these clusters are promising candidates for CRC targeting therapy worthy of further investigation.
C1 [Gil, Justyna; Karpinski, Pawel; Sasiadek, Maria M.] Wroclaw Med Univ, Dept Genet, Marcinkowskiego 1, PL-50368 Wroclaw, Poland.
   [Karpinski, Pawel] Polish Acad Sci, Inst Immunol & Expt Therapy, Lab Genom & Bioinformat, PL-53114 Wroclaw, Poland.
RP Gil, J (corresponding author), Wroclaw Med Univ, Dept Genet, Marcinkowskiego 1, PL-50368 Wroclaw, Poland.
RI Karpinski, Pawel/U-3313-2018
OI Karpinski, Pawel/0000-0003-3885-694X; Gil, Justyna/0000-0003-0991-7686;
   Sasiadek, Maria/0000-0002-7599-7074
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NR 66
TC 1
Z9 1
U1 0
U2 2
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 1422-0067
J9 INT J MOL SCI
JI Int. J. Mol. Sci.
PD OCT
PY 2020
VL 21
IS 19
AR 7101
DI 10.3390/ijms21197101
PG 14
WC Biochemistry & Molecular Biology; Chemistry, Multidisciplinary
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Chemistry
GA OO1QM
UT WOS:000587161100001
PM 32993062
OA Green Published, gold
DA 2022-04-25
ER

PT J
AU Sun, C
   Wang, FJ
   Zhang, HG
   Xu, XZ
   Jia, RC
   Yao, L
   Qiao, PF
AF Sun, Chen
   Wang, Fu-Jing
   Zhang, Hao-Gang
   Xu, Xun-Zheng
   Jia, Rui-Chun
   Yao, Lei
   Qiao, Peng-Fei
TI miR-34a mediates oxaliplatin resistance of colorectal cancer cells by
   inhibiting macroautophagy via transforming growth factor-beta/Smad4
   pathway
SO WORLD JOURNAL OF GASTROENTEROLOGY
LA English
DT Article
DE miR-34a; Oxaliplatin; Colorectal cancer; Macroautophagy; Transforming
   growth factor-alpha/Smad pathway
ID MESENCHYMAL TRANSITION; AUTOPHAGY; 5-FLUOROURACIL; MICRORNAS
AB AIM
   To investigate whether microRNA (miR)-34a mediates oxaliplatin (OXA) resistance of colorectal cancer (CRC) cells by inhibiting macroautophagy via the transforming growth factor (TGF)-alpha/Smad4 pathway.
   METHODS
   miR-34a expression levels were detected in CRC tissues and CRC cell lines by quantitative real-time polymerase chain reaction. Computational search, functional luciferase assay and western blotting were used to demonstrate the downstream target of miR-34a in CRC cells. Cell viability was measured with Cell Counting Kit-8. Apoptosis and macroautophagy of CRC cells were analyzed by flow cytometry and transmission electron microscopy, and expression of beclin I and LC3-II was detected by western blotting.
   RESULTS
   Expression of miR-34a was significantly reduced while expression of TGF-beta and Smad4 was increased in CRC patients treated with OXA-based chemotherapy. OXA treatment also resulted in decreased miR-34a levels and increased TGF-beta and Smad4 levels in both parental cells and the OXA-resistant CRC cells. Activation of macroautophagy contributed to OXA resistance in CRC cells. Expression levels of Smad4 and miR-34a in CRC patients had a significant inverse correlation and overexpressing miR-34a inhibited macroautophagy activation by directly targeting Smad4 through the TGF-alpha/Smad4 pathway. OXA-induced downregulation of miR-34a and increased drug resistance by activating macroautophagy in CRC cells.
   CONCLUSION
   miR-34a mediates OXA resistance of CRC by inhibiting macroautophagy via the TGF-alpha/Smad4 pathway.
C1 [Sun, Chen; Wang, Fu-Jing; Zhang, Hao-Gang; Xu, Xun-Zheng; Yao, Lei; Qiao, Peng-Fei] Harbin Med Univ, Affiliated Hosp 2, Dept Gen Surg, Harbin 150086, Heilongjiang Pr, Peoples R China.
   [Jia, Rui-Chun] Harbin Med Univ, Affiliated Hosp 2, Dept Blood Transfus, Harbin 150086, Heilongjiang Pr, Peoples R China.
RP Qiao, PF (corresponding author), Harbin Med Univ, Affiliated Hosp 2, Dept Gen Surg, Harbin 150086, Heilongjiang Pr, Peoples R China.
EM lunwenqpf@126.com
FU Science Foundation of Education Department of Heilongjiang Province,
   China [12541430]
FX Supported by Science Foundation of Education Department of Heilongjiang
   Province, China, no. 12541430.
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NR 25
TC 73
Z9 76
U1 1
U2 3
PU BAISHIDENG PUBLISHING GROUP INC
PI PLEASANTON
PA 8226 REGENCY DR, PLEASANTON, CA 94588 USA
SN 1007-9327
EI 2219-2840
J9 WORLD J GASTROENTERO
JI World J. Gastroenterol.
PD MAR 14
PY 2017
VL 23
IS 10
BP 1816
EP 1827
DI 10.3748/wjg.v23.i10.1816
PG 12
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA EN4AB
UT WOS:000395948200010
PM 28348487
OA hybrid, Green Submitted, Green Published
DA 2022-04-25
ER

PT J
AU Domart, MC
   Degli Esposti, D
   Sebagh, M
   Olaya, N
   Harper, F
   Pierron, G
   Franc, B
   Tanabe, KK
   Debuire, B
   Azoulay, D
   Brenner, C
   Lemoine, A
AF Domart, Marie-Charlotte
   Degli Esposti, Davide
   Sebagh, Mylene
   Olaya, Natalia
   Harper, Francis
   Pierron, Gerard
   Franc, Brigitte
   Tanabe, Kenneth K.
   Debuire, Brigitte
   Azoulay, Daniel
   Brenner, Catherine
   Lemoine, Antoinette
TI Concurrent induction of necrosis, apoptosis, and autophagy in ischemic
   preconditioned human livers formerly treated by chemotherapy
SO JOURNAL OF HEPATOLOGY
LA English
DT Article
DE Cell death; Ischemia/reperfusion; Ischemic preconditioning;
   Chemotherapy; Bcl-2; Beclin-1; Autophagy; Liver
ID MOUSE-LIVER; PREOPERATIVE CHEMOTHERAPY; REPERFUSION INJURY;
   COLORECTAL-CANCER; CELL-DEATH; IN-VIVO; BCL-2; METASTASES; OXALIPLATIN;
   MECHANISMS
AB Background/Aims: Liver pathology induced by chemotherapy (steatosis or vascular injury) is known to increase the liver's sensitivity to ischemia/reperfusion (I/R) injury, thereby increasing morbidity and mortality after liver resection. Our aim was to assess whether ischemic preconditioning (IP) reduces I/R injury to livers with chemotherapy-induced pathology.
   Methods: We analyzed a series of livers from patients treated with chemotherapy for colorectal cancer who underwent IP (n = 30) or not (n = 31) before hepatectomy. All but one of the livers exhibited chemotherapy-induced steatosis and/or peliosis before the I/R insult.
   Results: Necrosis was less frequent (p = 0.038) in livers with IP than in the others. IP had no influence on apoptosis as assessed by terminal transferase uridyl nick-end labeling (TUNEL) assay or caspase-3, -8 and -9 expression. I P induced a twofold increase in B-cell leukemia/lymphoma 2 (Bcl-2; p < 0.05), which was localized to hepatocytes of centrolobular and peliotic areas and colocalized with the autophagy protein beclin-1 in livers with IP, suggesting their coordinated role in autophagy. Increased expression of the phosphorylated Bcl-2 was observed in preconditioned livers and was associated with a decreased immunoprecipitation of beclin-1 and the increased expression of light chain 3 type II (LC3-II). The increased number of autophagic vacuoles seen by electron microscopy confirmed an association of autophagy in chemotherapy-injured livers following I P. However, the differences in protein expression were not reflected in postresection liver-injury tests or measure of patient morbidity.
   Conclusions: IP is associated with a reduction in necrosis of hepatocytes already damaged by chemotherapy and an activation of autophagy. Bcl-2 and beclin-1 could be major targets in the regulation of cell death during I/R injury. (C) 2009 European Association for the Study of the Liver. Published by Elsevier B.V. All rights reserved.
C1 [Domart, Marie-Charlotte; Degli Esposti, Davide; Olaya, Natalia; Debuire, Brigitte; Lemoine, Antoinette] Hop Paul Brousse, AP HP, Serv Biochim & Biol Mol, F-94804 Villejuif, France.
   [Domart, Marie-Charlotte; Degli Esposti, Davide; Olaya, Natalia] Univ Paris 11, INSERM, Inst Andre Lwoff IFR89, PRES Universud Paris,U602, Villejuif, France.
   [Degli Esposti, Davide; Lemoine, Antoinette] Univ Paris 11, Fac Pharm, Lab Biochim & Biol Cellulaire, F-92290 Chatenay Malabry, France.
   [Sebagh, Mylene] Univ Paris 11, AP HP, Hop Paul Brousse, Inst Andre Lwoff,Serv Anat Pathol,Inserm U785, F-94804 Villejuif, France.
   [Harper, Francis; Pierron, Gerard] Inst Andre Lwoff, Lab Replicat ADN & Ultrastruct Noyau, UPR 1983, Villejuif, France.
   [Franc, Brigitte] Univ Versailles St Quentin, Hop Ambroise Pare, AP HP, Serv Anat Pathol,PRES Universud Paris, Versailles, France.
   [Tanabe, Kenneth K.] Massachusetts Gen Hosp, Ctr Canc, Div Surg Oncol, Boston, MA USA.
   [Tanabe, Kenneth K.] Harvard Univ, Sch Med, Boston, MA USA.
   [Azoulay, Daniel] Univ Paris 11, Hop Paul Brousse, AP HP, Ctr Hepatobiliaire, Villejuif, France.
   [Brenner, Catherine] Univ Versailles St Quentin, CNRS, PRES Univsud Paris, UMR 8159, Versailles, France.
RP Lemoine, A (corresponding author), Hop Paul Brousse, AP HP, Serv Biochim & Biol Mol, 14 Ave Paul Vaillant Couturier, F-94804 Villejuif, France.
EM antoinette.lemoine@pbr.aphp.fr
RI Azoulay, Daniel/Q-7887-2018; Degli Esposti, Davide/M-1917-2015; SEBAGH,
   Mylène/T-7464-2018
OI Degli Esposti, Davide/0000-0003-1390-4845; Domart,
   Marie-Charlotte/0000-0002-5703-2922
FU Ligue Nationale Contre le Cancer (comite de l'Essonne); NRB-Vaincre le
   Cancer; Groupement Cooperatif de Transplantation de I'lle de France;
   Colciencias (Colombia)Departamento Administrativo de Ciencia, Tecnologia
   e Innovacion Colciencias
FX Marie-Charlotte Dorriart is a fellow of Ligue Nationale Contre le Cancer
   (comite de l'Essonne). Davide Degli Esposti is a fellow of NRB-Vaincre
   le Cancer and Groupement Cooperatif de Transplantation de I'lle de
   France. Natalia Olaya was supported by a grant from Colciencias
   (Colombia).
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NR 36
TC 40
Z9 43
U1 0
U2 13
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0168-8278
J9 J HEPATOL
JI J. Hepatol.
PD NOV
PY 2009
VL 51
IS 5
BP 881
EP 889
DI 10.1016/j.jhep.2009.06.028
PG 9
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA 519IY
UT WOS:000271760800007
PM 19765849
DA 2022-04-25
ER

PT J
AU Wu, WB
   Gou, H
   Dong, JY
   Yang, XL
   Zhao, YA
   Peng, H
   Chen, D
   Geng, RM
   Chen, LH
   Liu, J
AF Wu, Wenbing
   Gou, Hui
   Dong, Jingying
   Yang, Xiaolong
   Zhao, Yanan
   Peng, Heng
   Chen, Dan
   Geng, Ruiman
   Chen, Lihong
   Liu, Ji
TI Usnic Acid Inhibits Proliferation and Migration through ATM Mediated DNA
   Damage Response in RKO Colorectal Cancer Cell
SO CURRENT PHARMACEUTICAL BIOTECHNOLOGY
LA English
DT Article
DE Apoptosis; ATM; autophagy; DNA damage; miR-18a; usnic acid
ID INDUCED TOXICITY; APOPTOSIS; AUTOPHAGY; TRANSCRIPTION; ACTIVATION;
   MICRORNAS; MECHANISMS; CARCINOMA; ROS
AB Background: Usnic Acid (UA), also known as lichenol, has been reported to have inhibitory effects on a variety of cancer cells, but its specific mechanism remained to be elucidated. Tumor chemotherapy drugs, especially DNA damage chemotherapeutic drugs, target Chromosomal DNA, but their spontaneous and acquired drug resistance are also an urgent problem to be solved. Therefore, drug combination research has become the focus of researchers.
   Methods: Here, we evaluated the tumor- suppressing molecular mechanism of UA in colorectal cancer cells RKO from the perspective of the ATM-mediated DNA damage signaling pathway through H2O2 simulating DNA damage chemotherapeutic drugs. CCK8 cell proliferation assay was used to determine the inhibition of RKO cells by hydrogen peroxide and UA alone or in combination, and wound healing assay was applied to determine the effect of the drug on cell migration.
   Results: Transfected cells with miRNA18a-5p mimics and inhibitors, MDC and DCFH-DA staining for the measurement of autophagy and ROS, cell cycle and apoptosis were detected by flow cytometry, expressions of microRNA and mRNA were determined by fluorescence quantitative PCR, and protein by Western blot.
   Discussion: We found that UA can upregulate ATM via miR-18a to activate the DNA damage signaling pathway and inhibit the proliferation and migration of RKO cells in a concentration-dependent manner.
   Conclusion: At the same time, DNA damage responses, including cell cycle, autophagy, apoptosis and ROS levels, are also regulated by UA. Therefore, UA combined with DNA damage chemotherapeutic drugs may be an effective treatment for cancer.
C1 [Wu, Wenbing; Dong, Jingying; Yang, Xiaolong; Zhao, Yanan; Peng, Heng; Chen, Dan; Geng, Ruiman; Chen, Lihong; Liu, Ji] Sichuan Univ, West China Sch Basic Med Sci & Forens Med, Dept Biochem & Mol Biol, 17 Peoples South Rd, Chengdu 610041, Peoples R China.
   [Wu, Wenbing] Southwest Med Univ, Sch Basic Med Sci, Dept Biochem & Mol Biol, Luzhou 646000, Peoples R China.
   [Gou, Hui] Southwest Med Univ, Dept Pharm, Affiliated Hosp, Luzhou 646000, Peoples R China.
RP Liu, J (corresponding author), Sichuan Univ, West China Sch Basic Med Sci & Forens Med, Dept Biochem & Mol Biol, 17 Peoples South Rd, Chengdu 610041, Peoples R China.
EM liuji6103@163.com
OI Geng, Ruiman/0000-0002-9253-9171; wenbing, wu/0000-0002-8132-5100; dong,
   jingying/0000-0002-3841-1644
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NR 40
TC 3
Z9 3
U1 6
U2 19
PU BENTHAM SCIENCE PUBL LTD
PI SHARJAH
PA EXECUTIVE STE Y-2, PO BOX 7917, SAIF ZONE, 1200 BR SHARJAH, U ARAB
   EMIRATES
SN 1389-2010
EI 1873-4316
J9 CURR PHARM BIOTECHNO
JI Curr. Pharm. Biotechnol.
PY 2021
VL 22
IS 8
BP 1129
EP 1138
DI 10.2174/1389201021666201002155955
PG 10
WC Biochemistry & Molecular Biology; Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Pharmacology & Pharmacy
GA SF0KU
UT WOS:000652454500011
PM 33006536
DA 2022-04-25
ER

PT J
AU Wang, J
   Wang, J
   Li, L
   Feng, L
   Wang, YR
   Wang, Z
   Tan, NH
AF Wang, Jing
   Wang, Jia
   Li, Ling
   Feng, Li
   Wang, Yu-Rong
   Wang, Zhe
   Tan, Ning-Hua
TI RA-XII, a bicyclic hexapeptidic glucoside isolated from Rubia
   yunnanensis Diels, exerts antitumor activity by inhibiting protective
   autophagy and activating Akt-mTOR pathway in colorectal cancer cells
SO JOURNAL OF ETHNOPHARMACOLOGY
LA English
DT Article
DE Rubia yunnanensis Diels; Cyclopeptide; RA-XII; Colorectal cancer;
   Antitumor mechanism
AB Ethnopharmacological relevance: The roots of Rubia yunnanensis Diels (Chinese name 'Xiao-Hong-Shen'), a traditional Chinese medicine native to Yunnan province (China), have a long history of use for treating several diseases, such as tuberculosis, rheumatism and cancers. A bicyclic hexapeptidic glucoside named RA-XII was isolated from R. yunnanensis, which has been reported to exert anti-inflammatory and antitumor activities.
   Aim of the study: This study was designed to investigate the antitumor activity and potential mechanism of RA-XII on colorectal cancer (CRC) cell lines.
   Materials and methods: Sulforhodamine B assay, clonogenic assay and cell cycle analysis were conducted to assess the anti-proliferative activity of RA-XII on CRC cells. GFP-LC3B plasmid transfection, MDC and AO staining assays, cathepsin activity assay, and siRNAs against several genes were used to investigate the effect of RA-XII on autophagy. Western blotting was used to examine the expression levels of proteins associated with cell cycle arrest, apoptosis and autophagy. Human CRC xenograft-bearing BALB/c nude mice were used to evaluate the antitumor effect of RA-XII in vivo.
   Results: RA-XII showed favorable antineoplastic activity in SW620 and HT29 cells in vitro and in vivo. RA-XII did not induce apoptosis indicated by no obvious changes on mitochondrial membrane potential and apoptosisrelated marker proteins in SW620 or HT29 cells. Treatment of RA-XII inhibited the formation of autophagosomes, which is implied by the GFP-LC3 fluorescent dots, MDC-stained autophagic vesicles and LC3 protein expression. It was indicated that RA-XII suppressed autophagy by regulating several signaling pathways including mTOR and NF-kappa B pathways. Pharmacological or genetic inhibition of autophagy could enhance the cytotoxicity of RA-XII while autophagy inducer could rescue RA-XII-induced cell death. Besides, RA-XII could increase the susceptibility of CRC cells to bortezomib.
   Conclusion: Our study demonstrated that RA-XII exerted antitumor activity independent of apoptosis, and suppressed protective autophagy by regulating mTOR and NF-kappa B pathways in SW620 and HT29 cell lines, which suggested that RA-XII is a key active ingredient for the cancer treatment of Rubia yunnanensis and possesses a promising prospect as an autophagy inhibitor for CRC therapy.
C1 [Wang, Jing; Wang, Jia; Li, Ling; Feng, Li; Wang, Yu-Rong; Wang, Zhe; Tan, Ning-Hua] China Pharmaceut Univ, Sch Tradit Chinese Pharm, Dept TCMs Pharmaceut, Nanjing 211198, Peoples R China.
RP Wang, Z; Tan, NH (corresponding author), China Pharmaceut Univ, Sch Tradit Chinese Pharm, Dept TCMs Pharmaceut, Nanjing 211198, Peoples R China.
EM 18851107621@163.com; 1731020094@stu.cpu.edu.cn;
   1821020435@stu.cpu.edu.cn; cpu_fengli2012@163.com;
   yurong1987213@163.com; wangzhe@cpu.edu.cn; nhtan@cpu.edu
FU National New Drug Innovation Major Project of Ministry of Science and
   Technology of China [2017ZX09309027]; National Natural Science
   Foundation of ChinaNational Natural Science Foundation of China (NSFC)
   [21702231, 81803572]; Natural Science Foundation of Jiangsu
   ProvinceNatural Science Foundation of Jiangsu Province [BK20170745];
   Program of Innovative Research Team of Jiangsu Province; "Double
   First-Class" Project of China Pharmaceutical University [CPU2018GF05]
FX This work was supported by the National New Drug Innovation Major
   Project of Ministry of Science and Technology of China (2017ZX09309027),
   the National Natural Science Foundation of China (21702231, 81803572),
   the Natural Science Foundation of Jiangsu Province (BK20170745), the
   Program of Innovative Research Team of Jiangsu Province, and the "Double
   First-Class" Project of China Pharmaceutical University (CPU2018GF05).
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NR 42
TC 5
Z9 5
U1 10
U2 54
PU ELSEVIER IRELAND LTD
PI CLARE
PA ELSEVIER HOUSE, BROOKVALE PLAZA, EAST PARK SHANNON, CO, CLARE, 00000,
   IRELAND
SN 0378-8741
EI 1872-7573
J9 J ETHNOPHARMACOL
JI J. Ethnopharmacol.
PD FEB 10
PY 2021
VL 266
AR 113438
DI 10.1016/j.jep.2020.113438
PG 13
WC Plant Sciences; Chemistry, Medicinal; Integrative & Complementary
   Medicine; Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Plant Sciences; Pharmacology & Pharmacy; Integrative & Complementary
   Medicine
GA PE0JX
UT WOS:000598060900005
PM 33017635
DA 2022-04-25
ER

PT J
AU Chen, LX
   Sun, LB
   Dai, XF
   Li, T
   Yan, XJ
   Zhang, YT
   Xiao, HX
   Shen, XD
   Huang, G
   Xiang, W
   Zhang, Y
   Tan, DH
   Yang, SM
   Nie, YZ
   Huang, XQ
   Lian, JQ
   He, FT
AF Chen, Lingxi
   Sun, Liangbo
   Dai, Xufang
   Li, Tao
   Yan, Xiaojing
   Zhang, Yueting
   Xiao, Hanxi
   Shen, Xiaodong
   Huang, Gang
   Xiang, Wei
   Zhang, Yan
   Tan, Dehong
   Yang, Shiming
   Nie, Yongzhan
   Huang, Xuequan
   Lian, Jiqin
   He, Fengtian
TI LncRNA CRNDE Promotes ATG4B-Mediated Autophagy and Alleviates the
   Sensitivity of Sorafenib in Hepatocellular Carcinoma Cells
SO FRONTIERS IN CELL AND DEVELOPMENTAL BIOLOGY
LA English
DT Article
DE hepatocellular carcinoma; CRNDE; ATG4B; autophagy; sorafenib
ID LONG-NONCODING RNA; CANCER; CHEMOSENSITIVITY; PROLIFERATION; EXPRESSION;
   MECHANISM; INVASION; SPONGE; ATG4B; 5-FU
AB Autophagy is closely related to the growth and drug resistance of cancer cells, and autophagy related 4B (ATG4B) performs a crucial role in the process of autophagy. The long non-coding RNA (lncRNA) colorectal neoplasia differentially expressed (CRNDE) promotes the progression of hepatocellular carcinoma (HCC), but it is unclear whether the tumor-promoting effect of CRNDE is associated with the regulation of ATG4B and autophagy. Herein, we for the first time demonstrated that CRNDE triggered autophagy via upregulating ATG4B in HCC cells. Mechanistically, CRNDE enhanced the stability of ATG4B mRNA by sequestrating miR-543, leading to the elevation of ATG4B and autophagy in HCC cells. Moreover, sorafenib induced CRNDE and ATG4B as well as autophagy in HCC cells. Knockdown of CRNDE sensitized HCC cells to sorafenib in vitro and in vivo. Collectively, these results reveal that CRNDE drives ATG4B-mediated autophagy, which attenuates the sensitivity of sorafenib in HCC cells, suggesting that the pathway CRNDE/ATG4B/autophagy may be a novel target to develop sensitizing measures of sorafenib in HCC treatment.
C1 [Chen, Lingxi; Li, Tao; Yan, Xiaojing; Zhang, Yueting; Xiao, Hanxi; Shen, Xiaodong; Huang, Gang; Xiang, Wei; Zhang, Yan; Lian, Jiqin; He, Fengtian] Army Med Univ, Coll Basic Med Sci, Dept Biochem & Mol Biol, Chongqing, Peoples R China.
   [Sun, Liangbo; Lian, Jiqin] Army Med Univ, Fac Pharm & Lab Med, Dept Clin Biochem, Chongqing, Peoples R China.
   [Dai, Xufang] Chongqing Normal Univ, Coll Educ Sci, Chongqing, Peoples R China.
   [Tan, Dehong] Army Med Univ, Southwest Hosp, Inst Hepatopancreatobiliary Surg, Chongqing, Peoples R China.
   [Yang, Shiming] Army Med Univ, Xinqiao Hosp, Dept Gastroenterol, Chongqing, Peoples R China.
   [Nie, Yongzhan] Air Force Med Univ, State Key Lab Canc Biol, Xian, Peoples R China.
   [Huang, Xuequan] Army Med Univ, Southwest Hosp, Ctr Minimally Invas Intervent, Chongqing, Peoples R China.
RP Lian, JQ; He, FT (corresponding author), Army Med Univ, Coll Basic Med Sci, Dept Biochem & Mol Biol, Chongqing, Peoples R China.; Lian, JQ (corresponding author), Army Med Univ, Fac Pharm & Lab Med, Dept Clin Biochem, Chongqing, Peoples R China.; Huang, XQ (corresponding author), Army Med Univ, Southwest Hosp, Ctr Minimally Invas Intervent, Chongqing, Peoples R China.
EM hxuequan@163.com; lianjiqin@sina.com; hefengtian66@163.com
FU National Natural Science Foundation of ChinaNational Natural Science
   Foundation of China (NSFC) [81872024, 31671464, 82073300]; Natural
   Science Foundation of ChongqingNatural Science Foundation of Chongqing
   [cstc2017jcyjBX0079, cstc2018jcyjA2018]; Open Fund Research Projects of
   the State Key Laboratory of Cancer Biology of Air Force Medical
   University [CBSKL2019ZDKF07]; Basic and Clinical Integration Research
   Project of Army Medical University [2019JCLC04]
FX This study was supported by the National Natural Science Foundation of
   China (81872024, 31671464, and 82073300), the Natural Science Foundation
   of Chongqing (cstc2017jcyjBX0079 and cstc2018jcyjA2018), the Open Fund
   Research Projects of the State Key Laboratory of Cancer Biology of Air
   Force Medical University (CBSKL2019ZDKF07), and the Basic and Clinical
   Integration Research Project of Army Medical University (2019JCLC04).
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NR 52
TC 2
Z9 2
U1 3
U2 4
PU FRONTIERS MEDIA SA
PI LAUSANNE
PA AVENUE DU TRIBUNAL FEDERAL 34, LAUSANNE, CH-1015, SWITZERLAND
SN 2296-634X
J9 FRONT CELL DEV BIOL
JI Front. Cell. Dev. Biol.
PD AUG 2
PY 2021
VL 09
AR 687524
DI 10.3389/fcell.2021.687524
PG 16
WC Cell Biology; Developmental Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Cell Biology; Developmental Biology
GA UA6DC
UT WOS:000685249400001
PM 34409031
OA Green Published, gold
DA 2022-04-25
ER

PT J
AU Kim, MS
   Song, SY
   Lee, JY
   Yoo, NJ
   Lee, SH
AF Kim, Min Sung
   Song, Sang Yong
   Lee, Ji Youl
   Yoo, Nam Jin
   Lee, Sug Hyung
TI Expressional and mutational analyses of ATG5 gene in prostate cancers
SO APMIS
LA English
DT Article
DE ATG5; mutation; expression; prostate cancer; autophagy
ID AUTOPHAGY-RELATED GENE; MICROSATELLITE INSTABILITY; COLORECTAL CANCERS;
   CELL-DEATH; BECLIN-1; APOPTOSIS; TUMORIGENESIS; DISRUPTION; CARCINOMAS;
   THERAPY
AB Autophagy is an evolutionarily conserved mechanism that plays important roles in both cell death and cell survival. ATG5 is an essential constituent for autophagosome formation, which sequesters cytoplasmic materials before lysosomal delivery. Although both cell death and survival are important in cancer development, the role of autophagy in prostate cancer development remains unclear. The aim of this study was to see whether alterations of ATG5 protein expression and somatic mutations of the ATG5 gene are found in prostate cancers. In the present study, we analyzed ATG5 protein expression in 107 prostate carcinomas by immunohistochemistry; additionally, we assayed the presence of ATG5 somatic mutations in 45 prostate carcinomas by single-strand conformation polymorphism. Immunostaining of ATG5 in normal prostate cells was observed in 44.9% of the cases, whereas in prostate intraepithelial neoplasm (PIN) and prostate cancer cells, ATG5 was observed in 100% and 89.7% of the cases, respectively. Cytoplasmic expression of ATG5 that might be related to autophagy was seen in PIN (100%) and cancers (83.2%), but not in normal cells (0%). ATG5 expression was not associated with any of the pathologic characteristics, including size of the cancers, age, Gleason score, and stage. As for the ATG5 gene, we found no somatic mutations in the prostate cancers. In this study, we analyzed ATG5 expression and mutation in prostate cancers, and found that ATG5 expression was altered in prostate cancers. The expression of ATG5, especially in the cytoplasm, in the prostate cancers compared with normal prostate cells suggested that overexpression of this protein may be related to autophagy and might play a role in prostate tumorigenesis.
C1 [Kim, Min Sung; Yoo, Nam Jin; Lee, Sug Hyung] Catholic Univ Korea, Dept Pathol, Coll Med, Seoul 137701, South Korea.
   [Song, Sang Yong] Sungkyunkwan Univ, Sch Med, Samsung Med Ctr, Seoul, South Korea.
   [Lee, Ji Youl] Catholic Univ Korea, Dept Urol, Coll Med, Seoul 137701, South Korea.
RP Lee, SH (corresponding author), Catholic Univ Korea, Dept Pathol, Coll Med, 505 Banpo Dong, Seoul 137701, South Korea.
EM suhulee@catholic.ac.kr
FU Ministry for Health, Welfare and Family Affairs of KoreaMinistry of
   Health & Welfare, Republic of Korea [A100098]
FX This study was supported by a grant from Ministry for Health, Welfare
   and Family Affairs of Korea (A100098).
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NR 27
TC 31
Z9 35
U1 0
U2 8
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0903-4641
J9 APMIS
JI APMIS
PD NOV
PY 2011
VL 119
IS 11
BP 802
EP 807
DI 10.1111/j.1600-0463.2011.02812.x
PG 6
WC Immunology; Microbiology; Pathology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology; Microbiology; Pathology
GA 835TQ
UT WOS:000296059300010
PM 21995634
DA 2022-04-25
ER

PT J
AU Uscatu, CD
   Mixich, F
   Dumitrescu, TV
   Nicoli, ER
   Deliu, IC
   Man, GM
   Plesea, IE
AF Uscatu, Constantin Daniel
   Mixich, Francisc
   Dumitrescu, Theodor Viorel
   Nicoli, Elena-Raluca
   Deliu, Ionela Cristina
   Man, George Mihail
   Plesea, Iancu Emil
TI The influence of irradiation on autophagy process in normal and
   malignant colorectal epithelia
SO ROMANIAN JOURNAL OF MORPHOLOGY AND EMBRYOLOGY
LA English
DT Article
DE colorectal cancer; autophagy; LC3; preoperative irradiation
ID CANCER CELLS; PATTERNS
AB Aim: The authors assessed the influence of preoperative radiotherapy on autophagy process using a quantitative assessment of LC3 expression on both normal and tumoral colorectal tissues. Materials and Methods: Normal and malignant tissue samples were taken from 50 patients that underwent surgery for colorectal adenocarcinoma of which 11 received preoperative radiotherapy. Tissue samples were included in paraffin and sections were immunomarked for LC3 expression. LC3 percentage was assessed with dedicated software on 10 randomly selected fields with 40x objective from both normal and malignant tissue samples of each patient. The resulting data were assessed and compared with a statistical apparatus. Results: LC3 was overexpressed in tumoral tissue as compared with normal one. The LC3 percentage is different from person to person and the higher it is in normal epithelium, the higher will be in tumoral epithelium of the same person, regardless the irradiation. The LC3 expression levels are decreasing from tumoral non-irradiated epithelia to normal irradiated epithelia. LC3 expression in tumoral cells is granular, with particular perinuclear disposal and often "annular' pattern. Conclusions: The autophagy process has a basal level in the normal tissue, with interindividual variability. The autophagy process proved to be upregulated in the tumoral cells, with a particular morphological expression, namely the presence of cytoplasmic coarse granules disposed in an "annular' pattern. Preoperative radiotherapy is downregulating the autophagy process both in normal and tumoral tissue but to a lesser extent in the latter.
C1 [Uscatu, Constantin Daniel; Mixich, Francisc; Nicoli, Elena-Raluca] Univ Med & Pharm Craiova, Dept Cellular & Mol Biol, Craiova 200349, Romania.
   [Uscatu, Constantin Daniel; Plesea, Iancu Emil] Emergency Cty Hosp, Dept Pathol, 1 Tabaci St, Craiova 200642, Romania.
   [Dumitrescu, Theodor Viorel] Emergency Cty Hosp, Dept Surg, Craiova 200642, Romania.
   [Deliu, Ionela Cristina] Univ Med & Pharm Craiova, Dept Gastroenterol, Craiova 200349, Romania.
   [Man, George Mihail] Emergency Cty Hosp, Dept Pathol, Pitesti, Romania.
   [Plesea, Iancu Emil] Univ Med & Pharm Craiova, Dept Pathol, 2 Petru Rares St, Craiova 200349, Romania.
RP Plesea, IE (corresponding author), Emergency Cty Hosp, Dept Pathol, 1 Tabaci St, Craiova 200642, Romania.; Plesea, IE (corresponding author), Univ Med & Pharm Craiova, Dept Pathol, 2 Petru Rares St, Craiova 200349, Romania.
EM pie1956@yahoo.com
RI Nicoli, Elena-Raluca/F-3968-2011
OI Nicoli, Elena-Raluca/0000-0002-5545-630X; Dumitrescu, Theodor
   Viorel/0000-0002-2485-7821; Calota, Firmilian/0000-0002-2689-5477
FU European Social Fund, Human Resources Development Operational
   ProgramEuropean Social Fund (ESF) [POSDRU/159/1.5/136893]
FX This paper was published under the frame of European Social Fund, Human
   Resources Development Operational Program 2007-2013, Project No.
   POSDRU/159/1.5/136893.
CR Giatromanolaki A, 2010, J CLIN PATHOL, V63, P867, DOI 10.1136/jcp.2010.079525
   Guo GF, 2011, WORLD J GASTROENTERO, V17, P4779, DOI 10.3748/wjg.v17.i43.4779
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NR 9
TC 0
Z9 0
U1 0
U2 4
PU EDITURA ACAD ROMANE
PI BUCURESTI
PA CALEA 13 SEPTEMBRIE NR 13, SECTOR 5, BUCURESTI 050711, ROMANIA
SN 1220-0522
J9 ROM J MORPHOL EMBRYO
JI Rom. J. Morphol. Embryol.
PY 2016
VL 57
IS 1
BP 227
EP 232
PG 6
WC Developmental Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Developmental Biology
GA DM0PR
UT WOS:000376048800029
PM 27151712
DA 2022-04-25
ER

PT J
AU Lee, G
   Liang, CY
   Park, G
   Jang, C
   Jung, JU
   Chung, J
AF Lee, Gina
   Liang, Chengyu
   Park, Gihyun
   Jang, Cholsoon
   Jung, Jae U.
   Chung, Jongkyeong
TI UVRAG is required for organ rotation by regulating Notch endocytosis in
   Drosophila
SO DEVELOPMENTAL BIOLOGY
LA English
DT Article
DE UVRAG; Organ rotation; Vesicle trafficking; Notch endocytosis;
   Left-right body asymmetry
ID LEFT-RIGHT ASYMMETRY; PROGRAMMED CELL-DEATH; UNCONVENTIONAL MYOSIN;
   SIGNALING PATHWAY; TUMOR SUPPRESSORS; NODAL EXPRESSION; ENDOSOMAL ENTRY;
   MALE TERMINALIA; DOWN-REGULATION; COLON-CANCER
AB Heterotaxy characterized by abnormal left-right body asymmetry causes diverse congenital anomalies. Organ rotation is a crucial developmental process to establish the left-right patterning during animal development. However, the molecular basis of how organ rotation is regulated is poorly understood. Here we report that Drosophila UV-resistance associated gene (UVRAG), a tumor suppressor that regulates autophagy and endocytosis, plays unexpected roles in controlling organ rotation. Loss-of-function mutants of UVRAG show seriously impaired organ rotation phenotypes, which are associated with defects in endocytic trafficking rather than autophagy. Blunted endocytic degradation by UVRAG deficiency causes endosomal accumulation of Notch, resulting in abnormally enhanced Notch activity. Knockdown of Notch itself or expression of a dominant negative form of Notch transcriptional co-activator Mastermind is sufficient to rescue the rotation defect in UVRAG mutants. Consistently. UVRAG-mutated heterotaxy patient cells also display highly increased Notch protein levels. These results suggest evolutionarily conserved roles of UVRAG in organ rotation by regulating Notch endocytic degradation. (C) 2011 Elsevier Inc. All rights reserved.
C1 [Liang, Chengyu; Jung, Jae U.] Univ So Calif, Dept Mol Microbiol & Immunol, Los Angeles, CA 90033 USA.
   [Lee, Gina; Park, Gihyun; Chung, Jongkyeong] Seoul Natl Univ, Natl Creat Res Initiat Ctr, Seoul 151742, South Korea.
   [Lee, Gina; Park, Gihyun; Chung, Jongkyeong] Seoul Natl Univ, Sch Biol Sci, Seoul 151742, South Korea.
   [Lee, Gina; Park, Gihyun; Jang, Cholsoon; Chung, Jongkyeong] Korea Adv Inst Sci & Technol, Dept Biol Sci, Taejon 305701, South Korea.
   [Chung, Jongkyeong] Seoul Natl Univ, Inst Mol Biol & Genet, Seoul 151742, South Korea.
RP Jung, JU (corresponding author), Univ So Calif, Dept Mol Microbiol & Immunol, Los Angeles, CA 90033 USA.
EM jaeujung@usc.edu; jkc@snu.ac.kr
OI LIANG, CHENGYU/0000-0001-6082-2143
FU National Creative Research Initiatives ProgramMinistry of Education,
   Science and Technology, Republic of Korea [2010-0018291]; Priority
   Research Centers Program [2009-0094022]; Ministry of Education, Science,
   and Technology (MEST) of KoreaMinistry of Education, Science and
   Technology, Republic of Korea; U.S. Public Health ServiceUnited States
   Department of Health & Human ServicesUnited States Public Health Service
   [CA82057, CA91819, CA31363, CA115284, AI073099]; Fletcher Jones
   Foundation; Hastings Foundation; Korean GRL Program [K20815000001];
   Lymphoma and Leukemia Society of USA; Wright Foundation; Baxter
   Foundation;  [AI083841];  [CA140964]; NATIONAL CANCER INSTITUTEUnited
   States Department of Health & Human ServicesNational Institutes of
   Health (NIH) - USANIH National Cancer Institute (NCI) [R01CA031363,
   R21CA161436, R01CA082057, R01CA091819, R01CA140964, R01CA115284] Funding
   Source: NIH RePORTER; NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS
   DISEASESUnited States Department of Health & Human ServicesNational
   Institutes of Health (NIH) - USANIH National Institute of Allergy &
   Infectious Diseases (NIAID) [R01AI073099, R21AI083841] Funding Source:
   NIH RePORTER
FX We thank Drs. Ben-Zion Shilo, Denise Montell, Ernesto Sanchez-Herrero,
   Gary Struhl, Harald Stenmark, Hirofumi Ohashi, Hugo Bellen, Jaeseob Kim,
   Masayuki Miura, Pernille Rorth, Tetsuya Tabata and Thomas Neufeld for
   reagents and Drosophila lines. We are grateful to Drs. Kyung-Ok Cho,
   Kwang-Wook Choi and Young-Yun Kong for helpful discussion and kind
   support. We thank Bloomington Stock Center, Developmental Studies
   Hybridoma Bank, Drosophila Genetic Resource Center, Drosophila Genomics
   Resource Center, National Institute of Genetics and VDRC Stock Center
   for Drosophila stocks and antibodies, and Korea Basic Science Institute
   and National Instrumentation Center for Environmental Management (Seoul
   National University) for electron microscopic analysis. This work was
   supported by the National Creative Research Initiatives Program
   (2010-0018291) to J.C. and the Priority Research Centers Program
   (2009-0094022) to G.L. from the National Research Foundation (NRF) grant
   funded by the Ministry of Education, Science, and Technology (MEST) of
   Korea. J.J. was supported by U.S. Public Health Service grants CA82057,
   CA91819, CA31363, CA115284, AI073099, the Fletcher Jones Foundation, the
   Hastings Foundation and the Korean GRL Program (K20815000001). C.L was
   supported by AI083841, CA140964, the Lymphoma and Leukemia Society of
   USA, the Wright Foundation and the Baxter Foundation.
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NR 88
TC 30
Z9 31
U1 0
U2 3
PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 0012-1606
J9 DEV BIOL
JI Dev. Biol.
PD AUG 15
PY 2011
VL 356
IS 2
BP 588
EP 597
DI 10.1016/j.ydbio.2011.06.024
PG 10
WC Developmental Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Developmental Biology
GA 806JO
UT WOS:000293803900026
PM 21729695
OA Green Accepted, Bronze
DA 2022-04-25
ER

PT J
AU Park, SJ
   Park, SH
   Kim, JO
   Kim, JH
   Park, SJ
   Hwang, JJ
   Jin, DH
   Jeong, SY
   Lee, SJ
   Kim, JC
   Kim, I
   Cho, DH
AF Park, So Jung
   Park, Seong Ho
   Kim, Joo-Oh
   Kim, Jung Ho
   Park, So Jung
   Hwang, Jung Jin
   Jin, Dong-Hoon
   Jeong, Seong-Yun
   Lee, Seung Jin
   Kim, Jin Cheon
   Kim, InKi
   Cho, Dong-Hyung
TI Carnitine sensitizes TRAIL-resistant cancer cells to TRAIL-induced
   apoptotic cell death through the up-regulation of Bax
SO BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
LA English
DT Article
DE TRAIL; Resistance; Carnitine; A549; Apoptosis; Sensitization
ID GENE-EXPRESSION; LIGAND; MITOCHONDRIA; INHIBITION; ACTIVATION; PROTEIN;
   MCL-1; MECHANISMS; THERAPY; PATHWAY
AB Tumor necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL) is a member of the tumor necrosis factor family with apoptosis-inducing activity. Given that TRAIL selectively induces cell death in various tumors but has little or no toxicity to normal cells. TRAIL agonists have been considered as promising anti-cancer therapeutic agents. However, the resistance of many primary tumors and cancer cells to TRAIL poses a challenge. In our present study, we found that carnitine, a metabolite that transfers long-chain fatty acids into mitochondria for beta-oxidation and modulates protein kinase C activity, sensitizes TRAIL-resistant cancer cells to TRAIL. Combination of carnitine and TRAIL was found to synergistically induce apoptotic cell death through caspase activation, which was blocked by a pan caspase inhibitor, but not by an inhibitor of autophagy or an inhibitor of necrosis. The combination of carnitine and TRAIL reversed the resistance to TRAIL in lung cancer cells, colon carcinoma cells, and breast carcinoma cells. We further demonstrate that carnitine, either alone or in combination with TRAIL, enhances the expression of the pro-apoptotic Bcl-2 family protein, Bcl-2-associated X protein (Bax). The downregulation of Bax expression by small interfering RNA reduced caspase activation when cells were treated with TRAIL, and experiments with cells from Bax knockout mice confirmed this result. Taken together, our current results suggest that carnitine can reverse the resistance of cancer cells to TRAIL by up-regulating Bax expression. Thus, a combined delivery of carnitine and TRAIL may represent a new therapeutic strategy to treat TRAIL-resistant cancer cells. (C) 2012 Elsevier Inc. All rights reserved.
C1 [Park, So Jung; Kim, Joo-Oh; Kim, Jung Ho; Cho, Dong-Hyung] Kyung Hee Univ, Grad Sch EW Med Sci, Yongin 446701, Gyeoggi Do, South Korea.
   [Park, Seong Ho] Hallym Univ, Ilsong Inst Life Sci, Kangwon Do, South Korea.
   [Park, So Jung; Hwang, Jung Jin; Jin, Dong-Hoon; Jeong, Seong-Yun; Lee, Seung Jin; Kim, InKi] Univ Ulsan, Coll Med, Asan Med Ctr, Asan Inst Med Res, Seoul, South Korea.
   [Hwang, Jung Jin; Jin, Dong-Hoon; Jeong, Seong-Yun; Lee, Seung Jin; Kim, Jin Cheon] Asan Med Ctr, Inst Innovat Canc Res, Seoul 138736, South Korea.
   [Kim, Jin Cheon] Univ Ulsan, Coll Med, Asan Med Ctr, Dept Surg, Seoul, South Korea.
RP Kim, I (corresponding author), Asan Med Ctr, Asan Inst Med Reserch, Seoul 138736, South Korea.
EM ik.kim@amc.seoul.kr; dhcho@khu.ac.kr
RI Hwang, Jung Jin/F-3424-2014
FU Basic Science Research Program; National Research Foundation,
   KoreaNational Research Foundation of Korea [2010-0009164]; Korean Health
   Technology R&D Project, Ministry of Health & Welfare, Republic of Korea
   [A062254]
FX This research was supported by the Basic Science Research Program, the
   National Research Foundation, Korea (2010-0009164), and a grant of the
   Korean Health Technology R&D Project, Ministry of Health & Welfare,
   Republic of Korea (A062254).
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NR 37
TC 11
Z9 11
U1 0
U2 10
PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 0006-291X
J9 BIOCHEM BIOPH RES CO
JI Biochem. Biophys. Res. Commun.
PD NOV 9
PY 2012
VL 428
IS 1
BP 185
EP 190
DI 10.1016/j.bbrc.2012.10.038
PG 6
WC Biochemistry & Molecular Biology; Biophysics
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Biophysics
GA 043DN
UT WOS:000311523200032
PM 23068102
DA 2022-04-25
ER

PT J
AU Wei, FZ
   Cao, ZY
   Wang, X
   Wang, H
   Cai, MY
   Li, TT
   Hattori, N
   Wang, DL
   Du, YP
   Song, BY
   Cao, LL
   Shen, CC
   Wang, LN
   Wang, HY
   Yang, Y
   Xie, D
   Wang, F
   Ushijima, T
   Zhao, Y
   Zhu, WG
AF Wei, Fu-Zheng
   Cao, Ziyang
   Wang, Xi
   Wang, Hui
   Cai, Mu-Yan
   Li, Tingting
   Hattori, Naoko
   Wang, Donglai
   Du, Yipeng
   Song, Boyan
   Cao, Lin-Lin
   Shen, Changchun
   Wang, Lina
   Wang, Haiying
   Yang, Yang
   Xie, Dan
   Wang, Fan
   Ushijima, Toshikazu
   Zhao, Ying
   Zhu, Wei-Guo
TI Epigenetic regulation of autophagy by the methyltransferase EZH2 through
   an MTOR-dependent pathway
SO AUTOPHAGY
LA English
DT Article
DE autophagy; EZH2; histone modification; MTA2; MTOR pathway
ID REPRESSIVE COMPLEX 2; HISTONE DEACETYLASE; MI-2/NURD COMPLEX;
   TUMOR-SUPPRESSOR; CHROMATIN; NURD; METHYLATION; METASTASIS; GENE;
   RECRUITMENT
AB Macroautophagy is an evolutionarily conserved cellular process involved in the clearance of proteins and organelles. Although the autophagy regulation machinery has been widely studied, the key epigenetic control of autophagy process still remains unknown. Here we report that the methyltransferase EZH2 (enhancer of zeste 2 polycomb repressive complex 2 subunit) epigenetically represses several negative regulators of the MTOR (mechanistic target of rapamycin [serine/threonine kinase]) pathway, such as TSC2, RHOA, DEPTOR, FKBP11, RGS16 and GPI. EZH2 was recruited to these genes promoters via MTA2 (metastasis associated 1 family, member 2), a component of the nucleosome remodeling and histone deacetylase (NuRD) complex. MTA2 was identified as a new chromatin binding protein whose association with chromatin facilitated the subsequent recruitment of EZH2 to silenced targeted genes, especially TSC2. Downregulation of TSC2 (tuberous sclerosis 2) by EZH2 elicited MTOR activation, which in turn modulated subsequent MTOR pathway-related events, including inhibition of autophagy. In human colorectal carcinoma (CRC) tissues, the expression of MTA2 and EZH2 correlated negatively with expression of TSC2, which reveals a novel link among epigenetic regulation, the MTOR pathway, autophagy induction, and tumorigenesis.
C1 [Wei, Fu-Zheng; Cao, Ziyang; Wang, Xi; Wang, Hui; Wang, Donglai; Du, Yipeng; Song, Boyan; Cao, Lin-Lin; Shen, Changchun; Wang, Lina; Wang, Haiying; Yang, Yang; Zhao, Ying; Zhu, Wei-Guo] Peking Univ, Beijing Key Lab Prot Posttranslat Modificat & Cel, Dept Biochem & Mol Biol,Hlth Sci Ctr,Minist Educ, State Key Lab Nat & Biomimet Drugs,Key Lab Carcin, Beijing 100871, Peoples R China.
   [Cai, Mu-Yan; Xie, Dan] Sun Yat Sen Univ, Ctr Canc, State Key Lab Oncol South China, Guangzhou 510275, Guangdong, Peoples R China.
   [Li, Tingting] Peking Univ, Hlth Sci Ctr, Sch Basic Med Sci, Dept Biomed Informat, Beijing 100871, Peoples R China.
   [Hattori, Naoko; Ushijima, Toshikazu] Natl Canc Ctr, Div Epigen, Tokyo, Japan.
   [Wang, Fan] Peking Univ, Sch Basic Med Sci, Dept Radiat Med, Beijing 100871, Peoples R China.
   [Zhu, Wei-Guo] Peking Univ Tsinghua Univ Ctr Life Sci, Beijing, Peoples R China.
   [Zhu, Wei-Guo] Shenzhen Univ, Sch Med, Shenzhen, Peoples R China.
RP Zhu, WG (corresponding author), Peking Univ, Beijing Key Lab Prot Posttranslat Modificat & Cel, Dept Biochem & Mol Biol,Hlth Sci Ctr,Minist Educ, State Key Lab Nat & Biomimet Drugs,Key Lab Carcin, Beijing 100871, Peoples R China.
EM zhaoying0812@bjmu.edu.cn; zhuweiguo@bjmu.edu.cn
RI Ushijima, Toshikazu/AAP-5742-2021; Du, Yipeng/O-1223-2013
OI Ushijima, Toshikazu/0000-0003-3405-7817; Zhu,
   Wei-Guo/0000-0001-8385-6581; Yang, Yang/0000-0002-8737-590X; Hattori,
   Naoko/0000-0002-0901-4869; Wang, Haiying/0000-0001-7729-0649
FU 973 ProjectsNational Basic Research Program of China [2011CB910100,
   2011CB504200, 2013CB911000]; National Natural Science Foundation of
   ChinaNational Natural Science Foundation of China (NSFC) [81222028,
   81321003, 81472581, 81530074, 31570812, 91319302]; Ministry of Science
   and Technology of ChinaMinistry of Science and Technology, China
   [B70001]
FX This study was supported by the "973 Projects" (2011CB910100,
   2011CB504200 and 2013CB911000); National Natural Science Foundation of
   China (81222028, 81321003, 81472581, 81530074, 31570812 and 91319302),
   and grants (B70001) from the Ministry of Science and Technology of
   China.
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NR 60
TC 91
Z9 96
U1 9
U2 40
PU TAYLOR & FRANCIS INC
PI PHILADELPHIA
PA 530 WALNUT STREET, STE 850, PHILADELPHIA, PA 19106 USA
SN 1554-8627
EI 1554-8635
J9 AUTOPHAGY
JI Autophagy
PD DEC
PY 2015
VL 11
IS 12
BP 2309
EP 2322
DI 10.1080/15548627.2015.1117734
PG 14
WC Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Cell Biology
GA DA4XO
UT WOS:000367806300015
PM 26735435
OA Green Published, Bronze
DA 2022-04-25
ER

PT J
AU Li, H
   Chen, C
AF Li, Hai
   Chen, Chen
TI Inhibition of autophagy enhances synergistic effects of Salidroside and
   anti-tumor agents against colorectal cancer
SO BMC COMPLEMENTARY AND ALTERNATIVE MEDICINE
LA English
DT Article
DE Salidroside; Autophagy; AMPK signaling; Anti-tumor agents; Colorectal
   cancer
ID IN-VITRO; CELLS; JAK2/STAT3; APOPTOSIS; GROWTH
AB Background: Various plant extracts have been suggested to be used as auxiliary agents in chemotherapy considering their anti-proliferative effect on cancer cells. However, recent reports reveal that plant extracts may function as inducers of autophagy of cancer cells. In general, autophagy confers survival advantage for cells responding to stress conditions, thus representing an important mechanism for chemo-resistance. This study was aimed to investigate the effectiveness of combined use of Salidroside (Sal, a phenylpropanoid glycosides from Rhodiola rosea L) with anti-tumor agents against colorectal cancer (CRC) cells, and moreover to evaluate the potential role of autophagy in the combined therapy.
   Methods: CRC cells, HCT-116, were incubated with Sal alone or in combination with conventional chemotherapy agents including oxaliplatin (OXA), 5-fluorouracil (5-FU) and Doxorubicin (ADM). Cell proliferative characteristics were evaluated by cell viability and apoptosis rate. The protein expression was assessed by Immunofluorescent and Western blot assays.
   Results: Sal, alone or in combination with anti-tumor agents, increased expression of autophagic biomarkers, including LC3B and Becline-1, suggesting an autophagy induction. Except for the up-regulation of p-AMPK, p-mTOR, p-NF-kappa B (p65), TGF-beta, p-JAK2 and p-STAT3 were down-regulated by Sal. Because autophagy is positively correlated with the activation of AMPK/mTOR, NF-kappa B, TGF beta 1 and JAK2/STAT3 cascades, the autophagy induced by Sal may associate with AMPK activation. Indeed, blockage of AMPK signaling via Compound C or AMPK knockdown inhibited the autophagy. The blockage of AMPK signaling or a direct inhibition of autophagy via 3-MA increased effectiveness of combined use of Sal with anti-tumor agents against CRC.
   Conclusions: Inhibition of autophagy enhances synergistic effects of Sal and anti-tumor agents against colorectal cancer. This study provides experimental evidence and theoretical reference for improvement of a novel chemotherapy treatment protocol.
C1 [Li, Hai] Huazhong Univ Sci & Technol, Tongji Hosp, Dept Geriatr, Tongji Med Coll, Wuhan, Hubei, Peoples R China.
   [Chen, Chen] Huazhong Univ Sci & Technol, Tongji Med Coll, Dept Breast & Thyroid Surg, Union Hosp, Wuhan, Hubei, Peoples R China.
RP Li, H (corresponding author), Huazhong Univ Sci & Technol, Tongji Hosp, Dept Geriatr, Tongji Med Coll, Wuhan, Hubei, Peoples R China.
EM lihaiges@hust.edu.cn
OI Li, Hai/0000-0001-7937-5902
FU Shenzhen Municipal Commission of science and technology innovation
   [JCYJ20150402152005631]
FX This study was supported by the Shenzhen Municipal Commission of science
   and technology innovation (Grant No. JCYJ20150402152005631).
CR Bastola T, 2017, MOLECULES, V22, DOI 10.3390/molecules22020242
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NR 23
TC 30
Z9 36
U1 0
U2 15
PU BIOMED CENTRAL LTD
PI LONDON
PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND
SN 1472-6882
J9 BMC COMPLEM ALTERN M
JI BMC Complement. Altern. Med.
PD DEC 16
PY 2017
VL 17
AR 538
DI 10.1186/s12906-017-2046-z
PG 9
WC Integrative & Complementary Medicine
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Integrative & Complementary Medicine
GA FQ0XD
UT WOS:000418079400002
PM 29246220
OA Green Published, gold
DA 2022-04-25
ER

PT J
AU Gutierrez-Martinez, IZ
   Rubio, JF
   Piedra-Quintero, ZL
   Lopez-Mendez, O
   Serrano, C
   Reyes-Maldonado, E
   Salinas-Lara, C
   Betanzos, A
   Shibayama, M
   Silva-Olivares, A
   Candelario-Martinez, A
   Meraz-Rios, MA
   Schnoor, M
   Villegas-Sepulveda, N
   Nava, P
AF Gutierrez-Martinez, I. Z.
   Rubio, J. F.
   Piedra-Quintero, Z. L.
   Lopez-Mendez, O.
   Serrano, C.
   Reyes-Maldonado, E.
   Salinas-Lara, C.
   Betanzos, A.
   Shibayama, M.
   Silva-Olivares, A.
   Candelario-Martinez, A.
   Meraz-Rios, M. A.
   Schnoor, M.
   Villegas-Sepulveda, N.
   Nava, P.
TI mTORC1 Prevents Epithelial Damage During Inflammation and Inhibits
   Colitis-Associated Colorectal Cancer Development
SO TRANSLATIONAL ONCOLOGY
LA English
DT Article
ID DNA-DAMAGE; COLONIC EPITHELIUM; MAMMALIAN TARGET; KINASE INHIBITOR;
   E-CADHERIN; LITHIUM; AUTOPHAGY; CELLS; DOXORUBICIN; INTESTINE
AB Epithelial cells lining the intestinal mucosa constitute a selective-semipermeable barrier acting as first line of defense in the organism. The number of those cells remains constant during physiological conditions, but disruption of epithelial cell homeostasis has been observed in several pathologies. During colitis, epithelial cell proliferation decreases and cell death augments. The mechanism responsible for these changes remains unknown. Here, we show that the pro-inflammatory cytokine IFN gamma contributes to the inhibition of epithelial cell proliferation in intestinal epithelial cells (IECs) by inducing the activation of mTORC1. Activation of mTORC1 in response to IFN gamma was detected in IECs present along the crypt axis and in colonic macrophages. mTORC1 inhibition enhances cell proliferation, increases DNA damage in IEC. In macrophages, mTORC1 inhibition strongly reduces the expression of pro-inflammatory markers. As a consequence, mTORC1 inhibition exacerbated disease activity, increased mucosal damage, enhanced ulceration, augmented cell infiltration, decreased survival and stimulated tumor formation in a model of colorectal cancer CRC associated to colitis. Thus, our findings suggest that mTORC1 signaling downstream of IFN gamma prevents epithelial DNA damage and cancer development during colitis.
C1 [Gutierrez-Martinez, I. Z.; Rubio, J. F.; Lopez-Mendez, O.; Serrano, C.; Candelario-Martinez, A.; Nava, P.] CINVESTAV, Dept Physiol Biophys & Neurosci, Mexico City 07360, DF, Mexico.
   [Piedra-Quintero, Z. L.; Meraz-Rios, M. A.; Schnoor, M.; Villegas-Sepulveda, N.] CINVESTAV, Dept Mol Biomed, Mexico City 07360, DF, Mexico.
   [Reyes-Maldonado, E.] Natl Polytech, Natl Sch Biol Sci, Dept Morphol, Mexico City 11340, DF, Mexico.
   [Salinas-Lara, C.] UNAM, FES Iztacala, Surg & Med Sch, Histol & Pathol Unit, Tlalnepantla 54090, Mexico.
   [Betanzos, A.; Shibayama, M.; Silva-Olivares, A.] CINVESTAV, Dept Infect & Mol Pathogenesis, Mexico City 07360, DF, Mexico.
RP Serrano, C; Nava, P (corresponding author), Cinvestav Zacatenco, Dept Physiol Biophys & Neurosci, Av Inst Politecn Nacl 2508, Mexico City 07360, DF, Mexico.
EM serrano.cisg@gmail.com; pnava@fisio.cinvestav.mx
RI Meraz-Rios, Marco Antonio/F-4194-2016; Nava, Porfirio/D-8306-2012;
   SALINAS, CITLALTEPETL/AAG-4810-2020; Schnoor, Michael/H-1863-2016
OI Meraz-Rios, Marco Antonio/0000-0001-6748-8117; Nava,
   Porfirio/0000-0002-0506-1510; Schnoor, Michael/0000-0002-0269-5884;
   Villegas-Sepulveda, Nicolas/0000-0001-9489-2545
FU Premio Lisker 2016
FX This work was supported by the Premio Lisker 2016 (PND). We thank Norma
   Trejo for their excellent technical assistance.
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NR 43
TC 6
Z9 6
U1 1
U2 5
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1936-5233
J9 TRANSL ONCOL
JI Transl. Oncol.
PD JAN
PY 2019
VL 12
IS 1
BP 24
EP 35
DI 10.1016/j.tranon.2018.08.016
PG 12
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA HD9OU
UT WOS:000452892800004
PM 30265974
OA gold, Green Published
DA 2022-04-25
ER

PT J
AU Hao, HB
   Xia, GF
   Wang, C
   Zhong, FP
   Liu, LP
   Zhang, D
AF Hao, Haibin
   Xia, Guangfeng
   Wang, Chao
   Zhong, Fuping
   Liu, Laipeng
   Zhang, Dong
TI miR-106a suppresses tumor cells death in colorectal cancer through
   targeting ATG7
SO MEDICAL MOLECULAR MORPHOLOGY
LA English
DT Article
DE Colorectal cancer; miR-106a; ATG7; Cell death
ID GASTRIC-CANCER; AUTOPHAGY; EXPRESSION; PROLIFERATION; METASTASIS;
   RESISTANCE; APOPTOSIS; PATHWAY; BREAST
AB Autophagy-related gene 7 (ATG7) and miR-106a play an important role in cancer cell autophagy and apoptosis, but the outcome of ATG7 and miR-106a in colorectal cancer (CRC) still remains not clear. In this study, we found that ATG7 and miR-106a expression were mutually related with cell death and prognosis in CRC patients. In addition, we also showed that ATG7 and miR-106a expression were changeable in colorectal cancer cell lines when compared with normal cell lines, but ATG7 and miR-106a mRNA level was negatively correlated. Furthermore, ATG7 protein and mRNA levels decreased after over-expression of miR-106a, whereas the suppression of ATG7 had the opposite effect. We confirmed that miR-106a down-regulated ATG7 mRNA level by binding the specific sequence of ATG7 mRNA 3'UTR region. Moreover, the over-expression of ATG7 induced CRC cells death both in vitro and in vivo. Taken together, our study data demonstrated that ATG7 aggravated the cell death of CRC, which was inhibited by miR-106a.
C1 [Hao, Haibin; Xia, Guangfeng; Wang, Chao; Zhong, Fuping; Liu, Laipeng; Zhang, Dong] Nanchang Univ, Affiliated Hosp 2, Dept Gen Surg, Med Coll, 461 Bayi Rd, Nanchang 330006, Jiangxi, Peoples R China.
RP Hao, HB (corresponding author), Nanchang Univ, Affiliated Hosp 2, Dept Gen Surg, Med Coll, 461 Bayi Rd, Nanchang 330006, Jiangxi, Peoples R China.
EM haoweipei104@163.com
CR Arnold M, 2016, GUT
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NR 28
TC 25
Z9 27
U1 0
U2 8
PU SPRINGER JAPAN KK
PI TOKYO
PA SHIROYAMA TRUST TOWER 5F, 4-3-1 TORANOMON, MINATO-KU, TOKYO, 105-6005,
   JAPAN
SN 1860-1480
EI 1860-1499
J9 MED MOL MORPHOL
JI Med. Mol. Morphol.
PD JUN
PY 2017
VL 50
IS 2
BP 76
EP 85
DI 10.1007/s00795-016-0150-7
PG 10
WC Biology; Microscopy; Pathology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Life Sciences & Biomedicine - Other Topics; Microscopy; Pathology
GA EV5FW
UT WOS:000401788900003
PM 27981410
DA 2022-04-25
ER

PT J
AU Jang, JH
   Baerts, L
   Waumans, Y
   De Meester, I
   Yamada, Y
   Limani, P
   Gil-Bazo, I
   Weder, W
   Jungraithmayr, W
AF Jang, Jae-Hwi
   Baerts, Lesley
   Waumans, Yannick
   De Meester, Ingrid
   Yamada, Yoshito
   Limani, Perparim
   Gil-Bazo, Ignacio
   Weder, Walter
   Jungraithmayr, Wolfgang
TI Suppression of lung metastases by the CD26/DPP4 inhibitor Vildagliptin
   in mice
SO CLINICAL & EXPERIMENTAL METASTASIS
LA English
DT Article
DE CD26/DPP4; Lung metastases; Autophagy; Apoptosis
ID DIPEPTIDYL-PEPTIDASE-IV; ANTI-CD26 MONOCLONAL-ANTIBODY; IN-VITRO;
   COLORECTAL-CANCER; CD26 EXPRESSION; TUMOR-GROWTH; STEM-CELLS; AUTOPHAGY;
   VIVO; LOCALIZATION
AB Metastases rather than primary cancers determine nowadays the survival of patients. One of the most common primary malignancies is colorectal cancer and this type of tumor is characterized by a high tendency to spread metastases to the lung and liver. CD26/DPP4 is a transmembrane molecule with enzymatic functions which cleaves biologically active peptides. Recently, CD26/DPP4 has become the focus of cancer research and it was shown that CD26/DPP4-positive cancer cells display increased metastatic activity. Here, we tested if the CD26/DPP4-inhibitor Vildagliptin suppresses the development and growth of mouse colorectal lung metastases. This inhibitor of CD26/DPP4 was employed on mouse (C57BL/6) colorectal lung metastases, established by intravenous injection of the syngeneic cell line MC38. For mechanistic analysis, a subcutaneous tumor model was used. The treatment with Vildagliptin significantly suppressed both, the incidence and growth of lung metastases. Autophagy markers (LC3, p62, and ATF4) decreased, apoptosis increased (TUNEL, pH3/Ki-76), and the cell cycle regulator pCDC2 was inhibited. In conclusion, we here showed an anti-tumor effect of Vildagliptin via downregulation of autophagy resulting in increased apoptosis and modulation of the cell cycle. We therefore propose Vildagliptin for the evaluation as a new therapeutic approach for the treatment of colorectal cancer lung metastases.
C1 [Jang, Jae-Hwi; Yamada, Yoshito; Weder, Walter; Jungraithmayr, Wolfgang] Univ Zurich Hosp, Div Thorac Surg, CH-8091 Zurich, Switzerland.
   [Baerts, Lesley; Waumans, Yannick; De Meester, Ingrid] Univ Antwerp, Dept Pharmaceut Sci, Dept Med Biochem, B-2020 Antwerp, Belgium.
   [Limani, Perparim] Univ Zurich Hosp, Dept Visceral & Transplantat Surg, CH-8091 Zurich, Switzerland.
   [Gil-Bazo, Ignacio] Univ Navarra, Ctr Appl Med Res, Div Oncol, E-31080 Pamplona, Spain.
RP Jungraithmayr, W (corresponding author), Univ Zurich Hosp, Div Thorac Surg, Raemistr 100, CH-8091 Zurich, Switzerland.
EM wolfgang.jungraithmayr@usz.ch
RI Jungraithmayr, Wolfgang/F-3882-2015; De Meester, Ingrid/A-6881-2017;
   Gil-Bazo, Ignacio/E-4581-2019
OI Jungraithmayr, Wolfgang/0000-0002-1442-4862; De Meester,
   Ingrid/0000-0002-3421-0124; Gil-Bazo, Ignacio/0000-0002-2626-5109
FU Swiss National Science Foundation (SNF)Swiss National Science Foundation
   (SNSF) [310030 156876/1]; Stiftung fur wissenschaftliche Forschung';
   University of Antwerp [FFB3551]
FX We thank Dr. Lubor Borsig and Dr. Radovan Borojevic for kindly providing
   the MC38 (GFP) and GRX cell lines. This study is supported by Swiss
   National Science Foundation (SNF, 2014, 310030 156876/1) and the
   'Stiftung fur wissenschaftliche Forschung' 2015 to WJ and by a special
   research fund of the University of Antwerp (FFB3551).
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NR 35
TC 47
Z9 49
U1 2
U2 17
PU SPRINGER
PI DORDRECHT
PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS
SN 0262-0898
EI 1573-7276
J9 CLIN EXP METASTAS
JI Clin. Exp. Metastasis
PD OCT
PY 2015
VL 32
IS 7
BP 677
EP 687
DI 10.1007/s10585-015-9736-z
PG 11
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA CR9ZF
UT WOS:000361715300004
PM 26233333
OA Green Published, Green Accepted
DA 2022-04-25
ER

PT J
AU Grasso, S
   Pereira, GJS
   Palmeira-dos-Santos, C
   Calgarotto, AK
   Martinez-Lacaci, I
   Ferragut, JA
   Smaili, SS
   Bincoletto, C
AF Grasso, Silvina
   Pereira, Gustavo J. S.
   Palmeira-dos-Santos, Caroline
   Calgarotto, Andrana K.
   Martinez-Lacaci, Isabel
   Antonio Ferragut, Jose
   Smaili, Soraya S.
   Bincoletto, Claudia
TI Autophagy regulates Selumetinib (AZD6244) induced-apoptosis in
   colorectal cancer cells
SO EUROPEAN JOURNAL OF MEDICINAL CHEMISTRY
LA English
DT Article
DE Apoptosis; Autophagy; Selumetinib (AZD6244); CRC cells (SW480 and HT29)
ID INHIBITOR SELUMETINIB; DRUG-RESISTANCE; OPEN-LABEL; PHASE-II;
   ARRY-142886; PROTEIN; THERAPY; PATHWAYS; TRIAL; MELANOMA
AB Objective: As Selumetinib is a MEK1/2 inhibitor that has gained interest as an anti-tumor agent, the present study was designed to investigate autophagy involvement on Selumetinib-induced apoptosis in colorectal cancer (CRC) cells.
   Methods: CRC cells death and cycle studies were assessed by AnnexinV-FITC and PI staining, respectively. Autophagy flux was analysed by Western Blot (LC3II and p62 protein levels) and retroviral infection of SW480 cells for siBecn1 RNA interference experiments. Confocal microscopy was used to determine mCherry-EGFP-LC3 distribution.
   Key findings: The Selumetinib effects were concentration-dependent in SW480 cell line. Whereas 1 mu M exerted an arrest in the cell cycle (G1 phase), higher concentrations (10 mu M) induced cell death, which was accompanied by autophagy blockage in its last stages. Autophagy induction by Rapamycin (RAPA) increased cell survival, whereas pharmacology autophagy inhibition by Bafilomycin A1 (BAF), Chloroquine (CQ) or 3-Methyladenine (3-MA) increased Selumetinib-induced CRC cells death.
   Conclusions: Altogether, these results suggest that autophagy plays a fundamental role in CRC cells response to Selumetinib. In addition, the combination of Selumetinib with autophagy inhibitors may be a useful therapeutic strategy to enhance its activity against colorectal tumours. (C) 2016 Elsevier Masson SAS. All rights reserved.
C1 [Grasso, Silvina; Martinez-Lacaci, Isabel; Antonio Ferragut, Jose] Univ Miguel Hernandez, Inst Biol Mol & Celular, Alicante 03202, Spain.
   [Grasso, Silvina; Pereira, Gustavo J. S.; Palmeira-dos-Santos, Caroline; Calgarotto, Andrana K.; Smaili, Soraya S.; Bincoletto, Claudia] Univ Fed Sao Paulo UNIFESP, Escola Paulista Med, Dept Farmacol, Rua Tres Maio 100, Sao Paulo, SP, Brazil.
   [Martinez-Lacaci, Isabel] Hosp Univ Virgen de la Arrixaca, Unidad AECC Invest Traslac Canc, Inst Murciano Invest Biosanitaria, Murcia 30120, Spain.
RP Smaili, SS; Bincoletto, C (corresponding author), Univ Fed Sao Paulo UNIFESP, Escola Paulista Med, Dept Farmacol, Rua Tres Maio 100, Sao Paulo, SP, Brazil.
EM soraya.smaili23@gmail.com; claudia.bincoletto@unifesp.br
RI Bincoletto, Claudia/H-4936-2012; Pereira, Gustavo José
   Silva/ABH-1344-2020; Smaili, Soraya/AAH-2129-2019; Pereira,
   Gustavo/H-4636-2012
OI Pereira, Gustavo/0000-0002-6765-1276
FU FAPESPFundacao de Amparo a Pesquisa do Estado de Sao Paulo (FAPESP)
   [12/51215-4]; CAPESCoordenacao de Aperfeicoamento de Pessoal de Nivel
   Superior (CAPES); CNPqConselho Nacional de Desenvolvimento Cientifico e
   Tecnologico (CNPQ)
FX This work was supported by research grants from FAPESP (12/51215-4),
   CAPES and CNPq. The authors thank Dr. Hanako Hirata, Cicero Santos and
   Bruno Palmieri de Souza for excellent technical assistance.
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NR 38
TC 12
Z9 13
U1 1
U2 64
PU ELSEVIER FRANCE-EDITIONS SCIENTIFIQUES MEDICALES ELSEVIER
PI PARIS
PA 23 RUE LINOIS, 75724 PARIS, FRANCE
SN 0223-5234
EI 1768-3254
J9 EUR J MED CHEM
JI Eur. J. Med. Chem.
PD OCT 21
PY 2016
VL 122
BP 611
EP 618
DI 10.1016/j.ejmech.2016.06.043
PG 8
WC Chemistry, Medicinal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA DV5XL
UT WOS:000383003900052
PM 27448918
DA 2022-04-25
ER

PT J
AU Byun, HO
   Han, NK
   Lee, HJ
   Kim, KB
   Ko, YG
   Yoon, G
   Lee, YS
   Hong, SI
   Lee, JS
AF Byun, Hae-Ok
   Han, Na-Kyung
   Lee, Hae-June
   Kim, Ki-Bum
   Ko, Young-Gyu
   Yoon, Gyesoon
   Lee, Yun-Sil
   Hong, Seok-Il
   Lee, Jae-Seon
TI Cathepsin D and Eukaryotic Translation Elongation Factor 1 as Promising
   Markers of Cellular Senescence
SO CANCER RESEARCH
LA English
DT Article
ID ACCELERATED SENESCENCE; IN-VIVO; TUMOR-REGRESSION; CANCER CELLS;
   APOPTOSIS; P53; EXPRESSION; RADIATION; ARREST; DEATH
AB Induction of premature senescence may be a promising strategy for cancer treatment. However, biomarkers for senescent cancer cells are lacking. To identify such biomarkers, we performed comparative proteomic analysis of MCF7 human breast cancer cells undergoing cellular senescence in response to ionizing radiation (IR). IR-induced senescence was associated with up-regulation of cathepsin D (CD) and down-regulation of eukaryotic translation elongation factor 1 beta 2 (eEF1B2), as confirmed by Western blot. The other elongation factor, eukaryotic translation elongation factor 1 alpha 1 (eEF1A1), was also down-regulated. IR-induced senescence was associated with similar changes of CD and eEF1 (eEF1A1 and eEF1B2) levels in the HCT116 colon cancer cell line and the H460 lung cancer cell line. Up-regulation of CD and down-regulation of eEF1 seemed to be specific to senescence, as they were observed during cellular senescence induced by hydrogen peroxide or anticancer drugs (camptothecin, etoposide, or 50 ng doxorubicin) but not during apoptosis induced by Taxol or 10 mu g doxorubicin or autophagy induced by tamoxifen. The same alterations in CD and eEF1A1 levels were observed during replicative senescence and Ras oncogene-induced senescence. Transient cell cycle arrest did not alter levels of eEF1 or CD. Chemical inhibition of CD (pepstatin A) and small interfering RNA-mediated knockdown of CD and eEF1 revealed that these factors participate in cell proliferation. Finally, the senescence-associated alteration in CD and eEF1 levels observed in cell lines was also observed in IR-exposed xenografted tumors. These findings show that CD and eEF1 are promising markers for the detection of cellular senescence induced by a variety of treatments. [Cancer Res 2009;69(11):4638-47]
C1 [Byun, Hae-Ok; Han, Na-Kyung; Lee, Jae-Seon] Korea Inst Radiol & Med Sci, Div Radiat Canc Res, Seoul 139706, South Korea.
   [Lee, Hae-June; Lee, Yun-Sil] Korea Inst Radiol & Med Sci, Div Radiat Effects, Seoul 139706, South Korea.
   [Hong, Seok-Il] Korea Inst Radiol & Med Sci, Dept Lab Med & Clin Pathol, Seoul 139706, South Korea.
   [Han, Na-Kyung; Kim, Ki-Bum; Ko, Young-Gyu] Korea Univ, Grad Sch Life Sci & Biotechnol, Seoul, South Korea.
   [Yoon, Gyesoon] Ajou Univ, Sch Med, Dept Biochem, Suwon 441749, South Korea.
   [Yoon, Gyesoon] Ajou Univ, Grad Sch, Dept Mol Sci & Technol, Suwon 441749, South Korea.
RP Lee, JS (corresponding author), Korea Inst Radiol & Med Sci, Div Radiat Canc Res, Seoul 139706, South Korea.
EM jaeslee@kcch.re.kr
RI Lee, Yun-Sil/AAP-1378-2020
OI Lee, Yun-Sil/0000-0002-7538-8850
FU Ministry of Education, Science, and Technology of KoreaMinistry of
   Education, Science and Technology, Republic of Korea
FX National Nuclear Technology Program from The Ministry of Education,
   Science, and Technology of Korea.
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NR 49
TC 67
Z9 69
U1 0
U2 8
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD JUN 1
PY 2009
VL 69
IS 11
BP 4638
EP 4647
DI 10.1158/0008-5472.CAN-08-4042
PG 10
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA 455JL
UT WOS:000266755000014
PM 19487283
OA Green Published
DA 2022-04-25
ER

PT J
AU Mi, WN
   Wang, CY
   Luo, G
   Li, JH
   Zhang, YZ
   Jiang, MM
   Zhang, CC
   Liu, NN
   Jiang, XX
   Yang, G
   Zhang, LL
   Zhang, G
   Zhang, YJ
   Fu, Y
AF Mi, Wunan
   Wang, Chuyue
   Luo, Guang
   Li, Jiehan
   Zhang, Yizheng
   Jiang, Meimei
   Zhang, Chuchu
   Liu, Nannan
   Jiang, Xinxiu
   Yang, Ge
   Zhang, Lingling
   Zhang, Ge
   Zhang, Yingjie
   Fu, Yang
TI Targeting ERK induced cell death and p53/ROS-dependent protective
   autophagy in colorectal cancer
SO CELL DEATH DISCOVERY
LA English
DT Article
ID WILD-TYPE; APOPTOSIS; P53; ROS; STATISTICS
AB In recent years, many studies have shown that autophagy plays a vital role in the resistance of tumor chemotherapy. However, the interaction between autophagy and cell death has not yet been clarified. In this study, a new specific ERK inhibitor CC90003 was found to suppress colorectal cancer growth by inducing cell death both in vitro and in vivo. Studies have confirmed that higher concentrations of ROS leads to autophagy or cell death. In this research, the role of CC90003-induced ROS was verified. But after inhibiting ROS by two kinds of ROS inhibitors NAC and SFN, the autophagy induced by CC90003 decreased, while cell death strengthened. In parallel, protective autophagy was also induced, while in a p53-dependent manner. After silencing p53 or using the p53 inhibitor PFT alpha, the autophagy induced by CC90003 was weakened and the rate of cell death increases. Therefore, we confirmed that CC90003 could induce autophagy by activating ROS/p53. Furthermore, in the xenograft mouse model, the effect was obtained remarkably in the combinational treatment group of CC90003 plus CQ, comparing with that of the single treatment groups. In a word, our results demonstrated that targeting ERK leads to cell death and p53/ROS-dependent protective autophagy simultaneously in colorectal cancer, which offers new potential targets for clinical therapy.
C1 [Mi, Wunan; Li, Jiehan; Zhang, Yizheng; Zhang, Ge; Fu, Yang] Zhengzhou Univ, Affiliated Hosp 1, Dept Gastrointestinal Surg, Zhengzhou 450052, Peoples R China.
   [Mi, Wunan; Wang, Chuyue; Zhang, Yizheng; Jiang, Meimei; Zhang, Chuchu; Liu, Nannan; Jiang, Xinxiu; Zhang, Yingjie] Hunan Univ, Coll Biol, Changsha 410082, Peoples R China.
   [Mi, Wunan; Zhang, Yingjie] Hunan Univ, Sch Biomed Sci, Changsha 410082, Peoples R China.
   [Luo, Guang; Zhang, Lingling] Cent South Univ, Xiangya Hosp 3, Dept Lab Med, Changsha 410013, Peoples R China.
   [Yang, Ge] Zhengzhou Univ, Affiliated Hosp 1, Dept Ophthalmol, Zhengzhou 450052, Peoples R China.
   [Fu, Yang] Collaborat Innovat Ctr Henan Prov Canc Chemopreve, Zhengzhou 450052, Peoples R China.
RP Fu, Y (corresponding author), Zhengzhou Univ, Affiliated Hosp 1, Dept Gastrointestinal Surg, Zhengzhou 450052, Peoples R China.; Zhang, YJ (corresponding author), Hunan Univ, Coll Biol, Changsha 410082, Peoples R China.; Zhang, YJ (corresponding author), Hunan Univ, Sch Biomed Sci, Changsha 410082, Peoples R China.; Fu, Y (corresponding author), Collaborat Innovat Ctr Henan Prov Canc Chemopreve, Zhengzhou 450052, Peoples R China.
EM yingjiezhang@hnu.edu.cn; fuyang@zzu.edu.cn
FU Chinese National Natural Science FoundationNational Natural Science
   Foundation of China (NSFC) [81871995, 31801140, 31701132]; Project of
   Henan Health Department [YXKC2020029/2020054, SBGJ201901049/2020002041];
   Excellent Youth Fund of Henan Natural Science Foundation [212300410075];
   Natural Science Foundation of Hunan ProvinceNatural Science Foundation
   of Hunan Province [2020JJ4182, 2019JJ40366]; province-ministry joint
   construction project of Henan Provincial Health Commission [SB201901049]
FX This study was supported by Chinese National Natural Science Foundation
   (Nos. 81871995, 31801140, and 31701132), the Project of Henan Health
   Department (Nos. YXKC2020029/2020054 and SBGJ201901049/2020002041), the
   Excellent Youth Fund of Henan Natural Science Foundation (No.
   212300410075), the Natural Science Foundation of Hunan Province
   (2020JJ4182 and 2019JJ40366), and province-ministry joint construction
   project of Henan Provincial Health Commission (SB201901049).
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NR 43
TC 0
Z9 0
U1 1
U2 1
PU SPRINGERNATURE
PI LONDON
PA CAMPUS, 4 CRINAN ST, LONDON, N1 9XW, ENGLAND
EI 2058-7716
J9 CELL DEATH DISCOV
JI Cell Death Discov.
PD DEC 4
PY 2021
VL 7
IS 1
AR 375
DI 10.1038/s41420-021-00677-9
PG 11
WC Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Cell Biology
GA XI7LP
UT WOS:000726288400001
PM 34864826
OA Green Published, gold
DA 2022-04-25
ER

PT J
AU Lu, WY
   Lin, CH
   Li, YH
AF Lu, Wenyan
   Lin, Cuihong
   Li, Yonghe
TI Rottlerin induces Wnt co-receptor LRP6 degradation and suppresses both
   Wnt/beta-catenin and mTORC1 signaling in prostate and breast cancer
   Cells
SO CELLULAR SIGNALLING
LA English
DT Article
DE LRP6; Wnt signaling; mTORCI signaling; Rottlerin; Cancer; Drug discovery
ID DELTA-INDEPENDENT PATHWAY; COLON-CARCINOMA CELLS; CYCLIN D1 EXPRESSION;
   INDUCED APOPTOSIS; UP-REGULATION; BETA-CATENIN; AUTOPHAGY; INHIBITION;
   SURVIVIN; TARGET
AB Activation of Wnt/beta-catenin signaling can result in up-regulation of mTORC1 signaling in cancer cells. The low density lipoprotein receptor-related protein-6 (LRP6) is an essential Wnt co-receptor for Wnt/S-catenin signaling. We found that rottlerin, a natural plant polyphenol, suppressed LRP6 expression and phosphotylation, and inhibited Wnt43-catenin signaling in HEK293 cells. Furthermore, the inhibitory effects of rottlerin on LRP6 expression/phosphorylation and Wnt/beta-catenin signaling were confirmed in human prostate cancer PC-3 and DU145 cells and breast cancer MDA-MB-231 and T-47D cells. Mechanistically, rottlerin promoted LRP6 degradation, but had no effects on LRP6 transcriptional activity. In addition, rottlerin-mediated LRP6 downregulation was unrelated to activation of 5'-AMP-activated protein kinase (AMPK). Importantly, we also found that rottlerin inhibited mTORC1 signaling in prostate and breast cancer cells. Finally, we demonstrated that rottlerin was able to suppress the expression of cyclin D1 and survivin, two targets of both Wnt/S-catenin and mTORC1 signaling, in prostate and breast cancer cells, and displayed remarkable anticancer activity with IC50 values between 0.7 and 1.7 mu M for prostate cancer PC-3 and DU145 cells and breast cancer MDA-MB-231 and T-47D cells. The IC50 values are comparable to those shown to suppress the activities of Wnt/S-catenin and mTORC1 signaling in prostate and breast cancer cells. Our data indicate that rottlerin is a novel LRP6 inhibitor and suppresses both Wnt/S-catenin and mTORC1 signaling in prostate and breast cancer cells, and that LRP6 represents a potential therapeutic target for cancers. (c) 2014 Elsevier B.V. All rights reserved.
C1 [Lu, Wenyan; Lin, Cuihong; Li, Yonghe] So Res Inst, Dept Biochem & Mol Biol, Drug Discovery Div, Birmingham, AL 35205 USA.
   [Lin, Cuihong] Fujian Med Univ, Affiliated Hosp 1, Dept Pharm, Fuzhou, Peoples R China.
RP Li, YH (corresponding author), So Res Inst, Dept Biochem & Mol Biol, Drug Discovery Div, 2000 Ninth Ave South, Birmingham, AL 35205 USA.
EM y.li@souternresearch.org
FU National Institutes of HealthUnited States Department of Health & Human
   ServicesNational Institutes of Health (NIH) - USA [R01CAl24531,
   R21CA182056]; NATIONAL CANCER INSTITUTEUnited States Department of
   Health & Human ServicesNational Institutes of Health (NIH) - USANIH
   National Cancer Institute (NCI) [R01CA124531, R21CA182056] Funding
   Source: NIH RePORTER
FX We are grateful to Dr. Christof Niehrs (Deutsches
   Krebsforschungszentrum, Heidelberg, Germany) for providing LRP6 cDNA,
   Dr. Gail Johnson (University of Rochester) for providing GST-E Cadherin
   cDNA, and Dr. Randall T. Moon (University of Washington) for providing
   the Super8XTOPFlash luciferase construct. This work was supported by
   grants from the National Institutes of Health R01CAl24531 and
   R21CA182056 (to Y.L.).
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NR 63
TC 43
Z9 45
U1 2
U2 21
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA STE 800, 230 PARK AVE, NEW YORK, NY 10169 USA
SN 0898-6568
EI 1873-3913
J9 CELL SIGNAL
JI Cell. Signal.
PD JUN
PY 2014
VL 26
IS 6
BP 1303
EP 1309
DI 10.1016/j.cellsig.2014.02.018
PG 7
WC Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Cell Biology
GA AG0OH
UT WOS:000335114300015
PM 24607787
OA Green Accepted
DA 2022-04-25
ER

PT J
AU Neilsen, BK
   Kelly, DL
   Chakraborty, B
   Kim, HS
   White, MA
   Lewis, RE
   Fisher, KW
AF Neilsen, Beth K.
   Kelly, David L.
   Chakraborty, Binita
   Kim, Hyun Seok
   White, Michael A.
   Lewis, Robert E.
   Fisher, Kurt W.
TI High-throughput identification of protein functional similarities using
   a gene-expression-based siRNA screen
SO SCIENTIFIC DATA
LA English
DT Article; Data Paper
AB A gene expression-based siRNA screen was used to evaluate functional similarity between genetic perturbations to identify functionally similar proteins. A siRNA library (siGenome library, Dharmacon) consisting of multiple siRNAs per gene that have been pooled in to one well per gene was arrayed in a 384-well format and used to individually target 14,335 proteins for depletion in HCT116 colon cancer cells. For each protein depletion, the gene expression of eight genes was quantified using the multiplexed Affymetrix Quantigene 2.0 assay in technical triplicate. As a proof of concept, six genes (BNIP3, NDRG1, ALDOC, LOXL2, ACSL5, BNIP3L) whose expression pattern reliably reflect the disruption of the molecular scaffold KSR1 were measured upon each protein depletion. The remaining two genes (PPIB and HPRT) are housekeeping genes used for normalization. The gene expression signatures from this screen can be used to estimate the functional similarity between any two proteins and successfully identified functional relationships for specific proteins such as KSR1 and more generalized processes, such as autophagy.
C1 [Neilsen, Beth K.; Kelly, David L.; Lewis, Robert E.] Univ Nebraska Med Ctr, Fred & Pamela Buffett Canc Ctr, Eppley Inst, Omaha, NE 68198 USA.
   [Chakraborty, Binita] Duke Univ, Med Ctr, Pharmacol & Canc Biol, Durham, NC 27710 USA.
   [Kim, Hyun Seok] Yonsei Univ, Coll Med, Severance Biomed Sci Inst, Seoul, South Korea.
   [White, Michael A.] Univ Texas Southwestern Med Ctr Dallas, Dept Cell Biol, Dallas, TX 75390 USA.
   [Fisher, Kurt W.] Univ Nebraska Med Ctr, Dept Pathol & Microbiol, Omaha, NE 68198 USA.
RP Fisher, KW (corresponding author), Univ Nebraska Med Ctr, Dept Pathol & Microbiol, Omaha, NE 68198 USA.
EM kfisher@unmc.edu
OI Fisher, Kurt/0000-0002-8391-390X; Neilsen, Beth/0000-0002-4859-6486
FU NCIUnited States Department of Health & Human ServicesNational
   Institutes of Health (NIH) - USANIH National Cancer Institute (NCI)
   [CA157774, GM121316, CA203397, CA22287]; Eppley Institute in Cancer
   Biology training grant [NCI T32CA009476]; NPOD COBRE [NIH P20 GM104320];
   Fred & Pamela Buffett Cancer Center Support Grant [P30 CA036727]
FX We thank Amy Wells from the University of Nebraska Medical Center (UNMC)
   Eppley Institute high-throughput screening facility for her assistance.
   This work was supported by grants from NCI (CA157774 and GM121316 to
   R.E.L.; CA203397 to B.K.N., and CA22287 to K.W.F), Eppley Institute in
   Cancer Biology training grant (NCI T32CA009476), NPOD COBRE (NIH P20
   GM104320), and the Fred & Pamela Buffett Cancer Center Support Grant
   (P30 CA036727).
CR [Anonymous], 2019, MULTIPLEX GENE EXPRE
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NR 6
TC 1
Z9 1
U1 0
U2 1
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
EI 2052-4463
J9 SCI DATA
JI Sci. Data
PD JAN 21
PY 2020
VL 7
IS 1
DI 10.1038/s41597-020-0365-2
PG 9
WC Multidisciplinary Sciences
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Science & Technology - Other Topics
GA KI6DK
UT WOS:000511439400004
PM 31964871
OA gold, Green Published
DA 2022-04-25
ER

PT J
AU de Nigris, F
   Balestrieri, ML
   Napoli, C
AF de Nigris, Filomena
   Balestrieri, Maria Luisa
   Napoli, Claudio
TI Targeting c-Myc, Ras and IGF cascade to treat cancer and vascular
   disorders
SO CELL CYCLE
LA English
DT Review
DE c-Myc; Ras; IGF; cancer; atherosclerosis
ID GROWTH-FACTOR-I; SMOOTH-MUSCLE-CELLS; HUMAN ATHEROSCLEROTIC PLAQUES;
   ANTISENSE OLIGONUCLEOTIDES; COLON-CANCER; CARDIOVASCULAR-DISEASES;
   CAROTID ATHEROSCLEROSIS; HYPERLIPIDEMIC RABBITS; MORPHOLINO OLIGOMER;
   BINDING PROTEIN-3
AB Cancer and vascular diseases remain the predominant causes of morbidity and mortality in industrialized countries worldwide. The course of atherosclerosis with initiation, progression, and complication parallels the three stages of carcinogenesis with induction, growth, and invasion of tissue and neoangiogenesis. Within this framework, the oncogene c-Myc and growth factors pathways are acquiring increasing importance. Insulin-like growth factor-1 (IGF-1) pathway emerges among them for its versatile pleiotropic actions. A number of genes that permit extensive communication between IGF-1-AKT, p53, and mammalian target of rapamycin ( mTOR) pathways have been identified. In turn these pathways lead to p53 transcriptional program, the forkhead transcriptional programs, autophagy, and translational controls, which determine cell growth or arrest, cell survival or death. The increased understanding of the extensive communication and coordination between all these pathways may enable to targeting these events and to prevent neoplastic and vascular diseases. Great effort has been focused on the development of new agents designed to target various steps of c-Myc, Ras, and IGF cascade. However, what have we recently learned about their safety and effectiveness? Here, we review the very recent advances in the identification of novel inhibitors as well as antisense oligonuleotides (ASOs) and siRNA that are proving their usefulness in ongoing clinical trials both in therms of toxicity and specificity.
C1 Univ Naples Federico II, Dept Gen Pathol, Sch Med 1, Div Clin Pathol, I-80134 Naples, Italy.
   Univ Naples Federico II, Excellence Res Ctr Cardiovasc Dis, Sch Med 1, I-80134 Naples, Italy.
   Univ Naples Federico II, Dept Chem Biol & Phys, Sch Med 1, I-80134 Naples, Italy.
RP Napoli, C (corresponding author), Univ Naples Federico II, Dept Gen Pathol, Sch Med 1, Div Clin Pathol, Comlesso S Andrea Dame,Via L Crecchio 7, I-80134 Naples, Italy.
EM claunap@tin.it
OI Balestrieri, Maria Luisa/0000-0001-6001-1789; de nigris,
   filomena/0000-0002-2322-1557; Napoli, Claudio/0000-0002-5455-555X
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NR 100
TC 33
Z9 34
U1 0
U2 4
PU TAYLOR & FRANCIS INC
PI PHILADELPHIA
PA 530 WALNUT STREET, STE 850, PHILADELPHIA, PA 19106 USA
SN 1538-4101
EI 1551-4005
J9 CELL CYCLE
JI Cell Cycle
PD AUG 1
PY 2006
VL 5
IS 15
BP 1621
EP 1628
DI 10.4161/cc.5.15.3138
PG 8
WC Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Cell Biology
GA 086UK
UT WOS:000240698300008
PM 16921263
OA Bronze
DA 2022-04-25
ER

PT J
AU Yeon, M
   Lee, S
   Lee, JE
   Jung, HS
   Kim, Y
   Jeoung, D
AF Yeon, Minjeong
   Lee, Seungheon
   Lee, Joo-Eun
   Jung, Hyun Suk
   Kim, Youngmi
   Jeoung, Dooil
TI CAGE-miR-140-5p-Wnt1 Axis Regulates Autophagic Flux, Tumorigenic
   Potential of Mouse Colon Cancer Cells and Cellular Interactions Mediated
   by Exosomes
SO FRONTIERS IN ONCOLOGY
LA English
DT Article
DE cancer associated gene CAGE; cellular interactions; exosomes; micro
   RNA-140-5p; tumor microenvironment; wnt1
ID CANCER/TESTIS ANTIGEN CAGE; FEEDBACK LOOP; MAST-CELLS; EXPRESSION;
   PROLIFERATION; ACTIVATION; RESISTANCE; INHIBITION; INCREASES; CISPLATIN
AB Although the cancer/testis antigen CAGE has been implicated in tumorigenesis, the molecular mechanisms of CAGE-promoted tumorigenesis remain largely unknown. CT26(Flag-CAGE) cells, CT26 (mouse colon cancer cells) cells stably expressing CAGE, were established to investigate CAGE-promoted tumorigenesis. Down-regulation of CAGE led to decreased autophagic flux in CT26(Flag-CAGE) cells. CAGE interacted with Beclin1, a mediator of autophagy. The CT26(Flag-CAGE) cells showed enhanced autophagosome formation and displayed greater tumor spheroid-forming potential than CT26 cells. MicroRNA array analysis revealed that CAGE decreased the expression of various microRNAs, including miR-140-5p, in CT26 cells. CAGE was shown to bind to the promoter sequences of miR-140-5p. MiR-140-5p inhibition increased the tumorigenic potential of and autophagic flux in CT26 cells. A miR-140-5p mimic exerted negative effects on the tumorigenic potential of CT26(Flag-CAGE) cells and autophagic flux in CT26(Flag-CAGE) cells. MiR-140-5p was predicted to bind to the 3 '-UTR of Wnt1. CT26(Flag-CAGE) cells showed higher expression of Wnt1 than CT26 cells. Down-regulation of Wnt1 decreased autophagic flux. Luciferase activity assays showed the direct regulation of wnt1 by miR-140-5p. Tumor tissue derived from the CT26(Flag-CAGE) cells revealed higher expressions of factors associated with activated mast cells and tumor-associated macrophages than tumor tissue derived from CT26 cells. Culture medium from the CT26(Flag-CAGE) cells increased autophagic flux in CT26 cells, mast cells and macrophages. Culture medium from the CT26(Flag-CAGE) cells increased CD163 and autophagic flux in CT26 cells, mast cells, and macrophages in a Wnt1-dependent manner. Exosomes from CT26(Flag-CAGE) cells increased autophagc flux in CT26 cells, mast cells, and macrophages. Exosomes from CT26(Flag-CAGE) cells increased the tumorigenic potential of CT26 cells. Wnt1 was shown to be present within the exosomes. Recombinant Wnt1 protein increased autophagic flux in CT26, mast cells, and macrophages. Recombinant wnt1 protein mediated interactions between the CT26 cells, mast cells, and macrophages. Our results showed novel roles for the CAGE-miR-140-5p-Wnt1 axis in autophagic flux and cellular interactions mediated by exosomes.
C1 [Yeon, Minjeong; Lee, Seungheon; Lee, Joo-Eun; Jung, Hyun Suk; Jeoung, Dooil] Kangwon Natl Univ, Dept Biochem, Chuncheon Si, South Korea.
   [Kim, Youngmi] Hallym Univ, Coll Med, Inst New Frontier Res, Chuncheon Si, South Korea.
RP Jeoung, D (corresponding author), Kangwon Natl Univ, Dept Biochem, Chuncheon Si, South Korea.
EM jeoungd@kangwon.ac.kr
FU National Research Foundation [2017R1A2A2A05001029, 2017M3A9G7072417,
   2018R1D1A1B07043498]; BK21 plus Program; Korea Foundation for Cancer
   Research [KFCR-2018-002]
FX This work was supported by National Research Foundation Grants
   (2017R1A2A2A05001029, 2017M3A9G7072417, 2018R1D1A1B07043498), a grant
   from the BK21 plus Program. This work was also supported by Korea
   Foundation for Cancer Research (KFCR-2018-002).
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NR 59
TC 9
Z9 9
U1 3
U2 6
PU FRONTIERS MEDIA SA
PI LAUSANNE
PA AVENUE DU TRIBUNAL FEDERAL 34, LAUSANNE, CH-1015, SWITZERLAND
SN 2234-943X
J9 FRONT ONCOL
JI Front. Oncol.
PD NOV 14
PY 2019
VL 9
AR 1240
DI 10.3389/fonc.2019.01240
PG 20
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA JT8RC
UT WOS:000501249700001
PM 31799196
OA Green Published, gold
DA 2022-04-25
ER

PT J
AU Bhagwat, SV
   Gokhale, PC
   Crew, AP
   Cooke, A
   Yao, Y
   Mantis, C
   Kahler, J
   Workman, J
   Bittner, M
   Dudkin, L
   Epstein, DM
   Gibson, NW
   Wild, R
   Arnold, LD
   Houghton, PJ
   Pachter, JA
AF Bhagwat, Shripad V.
   Gokhale, Prafulla C.
   Crew, Andrew P.
   Cooke, Andy
   Yao, Yan
   Mantis, Christine
   Kahler, Jennifer
   Workman, Jennifer
   Bittner, Mark
   Dudkin, Lorina
   Epstein, David M.
   Gibson, Neil W.
   Wild, Robert
   Arnold, Lee D.
   Houghton, Peter J.
   Pachter, Jonathan A.
TI Preclinical Characterization of OSI-027, a Potent and Selective
   Inhibitor of mTORC1 and mTORC2: Distinct from Rapamycin
SO MOLECULAR CANCER THERAPEUTICS
LA English
DT Article
ID MAMMALIAN TARGET; KINASE INHIBITOR; IN-VITRO; GROWTH; AUTOPHAGY;
   THERAPY; RICTOR; ROLES
AB The phosphoinositide 3-kinase (PI3K)/AKT/mTOR pathway is frequently activated in human cancers, and mTOR is a clinically validated target. mTOR forms two distinct multiprotein complexes, mTORC1 and mTORC2, which regulate cell growth, metabolism, proliferation, and survival. Rapamycin and its analogues partially inhibit mTOR through allosteric binding to mTORC1, but not mTORC2, and have shown clinical utility in certain cancers. Here, we report the preclinical characterization of OSI-027, a selective and potent dual inhibitor of mTORC1 and mTORC2 with biochemical IC50 values of 22 nmol/L and 65 nmol/L, respectively. OSI-027 shows more than 100-fold selectivity for mTOR relative to PI3K alpha, PI3K beta, PI3K gamma, and DNA-PK. OSI-027 inhibits phosphorylation of the mTORC1 substrates 4E-BP1 and S6K1 as well as the mTORC2 substrate AKT in diverse cancer models in vitro and in vivo. OSI-027 and OXA-01 (close analogue of OSI-027) potently inhibit proliferation of several rapamycin-sensitive and -insensitive nonengineered and engineered cancer cell lines and also, induce cell death in tumor cell lines with activated PI3K-AKT signaling. OSI-027 shows concentration-dependent pharmacodynamic effects on phosphorylation of 4E-BP1 and AKT in tumor tissue with resulting tumor growth inhibition. OSI-027 shows robust antitumor activity in several different human xenograft models representing various histologies. Furthermore, in COLO 205 and GEO colon cancer xenograft models, OSI-027 shows superior efficacy compared with rapamycin. Our results further support the important role of mTOR as a driver of tumor growth and establish OSI-027 as a potent anticancer agent. OSI-027 is currently in phase I clinical trials in cancer patients. Mol Cancer Ther; 10(8); 1394-406. (C) 2011 AACR.
C1 [Bhagwat, Shripad V.] OSI Pharmaceut Inc, Biochem & Cellular Pharmacol, Canc Biol, Farmingdale, NY 11735 USA.
   [Crew, Andrew P.; Arnold, Lee D.] OSI Pharmaceut Inc, Canc Chem, Farmingdale, NY 11735 USA.
   [Gokhale, Prafulla C.; Cooke, Andy; Mantis, Christine; Workman, Jennifer; Bittner, Mark; Wild, Robert] OSI Pharmaceut Inc, Vivo Pharmacol, Boulder, CO USA.
   [Dudkin, Lorina; Houghton, Peter J.] Nationwide Childrens Hosp, Ctr Childhood Canc, Columbus, OH USA.
RP Bhagwat, SV (corresponding author), OSI Pharmaceut Inc, Biochem & Cellular Pharmacol, Canc Biol, Farmingdale, NY 11735 USA.
EM shripad.bhagwat@us.astellas.com
RI Houghton, Peter/E-3265-2011
OI Kahler, Jennifer/0000-0002-4088-0888
FU NATIONAL CANCER INSTITUTEUnited States Department of Health & Human
   ServicesNational Institutes of Health (NIH) - USANIH National Cancer
   Institute (NCI) [R01CA077776] Funding Source: NIH RePORTER; NCI NIH
   HHSUnited States Department of Health & Human ServicesNational
   Institutes of Health (NIH) - USANIH National Cancer Institute (NCI) [R01
   CA077776] Funding Source: Medline
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NR 35
TC 136
Z9 138
U1 1
U2 8
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 1535-7163
EI 1538-8514
J9 MOL CANCER THER
JI Mol. Cancer Ther.
PD AUG
PY 2011
VL 10
IS 8
BP 1394
EP 1406
DI 10.1158/1535-7163.MCT-10-1099
PG 13
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA 804YR
UT WOS:000293692500010
PM 21673091
DA 2022-04-25
ER

PT J
AU Wang, WY
   Wei, JL
   Zhang, HR
   Zheng, XR
   Zhou, H
   Luo, YJ
   Yang, JG
   Deng, QC
   Huang, SQ
   Fu, ZX
AF Wang, Wuyi
   Wei, Jinlai
   Zhang, Hairong
   Zheng, Xiangru
   Zhou, He
   Luo, Yajun
   Yang, Jianguo
   Deng, Qican
   Huang, Siqi
   Fu, Zhongxue
TI PRDX2 promotes the proliferation of colorectal cancer cells by
   increasing the ubiquitinated degradation of p53
SO CELL DEATH & DISEASE
LA English
DT Article
ID TUMOR-SUPPRESSOR PROTEIN; TRANSCRIPTIONAL REPRESSION; MDM2; ACTIVATION;
   L11; INHIBITION; CHECKPOINT; MUTATIONS; AUTOPHAGY; ARREST
AB Colorectal cancer is the most common gastrointestinal cancer and causes severe damage to human health. PRDX2 is a member of the peroxiredoxin family reported to have a high level of expression in colorectal cancer. However, the mechanisms by which PRDX2 promotes the proliferation of colorectal cancer are still unclear. Here, the results indicated that PRDX2 expression was upregulated in colorectal cancer and closely correlated with poor prognosis. Functionally, PRDX2 promoted the proliferation of colorectal cancer cells. Mechanistically, PRDX2 could bind RPL4, reducing the interaction between RPL4 and MDM2. These findings demonstrate that the oncogenic property of PRDX2 may be attributed to its regulation of the RPL4-MDM2-p53 pathway, leading to p53 ubiquitinated degradation.
C1 [Wang, Wuyi; Wei, Jinlai; Zhang, Hairong; Zheng, Xiangru; Zhou, He; Luo, Yajun; Yang, Jianguo; Deng, Qican; Huang, Siqi; Fu, Zhongxue] Chongqing Med Univ, Affiliated Hosp 1, Dept Gastrointestinal Surg, Chongqing, Peoples R China.
RP Fu, ZX (corresponding author), Chongqing Med Univ, Affiliated Hosp 1, Dept Gastrointestinal Surg, Chongqing, Peoples R China.
EM fzx19990521@126.com
FU National Natural Science Foundation of ChinaNational Natural Science
   Foundation of China (NSFC) [81572319]; Chongqing Natural Science
   FoundationNatural Science Foundation of Chongqing [cstc2017jcyjAX0127]
FX The research project was supported by the National Natural Science
   Foundation of China (Grant No. 81572319; Project recipient: F.Z.) and
   Chongqing Natural Science Foundation (Grant No. cstc2017jcyjAX0127;
   Project recipient: W.J.).
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NR 49
TC 2
Z9 2
U1 4
U2 4
PU SPRINGERNATURE
PI LONDON
PA CAMPUS, 4 CRINAN ST, LONDON, N1 9XW, ENGLAND
SN 2041-4889
J9 CELL DEATH DIS
JI Cell Death Dis.
PD JUN 11
PY 2021
VL 12
IS 6
AR 605
DI 10.1038/s41419-021-03888-1
PG 10
WC Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Cell Biology
GA SV0YJ
UT WOS:000663552600003
PM 34117220
OA Green Published, gold
DA 2022-04-25
ER

PT J
AU Kang, S
   Kim, JE
   Song, NR
   Jung, SK
   Lee, MH
   Park, JS
   Yeom, MH
   Bode, AM
   Dong, ZG
   Lee, KW
AF Kang, Soouk
   Kim, Jong-Eun
   Song, Nu Ry
   Jung, Sung Keun
   Lee, Mee Hyun
   Park, Jun Seong
   Yeom, Myeong-Hun
   Bode, Ann M.
   Dong, Zigang
   Lee, Ki Won
TI The Ginsenoside 20-O-beta-D-Glucopyranosyl-20(S)-Protopanaxadiol Induces
   Autophagy and Apoptosis in Human Melanoma via AMPK/JNK Phosphorylation
SO PLOS ONE
LA English
DT Article
ID HUMAN COLORECTAL-CANCER; COMPOUND-K; CELL-DEATH; B-RAF; ACTIVATION;
   MUTATIONS; NECROSIS; SURVIVAL; BRAF; RB1
AB Studies have shown that a major metabolite of the red ginseng ginsenoside Rb1, called 20-O-beta-D-glucopyranosyl-20(S)-protopanaxadiol (GPD), exhibits anticancer properties. However, the chemotherapeutic effects and molecular mechanisms behind GPD action in human melanoma have not been previously investigated. Here we report the anticancer activity of GPD and its mechanism of action in melanoma cells. GPD, but not its parent compound Rb1, inhibited melanoma cell proliferation in a dose-dependent manner. Further investigation revealed that GPD treatment achieved this inhibition through the induction of autophagy and apoptosis, while Rb1 failed to show significant effect at the same concentrations. The inhibitory effect of GPD appears to be mediated through the induction of AMPK and the subsequent attenuation of mTOR phosphorylation. In addition, GPD activated c-Jun by inducing JNK phosphorylation. Our findings suggest that GPD suppresses melanoma growth by inducing autophagic cell death and apoptosis via AMPK/JNK pathway activation. GPD therefore has the potential to be developed as a chemotherapeutic agent for the treatment of human melanoma.
C1 [Kang, Soouk; Kim, Jong-Eun; Song, Nu Ry; Jung, Sung Keun; Lee, Ki Won] Seoul Natl Univ, Dept Agr Biotechnol, WCU Biomodulat Major, Seoul, South Korea.
   [Kang, Soouk; Kim, Jong-Eun; Song, Nu Ry; Jung, Sung Keun; Lee, Ki Won] Seoul Natl Univ, Ctr Food & Bioconvergence, Seoul, South Korea.
   [Kang, Soouk; Kim, Jong-Eun; Jung, Sung Keun; Lee, Mee Hyun; Bode, Ann M.; Dong, Zigang] Univ Minnesota, Hormel Inst, Austin, MN 55912 USA.
   [Song, Nu Ry; Lee, Ki Won] Seoul Natl Univ, Adv Inst Convergence Technol, Suwon, South Korea.
   [Jung, Sung Keun] Korea Food Res Inst, Funct Food Resources Res Grp, Songnam, South Korea.
   [Park, Jun Seong; Yeom, Myeong-Hun] Amorepacif Corp R&D Ctr, Skin Res Inst, Yongin, South Korea.
   [Lee, Ki Won] Seoul Natl Univ, Inst Green Bio Sci & Technol, Res Inst Bio Food Ind, Pyeongchang, South Korea.
RP Dong, ZG (corresponding author), Univ Minnesota, Hormel Inst, 801 16th Ave NE, Austin, MN 55912 USA.
EM zgdong@hi.umn.edu; kiwon@snu.ac.kr
RI kim, jong-eun/B-3550-2017; Lee, Ki Won/M-4114-2018
OI kim, jong-eun/0000-0002-5030-6126; 
FU World Class Institute Program [WCI2009-002]; Leap Research Program Grant
   through the National Research Foundation, Ministry of Science, ICT and
   Future Planning, Republic of Korea [2010-0029233]
FX This work was supported by the World Class Institute Program
   (WCI2009-002) and the Leap Research Program Grant (2010-0029233) through
   the National Research Foundation, Ministry of Science, ICT and Future
   Planning, Republic of Korea. The funders had no role in study design,
   data collection and analysis, decision to publish, or preparation of the
   manuscript.
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NR 47
TC 23
Z9 23
U1 0
U2 16
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 1160 BATTERY STREET, STE 100, SAN FRANCISCO, CA 94111 USA
SN 1932-6203
J9 PLOS ONE
JI PLoS One
PD AUG 19
PY 2014
VL 9
IS 8
AR e104305
DI 10.1371/journal.pone.0104305
PG 10
WC Multidisciplinary Sciences
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Science & Technology - Other Topics
GA AN6XM
UT WOS:000340742100026
PM 25137374
OA Green Published, Green Submitted, gold
DA 2022-04-25
ER

PT J
AU Tian, W
   Chen, SY
AF Tian Wei
   Chen Si-yu
TI Recent advances in the molecular basis of anti-neoplastic mechanisms of
   oridonin
SO CHINESE JOURNAL OF INTEGRATIVE MEDICINE
LA English
DT Review
DE oridonin; anti-neoplasm; cell cycle arrest; apoptosis; autophagy
ID CARCINOMA HELA-CELLS; BREAST-CANCER CELLS; NF-KAPPA-B; INDUCED
   APOPTOSIS; RABDOSIA-RUBESCENS; SIGNALING PATHWAYS; COLORECTAL-CANCER;
   INDUCED AUTOPHAGY; LEUKEMIA-CELLS; CYCLE ARREST
AB Oridonin, a diterpenoid isolated from Rabdosia rubescens, has been proven to possess various pharmacological and physiological effects such as anti-inflammation, anti-bacterial, and anti-neoplastic, although in recent years, more attention has been paid to its anti-neoplastic effects. For example, oridonin can trigger cell cycle arrest, apoptosis, and autophagy in different neoplastic cell lines. This review summarizes the considerable knowledge about the action mechanisms of oridonin that has been studied in recent years. The present observations reveal the novel anti-neoplastic effects of oridonin, suggesting that it may be effective as a potent alternative or adjunct drug to conventional chemotherapy.
C1 [Tian Wei; Chen Si-yu] Shanghai Jiao Tong Univ, Dept Oncol, Xinhua Hosp, Sch Medcine, Shanghai 200092, Peoples R China.
RP Chen, SY (corresponding author), Shanghai Jiao Tong Univ, Dept Oncol, Xinhua Hosp, Sch Medcine, Shanghai 200092, Peoples R China.
EM siyu.chen@shsmu.edu.cn
FU National Natural Science Foundation of ChinaNational Natural Science
   Foundation of China (NSFC) [81274142, 30300139]; Natural Science
   Foundation of Science and Technology Commission of Shanghai
   MunicipalityScience & Technology Commission of Shanghai Municipality
   (STCSM) [11ZR1423400]; Key Project of Shanghai Municipal Education
   CommissionScience & Technology Commission of Shanghai Municipality
   (STCSM) [07zz43]
FX Supported by National Natural Science Foundation of China (No. 81274142,
   No. 30300139), Natural Science Foundation of Science and Technology
   Commission of Shanghai Municipality (No. 11ZR1423400), Key Project of
   Shanghai Municipal Education Commission (No. 07zz43)
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NR 51
TC 29
Z9 35
U1 5
U2 56
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 1672-0415
EI 1993-0402
J9 CHIN J INTEGR MED
JI Chin. J. Integr. Med.
PD APR
PY 2013
VL 19
IS 4
BP 315
EP 320
DI 10.1007/s11655-013-1437-3
PG 6
WC Integrative & Complementary Medicine
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Integrative & Complementary Medicine
GA 117QA
UT WOS:000316967000010
PM 23546635
DA 2022-04-25
ER

PT J
AU Kouhbanani, MAJ
   Sadeghipour, Y
   Sarani, M
   Sefidgar, E
   Ilkhani, S
   Amani, AM
   Beheshtkhoo, N
AF Kouhbanani, Mohammad Amin Jadidi
   Sadeghipour, Yasin
   Sarani, Mina
   Sefidgar, Erfan
   Ilkhani, Saba
   Amani, Ali Mohammad
   Beheshtkhoo, Nasrin
TI The inhibitory role of synthesized Nickel oxide nanoparticles against
   Hep-G2, MCF-7, and HT-29 cell lines: the inhibitory role of NiO NPs
   against Hep-G2, MCF-7, and HT-29 cell lines
SO GREEN CHEMISTRY LETTERS AND REVIEWS
LA English
DT Article
DE Nickel oxide nanoparticles; cyclic voltammetry; Hep-G2; MTT assay
ID CATALYTIC-ACTIVITY; OXIDATIVE STRESS; GREEN SYNTHESIS; ZINC-OXIDE;
   SOL-GEL; EXTRACT; AUTOPHAGY; DECOMPOSITION
AB Nickel oxide nanoparticles (NiO NPs) were synthesized via the facile sol-gel method. The synthesized NiO NPs were characterized using X-ray diffraction (XRD), Field-Emission Scanning Electron Microscopy (FESEM), Transmission Electron Microscopy (TEM), Raman and Fourier Transform Infrared (FT-IR) techniques. The effect of particle size was analyzed on structural alterations, electrochemical behaviors, and cytotoxic effect of synthesized NiO NPs. According to TEM results, the particle sizes of synthesized NiO NPs were 8.2, 15.4, and 21.7 nm at 300, 400, and 500 degrees C, respectively. Electrochemical behaviors of synthesized NiO NPs were assessed through the cyclic voltammetry (CV) technique. The results showed that the magnitude of the current density was decreased in treated samples exposed to higher temperature values. The cytotoxic activity of synthesized nanoparticles was investigated against human liver cancer cell (Hep-G2), breast cancer cell (MCF-7), and colon cancer cell (HT-29) lines using the MTT assay. The results demonstrated that synthesized NiO NPs had higher cytotoxicity at 300 C than at 400 and 500 C, because of their small particle size. Thus, synthesized NiO NPs exhibit acceptable cytotoxic effects against Hep-G2, MCF-7, and HT-29 cancer cell lines so that they could be a good choice for cancer treatment.
C1 [Kouhbanani, Mohammad Amin Jadidi; Sadeghipour, Yasin; Amani, Ali Mohammad; Beheshtkhoo, Nasrin] Shiraz Univ Med Sci, Sch Adv Med Sci & Technol, Dept Med Nanotechnol, Shiraz, Iran.
   [Sarani, Mina] Zabol Univ Med Sci, Zabol Med Plants Res Ctr, Zabol, Iran.
   [Sefidgar, Erfan] Inst Adv Studies Basic Sci, Dept Biol Sci, Zanjan, Iran.
   [Ilkhani, Saba] Shahid Beheshti Univ, Sch Med, Dept Biol & Anat Sci, Tehran, Iran.
   [Amani, Ali Mohammad] Shiraz Univ Med Sci, Pharmaceut Sci Res Ctr, Shiraz, Iran.
RP Amani, AM; Beheshtkhoo, N (corresponding author), Shiraz Univ Med Sci, Sch Adv Med Sci & Technol, Dept Med Nanotechnol, Shiraz, Iran.
EM Aliamani1400@gmail.com; beheshtkhoo.nano@gmail.com
FU Shiraz University of Medical Science [1396-0174-1526B]
FX This work was financially supported by research Grant of Shiraz
   University of Medical Science (No.1396-0174-1526B)
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NR 44
TC 3
Z9 3
U1 0
U2 2
PU TAYLOR & FRANCIS LTD
PI ABINGDON
PA 2-4 PARK SQUARE, MILTON PARK, ABINGDON OR14 4RN, OXON, ENGLAND
SN 1751-8253
EI 1751-7192
J9 GREEN CHEM LETT REV
JI Green Chem. Lett. Rev.
PD JUL 3
PY 2021
VL 14
IS 3
BP 443
EP 453
DI 10.1080/17518253.2021.1939435
PG 11
WC Chemistry, Multidisciplinary; Green & Sustainable Science & Technology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Chemistry; Science & Technology - Other Topics
GA SV2BV
UT WOS:000663630800001
OA gold
DA 2022-04-25
ER

PT J
AU Zou, L
   Sun, P
   Zhang, L
AF Zou, Lei
   Sun, Peng
   Zhang, Lei
TI miR-651-3p Enhances the Sensitivity of Hepatocellular Carcinoma to
   Cisplatin via Targeting ATG3-Mediated Cell Autophagy
SO JOURNAL OF ONCOLOGY
LA English
DT Article
ID GASTRIC-CANCER; COLON-CANCER; PROLIFERATION; METASTASIS; RESISTANCE;
   INVASION; PROMOTES; AXIS; ATG3; HCC
AB Drug resistance is a major challenge for hepatocellular carcinoma (HCC) treatment in a clinic, which limits the therapeutic effect of the chemotherapeutic drugs, including cisplatin (CDDP), in this disease. Mounting evidence has identified that miRNAs dysfunction is related to the resistance of tumor cells to CDDP, and miR-651-3p has been identified as a tumor inhibitor to suppress the progression of multiple tumors. However, the role of miR-651-3p in HCC remains unclear. In this study, the relative expression of miR-651-3p in HCC tissues and cell lines were measured, and the functions of miR-651-3p were also observed by CCK-8 assay, flow cytometry assay, and Western blot. Moreover, the downstream target of miR-651-3p was predicted and verified via TargetScan and dual-luciferase reporter assay, and its functions were also investigated. The results showed that miR-651-3p was significantly downregulated in HCC tissues and cell lines, and the decreased miR-651-3p was also observed in CDDP-induced cells. miR-651-3p upregulation could effectively inhibit the proliferation and induce the apoptosis of R-HepG2. It was also found that ATG3 was a downstream target of miR-651-3p, and ATG3 was highly upregulated in HCC tissues. Moreover, the upregulated ATG3 could partly reverse the effects of miR-651-3p on R-HepG2. Besides, miR-651-3p involved the autophagy pathway of the HCC cells via targeting ATG3. In conclusion, miR-651-3p could regulate the autophagy to enhance the sensitivity of HepG2 cells to CDDP via targeting ATG3.
C1 [Zou, Lei; Sun, Peng; Zhang, Lei] Zibo Cent Hosp, Dept Gastroenterol, Zibo 255036, Shandong, Peoples R China.
RP Zhang, L (corresponding author), Zibo Cent Hosp, Dept Gastroenterol, Zibo 255036, Shandong, Peoples R China.
EM shibayej@163.com
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NR 28
TC 0
Z9 0
U1 0
U2 1
PU HINDAWI LTD
PI LONDON
PA ADAM HOUSE, 3RD FLR, 1 FITZROY SQ, LONDON, W1T 5HF, ENGLAND
SN 1687-8450
EI 1687-8469
J9 J ONCOL
JI J. Oncol.
PD AUG 19
PY 2021
VL 2021
AR 5391977
DI 10.1155/2021/5391977
PG 7
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA UJ2AF
UT WOS:000691094200002
PM 34457004
OA gold, Green Published
DA 2022-04-25
ER

PT J
AU Yang, Z
   Chen, YS
   Wei, XY
   Wu, DJ
   Min, ZJ
   Quan, YJ
AF Yang, Zhou
   Chen, Yusheng
   Wei, Xiyi
   Wu, Dejun
   Min, Zhijun
   Quan, Yingjun
TI Upregulated NTF4 in colorectal cancer promotes tumor development via
   regulating autophagy
SO INTERNATIONAL JOURNAL OF ONCOLOGY
LA English
DT Article
DE neurotrophin-4; colorectal cancer; epithelial-to-mesenchymal transition;
   autophagy; mitogen-activated protein kinase pathway
ID GENE-EXPRESSION; APOPTOSIS; PATHWAYS; CELLS; EMT
AB Autophagy plays a key role in colorectal cancer (CRC) development and reduces the sensitivity of CRC cells to treatment. The present study reported a novel tumor-suppressive role for autophagy, which was demonstrated to be regulated through the novel oncogene neurotrophin-4 (NTF4). NTF4 was significantly overexpressed in tumor tissue compared with non-tumor mucosa, and the upregulation of NTF4 in CRC was associated with poor overall survival and advanced TNM stage. The genetic knockdown of NTF4 using short hairpin RNA in CRC cells prevented epithelial-to-mesenchymal transition and activated autophagy; this was regulated through the interaction between autophagy-associated gene 5 (Atg5) and the mitogen-activated protein kinase pathway. In addition, the knockdown of NTF4 inhibited cell invasion, migration, proliferation and colony formation, and promoted cell cycle arrest. Treatment of the cells with the autophagy inhibitor chloroquine (CQ) rescued these functions and promoted cell invasion, migration, proliferation and colony formation. Finally, the knockdown of NTF4 inhibited the growth of subcutaneous xenografts in Balb/c-nu mice. In conclusion, these findings suggested that NTF4 may be a diagnostic marker associated with the overall survival and progression of patients with CRC. NTF4 was found to promote tumorigenesis and CRC development through autophagy regulation.
C1 [Yang, Zhou; Chen, Yusheng; Wu, Dejun; Min, Zhijun; Quan, Yingjun] Fudan Univ, Pudong Med Ctr, Shanghai Pudong Hosp, Dept Gen Surg, 2800 Gongwei Rd, Shanghai 201399, Peoples R China.
   [Wei, Xiyi] Nanjing Med Univ, Clin Med Coll 1, Nanjing 210029, Jiangsu, Peoples R China.
   [Quan, Yingjun] Shanghai Jiao Tong Univ, Sch Med, Tongren Hosp, Shanghai 201399, Peoples R China.
RP Min, ZJ; Quan, YJ (corresponding author), Fudan Univ, Pudong Med Ctr, Shanghai Pudong Hosp, Dept Gen Surg, 2800 Gongwei Rd, Shanghai 201399, Peoples R China.
EM minzhijun@126.com; qyjasmine@126.com
FU Academic Leaders Training Program - Pudong Health Bureau of Shanghai
   [PWRd2016-05]; Scientific Research Foundation by Pudong Hospital
   [YJ2020-01]
FX The present study was funded by The Academic Leaders Training Program
   Supported by Pudong Health Bureau of Shanghai (grant no. PWRd2016-05)
   and the Scientific Research Foundation provided by Pudong Hospital
   affiliated to Fudan University (grant no. YJ2020-01).
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NR 29
TC 6
Z9 6
U1 2
U2 6
PU SPANDIDOS PUBL LTD
PI ATHENS
PA POB 18179, ATHENS, 116 10, GREECE
SN 1019-6439
EI 1791-2423
J9 INT J ONCOL
JI Int. J. Oncol.
PD JUN
PY 2020
VL 56
IS 6
BP 1442
EP 1454
DI 10.3892/ijo.2020.5027
PG 13
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA LJ8IE
UT WOS:000530403800008
PM 32236587
OA Green Published, hybrid
DA 2022-04-25
ER

PT J
AU BonakdarYazdi, B
   Khodagholi, F
   Shaerzadeh, F
   Sharifzadeh, A
   Ahmadi, R
   Sanati, M
   Mehdizadeh, H
   Payandehmehr, B
   Vali, L
   Jahromi, MM
   Taghizadeh, G
   Sharifzadeh, M
AF BonakdarYazdi, Behnoosh
   Khodagholi, Fariba
   Shaerzadeh, Fatemeh
   Sharifzadeh, Azadeh
   Ahmadi, Ramesh
   Sanati, Mehdi
   Mehdizadeh, Hajar
   Payandehmehr, Borna
   Vali, Leila
   Jahromi, Mehrnoush Moghaddasi
   Taghizadeh, Ghorban
   Sharifzadeh, Mohammad
TI The effect of arsenite on spatial learning: Involvement of autophagy and
   apoptosis
SO EUROPEAN JOURNAL OF PHARMACOLOGY
LA English
DT Article
DE Sodium arsenite; Autophagy; Apoptosis; Alzheimer disease; Spatial
   learning; Caspase-3; LC3
ID CASPASE-MEDIATED CLEAVAGE; COLON-CANCER CELLS; MORRIS WATER MAZE; SODIUM
   ARSENITE; CREB PHOSPHORYLATION; BECLIN 1; REGULATES AUTOPHAGY;
   SIGNAL-TRANSDUCTION; OXIDATIVE STRESS; NERVOUS-SYSTEM
AB Spatial learning plays a major role in one's information recording. Arsenic is one of ubiquitous environmental toxins with known neurological effects. However, studies investigating the effects of arsenic on spatial learning and related mechanisms are limited. This study was planned toexaminethe effects of bilateral intra-hippocampal infusion of different concentrations of sodium arsenite (5, 10 and 100 nM, 5 mu l/side) on spatial learning in Wistar rats. Moreover, we evaluated levels of LC3-II, Atg7 and Atg12 as reliable biomarkers of autophagy and caspase-3 and Bax/Bcl-2 ratio as indicators of apoptosis in the hippocampus. Interestingly, low concentrations of sodium arsenite (5 and 10 nM) significantly increased spatial acquisition but pre-training administration of sodium arsenite100 nM did not significantly alter spatial learning. LC3-II levels were significantly increased in groups treated with sodium arsenite 5 and 10 nM and decreased in the group receiving arsenite 100 nM compared to the control group. Atg7 and Atg12 levels were obviously higher in all groups treated with sodium arsenite compared to control. However, caspase-3 cleavage and Bax/Bcl-2 ratio were notably greater in 100 nM, and lesser in 5 nM arsenite group in comparison with control animals. The results of this study showed that the low concentrations of sodium arsenite could facilitate spatial learning. This facilitation could be attributed to neuronal autophagy induced by low concentrations of sodium arsenite. These findings may help to clarify the regulatory pathways for apoptosis and autophagy balance due to sodium arsenite.
C1 [BonakdarYazdi, Behnoosh; Sanati, Mehdi; Mehdizadeh, Hajar; Payandehmehr, Borna; Taghizadeh, Ghorban; Sharifzadeh, Mohammad] Univ Tehran Med Sci, Toxicol & Poisoning Res Ctr, Fac Pharm, Dept Pharmacol & Toxicol, Tehran, Iran.
   [Khodagholi, Fariba] Shahid Beheshti Univ Med Sci, Neurosci Res Ctr, Tehran, Iran.
   [Shaerzadeh, Fatemeh] Hormozgan Univ Med Sci, Dept Physiol, Fac Med, Bandar Abbas, Iran.
   [Sharifzadeh, Azadeh; Ahmadi, Ramesh] Azad Univ, Dept Physiol, Qom, Iran.
   [Mehdizadeh, Hajar; Taghizadeh, Ghorban; Sharifzadeh, Mohammad] Univ Tehran Med Sci, Sch Adv Technol Med, Dept Neurosci, Tehran, Iran.
   [Vali, Leila] Kuwait Univ, Fac Allied Hlth Sci, Dept Med Lab Sci, Sulibikhat, Kuwait.
   [Jahromi, Mehrnoush Moghaddasi] Lorestan Univ Med Sci, Sch Med, Dept Physiol, Khorramabad, Iran.
   [Taghizadeh, Ghorban] Iran Univ Med Sci, Fac Rehabil Sci, Dept Occupat Therapy, Tehran, Iran.
RP Sharifzadeh, M (corresponding author), Univ Tehran Med Sci, Fac Pharm, Dept Pharmacol & Toxicol, Tehran, Iran.
EM msharifzadeh@sina.tums.ac.ir
RI Taghizadeh, Ghorban/L-8609-2018; Taghizadeh, Ghorban/AAD-7167-2022;
   Khodagholi, Fariba/AAZ-4436-2020; Sanati, Mehdi/AAH-6634-2021
OI Taghizadeh, Ghorban/0000-0002-0145-9599; Taghizadeh,
   Ghorban/0000-0002-0145-9599; 
FU Tehran University of Medical Sciences (TUMS)Tehran University of Medical
   Sciences [92-02-33-23268]; Lorestan University of Medical Sciences
   [1283]
FX This work was supported by funds (No. 92-02-33-23268) from the Tehran
   University of Medical Sciences (TUMS) and Lorestan University of Medical
   Sciences (No. 1283). We thank Dr. Kian Azami and Dr. Ali Hosseini for
   their generous scientific advices and Mr. Ali Kazemi and Mr. Mehdi
   Gholami for their technical assistance.
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NR 67
TC 8
Z9 10
U1 0
U2 11
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0014-2999
EI 1879-0712
J9 EUR J PHARMACOL
JI Eur. J. Pharmacol.
PD FEB 5
PY 2017
VL 796
BP 54
EP 61
DI 10.1016/j.ejphar.2016.12.023
PG 8
WC Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA EJ9EL
UT WOS:000393529300007
PM 27993642
DA 2022-04-25
ER

PT J
AU Park, SH
   Park, SJ
   Kim, JO
   Shin, JH
   Kim, ES
   Jo, YK
   Kim, JS
   Park, SJ
   Jin, DH
   Hwang, JJ
   Lee, SJ
   Jeong, SY
   Lee, C
   Kim, I
   Cho, DH
AF Park, Seong Ho
   Park, So Jung
   Kim, Joo-Oh
   Shin, Ji Hyun
   Kim, Eun Sung
   Jo, Yoon Kyung
   Kim, Jae-Sung
   Park, So Jung
   Jin, Dong-Hoon
   Hwang, Jung Jin
   Lee, Seung Jin
   Jeong, Seong-Yun
   Lee, Chaeyoung
   Kim, InKi
   Cho, Dong-Hyung
TI Down-Regulation of Survivin by Nemadipine-A Sensitizes Cancer Cells to
   TRAIL-Induced Apoptosis
SO BIOMOLECULES & THERAPEUTICS
LA English
DT Article
DE TRAIL; Nemadipine-A; Sensitization; Cell death; H1299 cells
ID COLON-CARCINOMA CELLS; HUMAN-MELANOMA CELLS; MEDIATED APOPTOSIS;
   UP-REGULATION; EXPRESSION; ACTIVATION; RESISTANCE; PATHWAY; LIGAND;
   INHIBITION
AB The tumor necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL) is a member of the tumor necrosis factor family of cytokines. TRAIL selectively induces apoptotic cell death in various tumors and cancer cells, but it has little or no toxicity in normal cells. Agonism of TRAIL receptors has been considered to be a valuable cancer-therapeutic strategy. However, more than 85% of primary tumors are resistant to TRAIL, emphasizing the importance of investigating how to overcome TRAIL resistance. In this report, we have found that nemadipine-A, a cell-permeable L-type calcium channel inhibitor, sensitizes TRAIL-resistant cancer cells to this ligand. Combination treatments using TRAIL with nemadipine-A synergistically induced both the caspase cascade and apoptotic cell death, which were blocked by a pan caspase inhibitor (zVAD) but not by autophagy or a necrosis inhibitor. We further found that nemadipine-A, either alone or in combination with TRAIL, notably reduced the expression of survivin, an inhibitor of the apoptosis protein (IAP) family of proteins. Depletion of survivin by small RNA interference (siRNA) resulted in increased cell death and caspase activation by TRAIL treatment. These results suggest that nemadipine-A potentiates TRAIL-induced apoptosis by down-regulation of survivin expression in TRAIL resistant cells. Thus, combination of TRAIL with nemadipine-A may serve a new therapeutic scheme for the treatment of TRAIL resistant cancer cells, suggesting that a detailed study of this combination would be useful.
C1 [Park, Seong Ho] Hallym Univ, Ilsong Inst Life Sci, Anyang 431060, South Korea.
   [Park, So Jung; Kim, Joo-Oh; Shin, Ji Hyun; Kim, Eun Sung; Jo, Yoon Kyung; Cho, Dong-Hyung] Kyung Hee Univ, Grad Sch East West Med Sci, Yongin 446701, South Korea.
   [Kim, Jae-Sung] Korea Inst Radiol & Med Sci, Div Radiat Canc Res, Seoul 136706, South Korea.
   [Park, So Jung; Jin, Dong-Hoon; Hwang, Jung Jin; Lee, Seung Jin; Jeong, Seong-Yun; Kim, InKi] Asan Med Ctr, Asan Inst Life Sci, Seoul 138736, South Korea.
   [Jin, Dong-Hoon; Hwang, Jung Jin; Lee, Seung Jin; Jeong, Seong-Yun] Univ Ulsan, Coll Med, Asan Med Ctr, Inst Innovat Canc Res, Seoul 138736, South Korea.
   [Lee, Chaeyoung] Soongsil Univ, Dept Bioinformat & Life Sci, Seoul 156743, South Korea.
   [Kim, InKi] Univ Ulsan, Coll Med, Dept Med, Seoul 138736, South Korea.
RP Kim, I (corresponding author), Asan Med Ctr, Asan Inst Life Sci, Seoul 138736, South Korea.
EM ik.kim@amc.seoul.kr; dhcho@khu.ac.kr
RI Lee, Chaeyoung/C-7929-2012; Hwang, Jung Jin/F-3424-2014
OI Lee, Chaeyoung/0000-0002-2940-1778; Lee, Seung Jin/0000-0003-0625-7774
FU Kyung Hee University [KHU-20101839]
FX This research was supported by a grant from Kyung Hee University in 2010
   (KHU-20101839).
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U2 6
PU KOREAN SOC APPLIED PHARMACOLOGY
PI SEOUL
PA RM 805, KOREAN FEDERATION SCIENCE & TECHNOLOGY B/D, 635-4 YEOKSAM-DONG,
   KANGNAM-GU, SEOUL, 135-703, SOUTH KOREA
SN 1976-9148
EI 2005-4483
J9 BIOMOL THER
JI Biomol. Ther.
PD JAN 31
PY 2013
VL 21
IS 1
BP 29
EP 34
DI 10.4062/biomolther.2012.088
PG 6
WC Biochemistry & Molecular Biology; Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Pharmacology & Pharmacy
GA 284QK
UT WOS:000329334900004
PM 24009855
OA Green Published, Bronze, Green Submitted
DA 2022-04-25
ER

PT J
AU Ma, J
   Liu, L
   Ling, Y
   Zheng, JH
AF Ma, Jian
   Liu, Lei
   Ling, Yang
   Zheng, Jianhua
TI Polypeptide LTX-315 reverses the cisplatin chemoresistance of ovarian
   cancer cells via regulating Beclin-1/PI3K/mTOR signaling pathway
SO JOURNAL OF BIOCHEMICAL AND MOLECULAR TOXICOLOGY
LA English
DT Article
DE autophagy; cisplatin chemoresistance; LTX-315; ovarian cacner
ID ONCOLYTIC PEPTIDE LTX-315; COLON-CANCER; AUTOPHAGY; RESISTANCE; TUMOR
AB Objective Polypeptide LTX-315 induces immunogenic cell death, thus having the potential to improve the effect of anticancer treatment. However, the function of LTX-315 in reversing chemoresistance in ovarian cancer (OC) still remains elusive. Our study aims to decipher the effect of LTX-315 on reversing the chemoresistance of OC cells and explore its mechanism. Methods SKOV3, A2780, SKOV3/DDP, and A2780/DDP cells (cisplatin [DDP]-resistant cells] were treated with different concentrations of LTX-315 (10 and 20 mu mol/L), respectively. Cell counting kit-8 assay, Transwell assay, and flow cytometry were used to assess cell viability, migration, invasion, apoptosis rate, and cell cycle of the cells. Western blot was performed to examine the expression of cleaved caspase 3, caspase 3, cleaved Poly (ADP-ribose) polymerase (PARP), PARP, Bax, Bcl-2, Beclin-1, p-Akt, Akt, p-mammalian target of rapamycin (mTOR), and mTOR. Furthermore, OC cells were treated with autophagy inhibitor 3-methyladenine (3-MA), and "rescue experiments" were performed. Results DDP-resistant OC cell models were established, and LTX-315 treatment resulted in lower IC50 of DDP. In OC cells treated with LTX-315, the viability, migration, invasion and the expression of Bcl-2 of were repressed, but the apoptotic rate and the expression of cleaved caspase 3, cleaved PARP and Bax were increased, and the cell cycle was arrested. Moreover, LTX-315 promoted Beclin-1 expression level and inhibited p-Akt and p-mTOR expression levels, whereas 3-MA could partially reverse the biological effects of LTX-315 on OC cells. Conclusion LTX-315 can inhibit the resistance of OC cells to DDP in vitro and plays a role by regulating Beclin-1/phosphatidylinositol-3-kinase/mTOR signaling pathway.
C1 [Ma, Jian] Soochow Univ, Affiliated Hosp 3, Dept Med Oncol, Changzhou, Peoples R China.
   [Ma, Jian; Ling, Yang] Soochow Univ, Changzhou Tumor Hosp, Dept Med Oncol, Changzhou 213000, Jiangsu, Peoples R China.
   [Liu, Lei; Zheng, Jianhua] Harbin Med Univ, Clin Med Coll 1, Dept Obstet & Gynecol, Harbin, Peoples R China.
   [Liu, Lei] Harbin Med Univ, Affiliated Canc Hosp, Dept Obstet & Gynecol, Harbin, Peoples R China.
RP Ling, Y (corresponding author), Soochow Univ, Changzhou Tumor Hosp, Dept Med Oncol, Changzhou 213000, Jiangsu, Peoples R China.; Zheng, JH (corresponding author), Harbin Med Univ, Clin Med Coll 1, 23 Youzheng St, Harbin 150001, Heilongjiang, Peoples R China.
EM 2559512439@qq.com; kelanba5@163.com
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NR 25
TC 1
Z9 1
U1 9
U2 9
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1095-6670
EI 1099-0461
J9 J BIOCHEM MOL TOXIC
JI J. Biochem. Mol. Toxicol.
PD SEP
PY 2021
VL 35
IS 9
AR e22853
DI 10.1002/jbt.22853
EA JUL 2021
PG 8
WC Biochemistry & Molecular Biology; Toxicology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Toxicology
GA UQ0FH
UT WOS:000678805100001
PM 34309113
DA 2022-04-25
ER

PT J
AU de Franca, MNF
   Isidorio, RG
   Bonifacio, JHO
   dos Santos, EWP
   Santos, JF
   Ottoni, FM
   de Lucca, W
   Scher, R
   Alves, RJ
   Correa, CB
AF Farias de Franca, Mariana Nobre
   Isidorio, Raquel Geralda
   Oliveira Bonifacio, Joao Henrique
   Propheta dos Santos, Edmilson Willian
   Santos, Jileno Ferreira
   Ottoni, Flaviano Melo
   de Lucca Junior, Waldecy
   Scher, Ricardo
   Alves, Ricardo Jose
   Correa, Cristiane Bani
TI Anti-proliferative and pro-apoptotic activity of glycosidic derivatives
   of lawsone in melanoma cancer cell
SO BMC CANCER
LA English
DT Article
DE Lawsone; Melanoma; Cytotoxicity; Apoptosis; Flow cytometer; Migration;
   Clonogenic assay
ID MOLECULAR-MECHANISMS; COLON-CANCER; IN-VITRO; ASSAY; PROLIFERATION;
   THERAPEUTICS; CYTOTOXICITY; AUTOPHAGY
AB BackgroundMelanoma is a malignant cancer that affects melanocytes and is considered the most aggressive skin-type cancer. The prevalence for melanoma cancer for the last five year is about one million cases. The impact caused of this and other types of cancer, revel the importance of research into potential active compounds. The natural products are an important source of compounds with biological activity and research with natural products may enable the discovery of compounds with potential activity in tumor cells.MethodsThe Sulforhodamine B was used to determine cell density after treatment with lawsone derivatives. Apoptosis and necrosis were analyzed by flow cytometer. Morphological changes were observed by fluorescence using the Phalloidin/FITC and DAPI stains. The clonogenic and wound healing assays were used to analyze reduction of colonies formation and migratory capacity of melanoma cells, respectability.ResultsIn pharmacological screening, seven compounds derived from lawsone were considered to have high cytotoxic activity (GI>75%). Three compounds were selected to assess the inhibitory concentration for 50% of cells (IC50), and the compound 9, that has IC50 5.3 mu M in melanoma cells, was selected for further analyses in this cell line. The clonogenic assay showed that the compound is capable of reducing the formation of melanoma colonies at 10.6 mu M concentration. The compound induced apoptotic morphological changes in melanoma cells and increased by 50% the cells dying from apoptosis. Also, this compound reduced the migratory capacity of melanoma cells.ConclusionsThe results of this study showed that the evaluated lawsone derivatives have potential activity on tumor cells. The compound 9 is capable of inducing cell death by apoptosis in melanoma cells (B16F10).
C1 [Farias de Franca, Mariana Nobre; Oliveira Bonifacio, Joao Henrique; Propheta dos Santos, Edmilson Willian; Santos, Jileno Ferreira; Scher, Ricardo; Correa, Cristiane Bani] Univ Fed Sergipe, Dept Morphol, Lab Biol & Immunol Canc & Leishmania, Sao Cristovao, Sergipe, Brazil.
   [Farias de Franca, Mariana Nobre; Propheta dos Santos, Edmilson Willian; Correa, Cristiane Bani] Univ Fed Sergipe, Grad Program Hlth Sci, Aracaju, Sergipe, Brazil.
   [Isidorio, Raquel Geralda; Ottoni, Flaviano Melo; Alves, Ricardo Jose] Univ Fed Minas Gerais, Fac Pharm, Dept Pharmaceut Prod, Lab Pharmaceut Chem, Belo Horizonte, MG, Brazil.
   [de Lucca Junior, Waldecy] Univ Fed Sergipe, Dept Morphol, Lab Mol Neurosci Sergipe, Sao Cristovao, Sergipe, Brazil.
RP Correa, CB (corresponding author), Univ Fed Sergipe, Dept Morphol, Lab Biol & Immunol Canc & Leishmania, Sao Cristovao, Sergipe, Brazil.; Correa, CB (corresponding author), Univ Fed Sergipe, Grad Program Hlth Sci, Aracaju, Sergipe, Brazil.
EM crisbani@gmail.com
RI Correa, Cristiane Bani/AAR-9384-2020
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NR 56
TC 2
Z9 2
U1 0
U2 0
PU BMC
PI LONDON
PA CAMPUS, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
EI 1471-2407
J9 BMC CANCER
JI BMC Cancer
PD JUN 2
PY 2021
VL 21
IS 1
AR 662
DI 10.1186/s12885-021-08404-4
PG 13
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA SQ8TS
UT WOS:000660623100008
PM 34078316
OA gold, Green Published
DA 2022-04-25
ER

PT J
AU Xie, CM
   Wei, DP
   Zhao, LL
   Marchetto, S
   Mei, L
   Borg, JP
   Sun, Y
AF Xie, Chuan-Ming
   Wei, Dongping
   Zhao, Lili
   Marchetto, Sylvie
   Mei, Lin
   Borg, Jean-Paul
   Sun, Yi
TI Erbin is a novel substrate of the Sag-beta TrCP E3 ligase that regulates
   Kras(G12D)-induced skin tumorigenesis
SO JOURNAL OF CELL BIOLOGY
LA English
DT Article
ID COLON-CANCER CELLS; F-BOX PROTEIN; UBIQUITIN LIGASE;
   FUNCTIONAL-CHARACTERIZATION; ERBB2/HER2 RECEPTOR; KAPPA-B; K-RAS;
   AUTOPHAGY; DEGRADATION; SENESCENCE
AB SAG/RBX2 is the RING (really interesting new gene) component of Cullin-RING ligase, which is required for its activity. An organ-specific role of SAG in tumorigenesis is unknown. We recently showed that Sag/Rbx2, upon lung-targeted deletion, suppressed Kras(G12D)-induced tumorigenesis via inactivating NF-kappa B and mammalian target of rapamycin pathways. In contrast, we report here that, upon skin-targeted deletion, Sag significantly accelerated Kras(G12D)-induced papillomagenesis. In Kras(G12D)-expressing primary keratinocytes, Sag deletion promotes proliferation by inhibiting autophagy and senescence, by inactivating the Ras-Erk pathway, and by blocking reactive oxygen species (ROS) generation. This is achieved by accumulation of Erbin to block Ras activation of Raf and Nrf2 to scavenge ROS and can be rescued by knockdown of Nrf2 or Erbin. Simultaneous one-allele deletion of the Erbin-encoding gene Erbb2ip partially rescued the phenotypes. Finally, we characterized Erbin as a novel substrate of SAG-beta TrCP E3 ligase. By degrading Erbin and Nrf2, Sag activates the Ras-Raf pathway and causes ROS accumulation to trigger autophagy and senescence, eventually delaying Kras(G12D)-induced papillomagenesis and thus acting as a skin-specific tumor suppressor.
C1 [Xie, Chuan-Ming; Wei, Dongping] Univ Michigan, Dept Radiat Oncol, Div Radiat & Canc Biol, Ann Arbor, MI 48109 USA.
   [Zhao, Lili] Univ Michigan, Dept Radiat Oncol, Dept Biostat, Ann Arbor, MI 48109 USA.
   [Sun, Yi] Zhejiang Univ, Sch Med, Inst Translat Med, Hangzhou 310058, Zhejiang, Peoples R China.
   [Sun, Yi] Zhejiang Univ, Collaborat Innovat Ctr Diag & Treatment Infect Di, Hangzhou 310058, Zhejiang, Peoples R China.
   [Marchetto, Sylvie; Borg, Jean-Paul] INSERM, U1068, Canc Res Ctr Marseille Cell Polar Cell Signalling, F-13009 Marseille, France.
   [Marchetto, Sylvie; Borg, Jean-Paul] Inst J Paoli I Calmettes, F-13009 Marseille, France.
   [Marchetto, Sylvie; Borg, Jean-Paul] Aix Marseille Univ, F-13284 Marseille, France.
   [Marchetto, Sylvie; Borg, Jean-Paul] CNRS, UMR7258, F-13009 Marseille, France.
   [Mei, Lin] Georgia Regents Univ, Dept Neurosci & Regenerat Med, Med Coll Georgia, Augusta, GA 30912 USA.
   [Mei, Lin] Georgia Regents Univ, Dept Neurol, Med Coll Georgia, Augusta, GA 30912 USA.
RP Sun, Y (corresponding author), Univ Michigan, Dept Radiat Oncol, Div Radiat & Canc Biol, Ann Arbor, MI 48109 USA.
EM sunyi@umich.edu
RI Sun, Yi/K-1025-2014; Borg, Jean-Paul/AAX-8096-2020; Xie,
   Chuan-Ming/AAT-9557-2021
OI Sun, Yi/0000-0002-5841-4287; Borg, Jean-Paul/0000-0001-8418-3382; Xie,
   Chuan-Ming/0000-0003-4362-6612
FU National Cancer InstituteUnited States Department of Health & Human
   ServicesNational Institutes of Health (NIH) - USANIH National Cancer
   Institute (NCI) [CA118762, CA156744, CA171277]; La Ligue Contre le
   Cancer (Label Ligue); Institut Paoli-Calmettes grants; NATIONAL CANCER
   INSTITUTEUnited States Department of Health & Human ServicesNational
   Institutes of Health (NIH) - USANIH National Cancer Institute (NCI)
   [R01CA156744, R01CA118762, R01CA171277, P30CA046592] Funding Source: NIH
   RePORTER
FX This work was supported by National Cancer Institute grants (CA118762,
   CA156744, and CA171277) to Y. Sun and by La Ligue Contre le Cancer
   (Label Ligue) and Institut Paoli-Calmettes grants to J.-P. Borg. J.-P.
   Borg is a member of Institut Universitaire de France.
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NR 70
TC 19
Z9 19
U1 1
U2 11
PU ROCKEFELLER UNIV PRESS
PI NEW YORK
PA 950 THIRD AVE, 2ND FLR, NEW YORK, NY 10022 USA
SN 0021-9525
EI 1540-8140
J9 J CELL BIOL
JI J. Cell Biol.
PD JUN 8
PY 2015
VL 209
IS 5
BP 721
EP 737
DI 10.1083/jcb.201411104
PG 17
WC Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Cell Biology
GA CK1AR
UT WOS:000355938200008
PM 26056141
OA Bronze, Green Published, Green Submitted
DA 2022-04-25
ER

PT J
AU Pellegrini, P
   Serviss, JT
   Lundback, T
   Bancaro, N
   Mazurkiewicz, M
   Kolosenko, I
   Yu, D
   Haraldsson, M
   D'Arcy, P
   Linder, S
   De Milito, A
AF Pellegrini, Paola
   Serviss, Jason T.
   Lundback, Thomas
   Bancaro, Nicolo
   Mazurkiewicz, Magdalena
   Kolosenko, Iryna
   Yu, Di
   Haraldsson, Martin
   D'Arcy, Padraig
   Linder, Stig
   De Milito, Angelo
TI A drug screening assay on cancer cells chronically adapted to acidosis
SO CANCER CELL INTERNATIONAL
LA English
DT Article
DE Tumor acidosis; Drug resistance; RNAseq; Verteporfin; Drug screening
ID VERTEPORFIN-PHOTODYNAMIC THERAPY; EXTRACELLULAR PH; MELANOMA-CELLS;
   TUMOR ACIDITY; RESISTANCE; AUTOPHAGY; LIGHT; PROLIFERATION; YAP
AB Background: Drug screening for the identification of compounds with anticancer activity is commonly performed using cell lines cultured under normal oxygen pressure and physiological pH. However, solid tumors are characterized by a microenvironment with limited access to nutrients, reduced oxygen supply and acidosis. Tumor hypoxia and acidosis have been identified as important drivers of malignant progression and contribute to multicellular resistance to different forms of therapy. Tumor acidosis represents an important mechanism mediating drug resistance thus the identification of drugs active on acid-adapted cells may improve the efficacy of cancer therapy.
   Methods: Here, we characterized human colon carcinoma cells (HCT116) chronically adapted to grow at pH 6.8 and used them to screen the Prestwick drug library for cytotoxic compounds. Analysis of gene expression profiles in parental and low pH-adapted cells showed several differences relating to cell cycle, metabolism and autophagy.
   Results: The screen led to the identification of several compounds which were further selected for their preferential cytotoxicity towards acid-adapted cells. Amongst 11 confirmed hits, we primarily focused our investigation on the benzoporphyrin derivative Verteporfin (VP). VP significantly reduced viability in low pH-adapted HCT116 cells as compared to parental HCT116 cells and normal immortalized epithelial cells. The cytotoxic activity of VP was enhanced by light activation and acidic pH culture conditions, likely via increased acid-dependent drug uptake. VP displayed the unique property to cause light-dependent cross-linking of proteins and resulted in accumulation of polyubiquitinated proteins without inducing inhibition of the proteasome.
   Conclusions: Our study provides an example and a tool to identify anticancer drugs targeting acid-adapted cancer cells.
C1 [Pellegrini, Paola; Serviss, Jason T.; Bancaro, Nicolo; Mazurkiewicz, Magdalena; Kolosenko, Iryna; Yu, Di; De Milito, Angelo] Karolinska Inst, Dept Oncol Pathol, Canc Ctr Karolinska, R8 00, S-17176 Stockholm, Sweden.
   [Lundback, Thomas; Haraldsson, Martin] Chem Biol Consortium Sweden, Sci Life Lab, Stockholm, Sweden.
   [D'Arcy, Padraig; Linder, Stig] Linkoping Univ, Dept Med & Hlth Sci, S-58183 Linkoping, Sweden.
   [Lundback, Thomas] AstraZeneca, IMED Biotech Unit, Discovery Sci, Gothenburg, Sweden.
RP De Milito, A (corresponding author), Karolinska Inst, Dept Oncol Pathol, Canc Ctr Karolinska, R8 00, S-17176 Stockholm, Sweden.
EM angelo.de-milito@ki.se
RI Lundbäck, Thomas/G-8076-2018; D'Arcy, Pádraig/F-7633-2018; D'Arcy,
   Pádraig/AAB-5045-2019
OI Lundbäck, Thomas/0000-0002-8145-7808; D'Arcy,
   Pádraig/0000-0001-6671-7600; D'Arcy, Pádraig/0000-0001-6671-7600; De
   Milito, Angelo/0000-0003-2591-2914; Serviss, Jason/0000-0002-5778-7014
FU Swedish Cancer SocietySwedish Cancer Society [CAN 2012/415]; Association
   for International Cancer Research [11-0522]; Robert Lundberg Foundation
FX This work was supported by Grants from the Swedish Cancer Society (Grant
   #CAN 2012/415), the Association for International Cancer Research (Grant
   #11-0522) and the Robert Lundberg Foundation.
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EI 1475-2867
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PD SEP 25
PY 2018
VL 18
AR 147
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PG 15
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA GV1GK
UT WOS:000445819100001
PM 30263014
OA Green Published, gold
DA 2022-04-25
ER

PT J
AU Kumari, M
   Purohit, MP
   Patnaik, S
   Shukla, Y
   Kumar, P
   Gupta, KC
AF Kumari, Manisha
   Purohit, Mahaveer Prasad
   Patnaik, Satyakam
   Shukla, Yogeshwer
   Kumar, Pradeep
   Gupta, Kailash Chand
TI Curcumin loaded selenium nanoparticles synergize the anticancer
   potential of doxorubicin contained in self-assembled, cell receptor
   targeted nanoparticles
SO EUROPEAN JOURNAL OF PHARMACEUTICS AND BIOPHARMACEUTICS
LA English
DT Article
DE Doxorubicin; Nanoparticles; Selenium; Curcumin; Apoptosis; Ehrlich's
   ascites carcinoma
ID NF-KAPPA-B; EPITHELIAL-MESENCHYMAL TRANSITION; COLON-CANCER CELLS;
   DRUG-DELIVERY; TUMOR-CELLS; HYDROGEN-PEROXIDE; HYALURONIC-ACID;
   IN-VITRO; APOPTOSIS; MECHANISMS
AB Doxorubicin (DOX) has been extensively used to treat a wide range of cancers in free and nanotized form. Nanotization of DOX has alleviated its toxicity and efflux-mediated resistance. However, frequent upregulation of anti-apoptotic pathways, chemotherapy-enhanced inflammation, and epithelial-mesenchymal transition (EMT), present additional aspects of cellular DOX resistance. Nanoparticle-mediated combination therapy of DOX with additional anticancer agents is expected to offer greater therapeutic benefit by alleviating the overall drug resistance. We synthesized CD44-targeted DOX loaded nanoparticles (PSHA-DOXNPs) and evaluated their anticancer efficacy in combination with curcumin loaded selenium nanoparticles (Se-Cur NPs), previously developed by our group (Kumari et al., 2017). Combination of these nanoparticles (NPs) increased ROS level, decreased mitochondrial membrane potential, induced cell cycle arrest and apoptosis in HCT116 cells. This combination decreased the expressions of NF kappa B, Phospho-NF kappa B, EMT-metastasis-associated proteins (Snail, Vimentin, N-cadherin, CD44, MMP-2 and MMP-9), autophagy-associated proteins (Beclin-1 and LC-3BII), as well as anti-apoptotic protein Bcl-2, increased the expression of pro-apoptotic protein Bax, and increased cyt c release, which indicated decrease in inflammation, metastasis, and autophagy with increase in apoptosis. Moreover, the combination of NPs decreased tumor burden and increased survival of Ehrlich's ascites carcinoma (EAC)-bearing mice.
C1 [Kumari, Manisha; Kumar, Pradeep; Gupta, Kailash Chand] CSIR Inst Genom & Integrat Biol, Delhi Univ Campus,Mall Rd, Delhi 110007, India.
   [Purohit, Mahaveer Prasad; Patnaik, Satyakam; Shukla, Yogeshwer] CSIR Indian Inst Toxicol Res, MG Marg, Lucknow 226001, Uttar Pradesh, India.
   [Kumari, Manisha; Purohit, Mahaveer Prasad] Acad Sci & Innovat Res AcSIR, New Delhi, India.
RP Gupta, KC (corresponding author), CSIR Inst Genom & Integrat Biol, Delhi Univ Campus,Mall Rd, Delhi 110007, India.
EM kcgupta9@gmail.com
RI Kumari, Manisha/AAX-5517-2021; Patnaik, Satyakam/O-3617-2019
OI Patnaik, Satyakam/0000-0003-4920-236X; KUMAR,
   PRADEEP/0000-0001-5874-8191
FU CSIR network projectCouncil of Scientific & Industrial Research (CSIR) -
   India [BSC0112]; Indian Council of Medical Research (ICMR), New
   DelhiIndian Council of Medical Research (ICMR); CSIRCouncil of
   Scientific & Industrial Research (CSIR) - India
FX The authors gratefully acknowledge the financial support from CSIR
   network project BSC0112. KCG thanks, Indian Council of Medical Research
   (ICMR), New Delhi for awarding Dr. A.S. Paintal Distinguished Scientist
   Chair of ICMR. MK thanks CSIR for providing Senior Research Fellowship.
   Dr. P.N. Saxena, CSIR-IITR is acknowledged for helping in SEM studies.
   Mr. Jaishankar, CSIR-IITR and Ms. N. Arjaria, CSIR-IITR, are
   acknowledged for their help in TEM studies. Mr. Puneet Khare, CSIR-IITR
   is acknowledged for helping in flow cytometry-based experiments. Mr.
   S.H.N. Naqvi, CSIR-IITR is acknowledged for helping in animal studies.
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NR 70
TC 21
Z9 21
U1 4
U2 74
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0939-6411
EI 1873-3441
J9 EUR J PHARM BIOPHARM
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BP 185
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DI 10.1016/j.ejpb.2018.06.030
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SC Pharmacology & Pharmacy
GA GQ6SN
UT WOS:000441855500020
PM 29969665
DA 2022-04-25
ER

PT J
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   Pudelko, K
   Stadler, M
   Walter, S
   Unterleuthner, D
   Unger, C
   Kramer, N
   Hengstschlager, M
   Kenner, L
   Pfeiffer, D
   Krupitza, G
   Dolznig, H
AF Riedl, Angelika
   Schlederer, Michaela
   Pudelko, Karoline
   Stadler, Mira
   Walter, Stefanie
   Unterleuthner, Daniela
   Unger, Christine
   Kramer, Nina
   Hengstschlager, Markus
   Kenner, Lukas
   Pfeiffer, Dagmar
   Krupitza, Georg
   Dolznig, Helmut
TI Comparison of cancer cells in 2D vs 3D culture reveals differences in
   AKT-mTOR-S6K signaling and drug responses
SO JOURNAL OF CELL SCIENCE
LA English
DT Article
DE AKT-mTOR-S6K signaling; MAPK signaling; Spheroid; Drug response
ID TUMOR-CELLS; LINE CACO-2; MTOR; APOPTOSIS; MODELS; FIBROBLASTS;
   ACTIVATION; RESISTANCE; SPHEROIDS; AUTOPHAGY
AB Three-dimensional (3D) cancer models are used as preclinical systems to mimic physiologic drug responses. We provide evidence for strong changes of proliferation and metabolic capacity in three dimensions by systematically analyzing spheroids of colon cancer cell lines. Spheroids showed relative lower activities in the AKT, mammalian target of rapamycin (mTOR) and S6K (also known as RPS6KB1) signaling pathway compared to cells cultured in two dimensions. We identified spatial alterations in signaling, as the level of phosphorylated RPS6 decreased from the spheroid surface towards the center, which closely coordinated with the tumor areas around vessels in vivo. These 3D models displayed augmented antitumor responses to AKT-mTOR-S6K or mitogen-activated protein kinase (MAPK) pathway inhibition compared to those in 2D models. Inhibition of AKT-mTOR-S6K resulted in elevated ERK phosphorylation in 2D culture, whereas under these conditions, ERK signaling was reduced in spheroids. Inhibition of MEK1 (also known as MAP2K1) led to decreased AKT-mTOR-S6K signaling in 3D but not in 2D culture. These data indicate a distinct rewiring of signaling in 3D culture and during treatment. Detached tumor-cell clusters in vessels, in addition to circulating single tumor cells, play a putative role inmetastasis in human cancers. Hence, the understanding of signaling in spheroids and the responses in the 3D models upon drug treatment might be beneficial for anti-cancer therapies.
C1 [Riedl, Angelika; Pudelko, Karoline; Stadler, Mira; Walter, Stefanie; Unterleuthner, Daniela; Unger, Christine; Kramer, Nina; Hengstschlager, Markus; Dolznig, Helmut] Med Univ Vienna, Inst Med Genet, Wahringer Str 10, A-1090 Vienna, Austria.
   [Schlederer, Michaela; Kenner, Lukas; Krupitza, Georg] Med Univ Vienna, Clin Inst Pathol, Wahringer Gurtel 18-20, A-1090 Vienna, Austria.
   [Schlederer, Michaela; Kenner, Lukas] Ludwig Boltzmann Inst Canc Res, Wahringer Str 13A, A-1090 Vienna, Austria.
   [Kenner, Lukas] Univ Vet Med Vienna, UPLA, A-1210 Vienna, Austria.
   [Pfeiffer, Dagmar] Med Univ Graz, Inst Cell Biol Histol & Embryol, Harrachgasse 21, A-8010 Graz, Austria.
   [Riedl, Angelika] Boehringer Ingelheim RCV GmbH & Co KG, Dr Boehringer Gasse 5-11, A-1121 Vienna, Austria.
RP Dolznig, H (corresponding author), Med Univ Vienna, Inst Med Genet, Wahringer Str 10, A-1090 Vienna, Austria.
EM helmut.dolznig@meduniwien.ac.at
RI Dolznig, Helmut/L-7005-2015
OI Dolznig, Helmut/0000-0002-6063-3585; Kenner, Lukas/0000-0003-2184-1338;
   Brislinger, Dagmar/0000-0002-7319-5377; Kramer,
   Nina/0000-0002-9058-8076; Krupitza, Georg/0000-0003-2949-7906
FU Niederosterreichische Forschungs- und Bildungsges.m.b.H (NFB); Austrian
   Academy of Sciences (OAW)
FX This work was supported by the Niederosterreichische Forschungs- und
   Bildungsges.m.b.H (NFB). A.R. was a recipient of a DOC fellowship from
   the Austrian Academy of Sciences (OAW).
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NR 50
TC 215
Z9 221
U1 7
U2 42
PU COMPANY BIOLOGISTS LTD
PI CAMBRIDGE
PA BIDDER BUILDING, STATION RD, HISTON, CAMBRIDGE CB24 9LF, ENGLAND
SN 0021-9533
EI 1477-9137
J9 J CELL SCI
JI J. Cell Sci.
PD JAN 1
PY 2017
VL 130
IS 1
SI SI
BP 203
EP 218
DI 10.1242/jcs.188102
PG 16
WC Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Cell Biology
GA EG5ST
UT WOS:000391105300023
PM 27663511
OA Green Published
HC Y
HP N
DA 2022-04-25
ER

PT J
AU Bhol, CS
   Panigrahi, DP
   Praharaj, PP
   Mahapatra, KK
   Patra, S
   Mishra, SR
   Behera, BP
   Bhutia, SK
AF Bhol, Chandra S.
   Panigrahi, Debasna P.
   Praharaj, Prakash P.
   Mahapatra, Kewal K.
   Patra, Srimanta
   Mishra, Soumya R.
   Behera, Bishnu P.
   Bhutia, Sujit K.
TI Epigenetic modifications of autophagy in cancer and cancer therapeutics
SO SEMINARS IN CANCER BIOLOGY
LA English
DT Article
DE Autophagy; Epigenetics; Cancer; DNA methylation; Histone modification;
   miRNA
ID INCREASES DRUG-RESISTANCE; INDUCED DOWN-REGULATION; TUMOR-SUPPRESSOR;
   CELL-PROLIFERATION; GASTRIC-CANCER; INHIBITS AUTOPHAGY; DNA METHYLATION;
   HEPATOCELLULAR-CARCINOMA; ACTIVATING AUTOPHAGY; COLORECTAL-CANCER
AB Epigenetic alterations, such as DNA methylation, histone modifications and miRNAs, have a significant role play in malignant cellular transformation and metastasis. On the other hand, autophagy has been reported to perform context-dependent roles in cancer; at times, it becomes lethal and abolishes tumorigenesis, whereas, at other instances, it protects cancer cells by providing a rescue mechanism under adverse conditions. Although epigenetics and autophagy are two important and independent cellular processes, various oncogenic and oncosuppressor proteins involve autophagy through epigenetic modifications and different signaling pathways, thereby regulating tumor growth and therapeutic response. Moreover, the importance of epigenetic modification of autophagy in cancer is reflected through its involvement in cancer stem cell maintenance, which in turn, contributes to tumor cell viability during dormancy leading to tumor recurrence. The effects of epigenetic modifications of autophagy in cancer is still ambiguous and less acknowledged; therefore, efforts have been made to understand its detail underlying mechanism to unveil new targets and avenues for better prognosis and diagnosis of cancer.
C1 [Bhol, Chandra S.; Panigrahi, Debasna P.; Praharaj, Prakash P.; Mahapatra, Kewal K.; Patra, Srimanta; Mishra, Soumya R.; Behera, Bishnu P.; Bhutia, Sujit K.] Natl Inst Technol Rourkela, Dept Life Sci, Canc & Cell Death Lab, Sundergarh, Odisha, India.
RP Bhutia, SK (corresponding author), Natl Inst Technol Rourkela, Dept Life Sci, Canc & Cell Death Lab, Sundergarh, Odisha, India.
EM sujitb@nitrkl.ac.in
RI Bhol, Chandra Sekhar/W-6462-2019; Praharaj, Prakash P./J-5515-2018
OI Bhol, Chandra Sekhar/0000-0003-3397-6483; Praharaj, Prakash
   P./0000-0003-0425-5118; Patra, Srimanta/0000-0002-0166-0903; Behera,
   Bishnu Prasad/0000-0003-0326-6050
FU Government of India, Ministry of Human Resource DevelopmentMinistry of
   Human Resource Development (MHRD), Government of India; Board of
   Research in Nuclear Sciences (BRNS), Department of Atomic Energy
   (DAE)Department of Atomic Energy (DAE)Board of Research in Nuclear
   Sciences (BRNS) [37 (1)/14/38/2016-BRNS/37276]; Science and Engineering
   Research Board (SERB), Department of Science and Technology
   [EMR/2016/001246]
FX We thank National Institute of Technology Rourkela for providing the
   facility for this research work. CSB is obliged to Government of India,
   Ministry of Human Resource Development for providing fellowship.
   Research support was partly provided by the Board of Research in Nuclear
   Sciences (BRNS) [Number: 37 (1)/14/38/2016-BRNS/37276], Department of
   Atomic Energy (DAE); Science and Engineering Research Board (SERB)
   [Number: EMR/2016/001246], Department of Science and Technology.
   Moreover, the authors apologize to investigators whose original
   contributions have not been cited; we have chosen to cite recent
   publications in which details of such contributions can be found.
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NR 148
TC 14
Z9 15
U1 3
U2 20
PU ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD
PI LONDON
PA 24-28 OVAL RD, LONDON NW1 7DX, ENGLAND
SN 1044-579X
EI 1096-3650
J9 SEMIN CANCER BIOL
JI Semin. Cancer Biol.
PD NOV
PY 2020
VL 66
SI SI
BP 22
EP 33
DI 10.1016/j.semcancer.2019.05.020
PG 12
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA OA7YO
UT WOS:000577996900004
PM 31158463
DA 2022-04-25
ER

PT J
AU Lenis-Rojas, OA
   Fernandes, AR
   Roma-Rodrigues, C
   Baptista, PV
   Marques, F
   Perez-Fernandez, D
   Guerra-Varela, J
   Sanchez, L
   Vazquez-Garcia, D
   Torres, ML
   Fernandez, A
   Fernandez, JJ
AF Lenis-Rojas, O. A.
   Fernandes, A. R.
   Roma-Rodrigues, C.
   Baptista, P. V.
   Marques, F.
   Perez-Fernandez, D.
   Guerra-Varela, J.
   Sanchez, L.
   Vazquez-Garcia, D.
   Lopez Torres, M.
   Fernandez, A.
   Fernandez, J. J.
TI Heteroleptic mononuclear compounds of ruthenium(II): synthesis,
   structural analyses, in vivo antitumor activity and in vivo toxicity on
   zebrafish embryost
SO DALTON TRANSACTIONS
LA English
DT Article
ID AUTOPHAGIC CELL-DEATH; POLYPYRIDYL COMPLEXES; DNA-BINDING; DEVELOPMENTAL
   TOXICITY; ANTICANCER ACTIVITY; MODEL SYSTEM; DRUG; PLATINUM; MECHANISMS;
   LIGANDS
AB The limitations of platinum complexes in cancer treatment have motivated the extensive investigation into other metal complexes such as ruthenium. We herein present the synthesis and characterization of a new family of ruthenium compounds 1a-5a with the general formula [Ru(bipy)(2)L][CF3SO3](2) (bipy = 2,2'-bipyridine; L = bidentate ligand: N,N; N,P; P,P; P,As) which have been characterized by elemental analysis, ES-MS, H-1 and P-31-{H-1} NMR, FTIR and conductivity measurements. The molecular structures of four Ru(II) complexes were determined by single crystal X-ray diffraction. All compounds displayed moderate cytotoxic activity in vitro against human A2780 ovarian, MCF7 breast and HCT116 colorectal tumor cells. Compound 5a was the most cytotoxic compound against A2780 and MCF7 tumor cells with an IC50 of 4.75 +/- 2.82 mu M and 20.02 +/- 1.46 mu M, respectively. The compounds showed no cytotoxic effect on normal human primary fibroblasts but rather considerable selectivity for A2780, MCF7 and HCT116 tumor cells. All compounds induce apoptosis and autophagy in A2780 ovarian carcinoma cells and some nuclear DNA fragmentation. All compounds interact with CT-DNA with intrinsic binding constants in the order 1a > 4a > 2a > 3a > 5a. The observed hyperchromic effect may be due to the electrostatic interaction between positively charged cations and the negatively charged phosphate backbone at the periphery of the double helix-CT-DNA. Interestingly, compound la shows a concentration dependent DNA double strand cleavage. In addition in vivo toxicity has been evaluated on zebrafish embryos unveiling the differential toxicity between the compounds, with LC50 ranging from 8.67 mg L-1 for compound la to 170.30 mg L-1 for compound 2a.
C1 [Lenis-Rojas, O. A.; Vazquez-Garcia, D.; Lopez Torres, M.; Fernandez, A.; Fernandez, J. J.] Univ A Coruna, Dept Quim Fundamental, La Coruna 15008, Spain.
   [Lenis-Rojas, O. A.; Vazquez-Garcia, D.; Lopez Torres, M.; Fernandez, A.; Fernandez, J. J.] Univ A Coruna, CICA, La Coruna 15008, Spain.
   [Fernandes, A. R.; Roma-Rodrigues, C.; Baptista, P. V.] Univ Nova Lisboa, Fac Ciencias & Tecnol, Dept Ciencias Vida, UCIBIO, Campus Caparica, P-2829516 Caparica, Portugal.
   [Marques, F.] Univ Lisbon, Inst Super Tecn, C2TN, Estr Nacl 10 Km 139-7, P-2695066 Bobadela, Lrs, Portugal.
   [Perez-Fernandez, D.; Guerra-Varela, J.; Sanchez, L.] Univ Santiago de Compostela, Fac Vet, Dept Zool Genet & Antropol Fis, Lugo 27002, Spain.
RP Fernandez, JJ (corresponding author), Univ A Coruna, Dept Quim Fundamental, La Coruna 15008, Spain.; Fernandez, JJ (corresponding author), Univ A Coruna, CICA, La Coruna 15008, Spain.; Fernandes, AR (corresponding author), Univ Nova Lisboa, Fac Ciencias & Tecnol, Dept Ciencias Vida, UCIBIO, Campus Caparica, P-2829516 Caparica, Portugal.
EM ma.fernandes@fct.unl.pt; lujjfs@udc.es
RI Digna, Vázquez García/L-6288-2014; Pérez-Fernández, David/D-3762-2017;
   Baptista, Pedro/P-3182-2019; López-Torres, Margarita/L-6072-2014;
   Fernández Sánchez, Jesús José/L-5960-2014; Roma-Rodrigues,
   Catarina/AAT-5658-2021; López, Alberto A. Fernández/L-6449-2014; Gómez,
   ACUIGEN/ABD-5337-2020; Rojas, Oscar/ABE-2206-2021; Sánchez,
   Laura/L-2411-2014; Roma-Rodrigues, Catarina/S-6144-2016; Marques,
   Fernanda M/J-9790-2013; Fernandes, Alexandra R/C-7465-2011
OI Digna, Vázquez García/0000-0002-2255-5651; Baptista,
   Pedro/0000-0001-5255-7095; López-Torres, Margarita/0000-0003-1288-5128;
   Fernández Sánchez, Jesús José/0000-0003-4938-0342; Roma-Rodrigues,
   Catarina/0000-0002-8676-6562; López, Alberto A.
   Fernández/0000-0003-2504-6016; Rojas, Oscar/0000-0002-5914-5787;
   Sánchez, Laura/0000-0001-7927-5303; Roma-Rodrigues,
   Catarina/0000-0002-8676-6562; Marques, Fernanda M/0000-0001-8440-5299;
   Fernandes, Alexandra R/0000-0003-2054-4438; Guerra-Varela,
   Jorge/0000-0002-8365-7125
FU Xunta de Galicia (Galicia, Spain) under the Grupos de Referencia
   Competitiva Programme [GRC2014/042]; Universidade da Coruna; Universidad
   de Santiago de Compostela [GRC2014/010]; Xunta de GaliciaXunta de
   GaliciaEuropean Commission [EM2014/056]; FCTPortuguese Foundation for
   Science and TechnologyEuropean Commission [UID/Multi/04349/2013];
   FCT/MEC [UID/Multi/04378/2013]; ERDFEuropean Commission
   [POCI-01-0145-FEDER-007728]
FX This work was made possible thanks to the financial support received
   from the Xunta de Galicia (Galicia, Spain) under the Grupos de
   Referencia Competitiva Programme: Project GRC2014/042, Universidade da
   Coruna; and Project GRC2014/010, Universidad de Santiago de Compostela.
   DVG gratefully acknowledge the Xunta de Galicia support through
   EM2014/056 project. C2TN/IST author gratefully acknowledge the FCT
   support through UID/Multi/04349/2013 project. UCIBIO authors were
   financed by national funds from FCT/MEC (UID/Multi/04378/2013) and
   co-financed by the ERDF under the PT2020 Partnership Agreement
   (POCI-01-0145-FEDER-007728).
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NR 96
TC 37
Z9 37
U1 0
U2 52
PU ROYAL SOC CHEMISTRY
PI CAMBRIDGE
PA THOMAS GRAHAM HOUSE, SCIENCE PARK, MILTON RD, CAMBRIDGE CB4 0WF, CAMBS,
   ENGLAND
SN 1477-9226
EI 1477-9234
J9 DALTON T
JI Dalton Trans.
PD DEC 21
PY 2016
VL 45
IS 47
BP 19127
EP 19140
DI 10.1039/c6dt03591d
PG 14
WC Chemistry, Inorganic & Nuclear
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Chemistry
GA EF1KE
UT WOS:000390082900039
PM 27868117
DA 2022-04-25
ER

PT J
AU Lee, MS
   Kim, MS
   Yoo, JK
   Lee, JY
   Ju, JE
   Jeong, YK
AF Lee, Mi So
   Kim, Mi-Sook
   Yoo, Jae Kuk
   Lee, Ji Young
   Ju, Jae Eun
   Jeong, Youn Kyoung
TI Enhanced anticancer effects of a mixture of low-dose mushrooms and Panax
   ginseng root extracts in human colorectal cancer cells
SO ONCOLOGY REPORTS
LA English
DT Article
DE anticancer effect; G2/M arrest; human colorectal cancer; mushroom; Panax
   ginseng; apoptosis; autophagy; DNA damage repair
ID PHELLINUS-LINTEUS; CYCLE ARREST; CORDYCEPS-MILITARIS; APOPTOSIS;
   POLYSACCHARIDE
AB Worldwide, colorectal cancer is the third most common cancer in men and the second most common in women. As conventional colorectal cancer therapies result in various side effects, there is a need for adjuvant therapy that can enhance the conventional therapies without complications. In this study, we investigated the anticancer effects of combined mixture of the several medicinal mushrooms and Panax ginseng root extracts (also called Amex7) as an adjuvant compound in the treatment of human colorectal cancer. We observed the in vivo inhibitory effect of Amex7 (1.25, 6.25, and 12.5 ml/kg, oral administration, twice daily) on tumor growth in a mouse model xenografted with HT-29 human colorectal cancer cells. In vitro, at 6, 12, and 24 h after 4% Amex7 treatment, we analyzed cell cycle by flow cytometry and the expression levels of cell cycle progression, apoptosis, and DNA damage repair-related proteins using immunoblotting and immunofluorescence staining in HT-29 cell line. As a result, Amex7 significantly suppressed tumor growth in HT-29 human colorectal cancer cells and xenografts. In vitro, Amex7 induced G2/M arrest through the regulation of cell cycle proteins and cell death by apoptosis and autophagy. Additionally, Amex7 consistently induced DNA damage and delayed the repair of Amex7-induced DNA damage by reducing the level of HR repair proteins. In conclusion, Amex7 enhanced anticancer effects through the induction of G2/M arrest and cell death, including apoptosis and autophagy. Furthermore, Amex7 impaired DNA damage repair. The present study provides a scientific rationale for the clinical use of a combined mixture of medicinal mushrooms and P. ginseng root extracts as an adjuvant treatment in human colorectal cancer.
C1 [Lee, Mi So; Lee, Ji Young; Ju, Jae Eun; Jeong, Youn Kyoung] Korea Inst Radiol & Med Sci, Radiat Nonclin Ctr, 75 Nowon Ro, Seoul 01812, South Korea.
   [Kim, Mi-Sook] Korea Inst Radiol & Med Sci, Dept Radiat Oncol, 75 Nowon Ro, Seoul 01812, South Korea.
   [Yoo, Jae Kuk] Han Kook Shin Yak Pharmaceut Co Ltd, Nonsan 33023, South Korea.
RP Jeong, YK (corresponding author), Korea Inst Radiol & Med Sci, Radiat Nonclin Ctr, 75 Nowon Ro, Seoul 01812, South Korea.; Kim, MS (corresponding author), Korea Inst Radiol & Med Sci, Dept Radiat Oncol, 75 Nowon Ro, Seoul 01812, South Korea.
EM mskim@kirams.re.kr; amy3523@kirams.re.kr
FU Korea Institute of Radiological and Medical Sciences (KIRAMS) - Ministry
   of Science, ICT and Future Planning, Republic of Korea [1711045548]
FX This study was supported by a grant of the Korea Institute of
   Radiological and Medical Sciences (KIRAMS), funded by Ministry of
   Science, ICT and Future Planning, Republic of Korea (no. 1711045548).
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NR 27
TC 1
Z9 2
U1 0
U2 21
PU SPANDIDOS PUBL LTD
PI ATHENS
PA POB 18179, ATHENS, 116 10, GREECE
SN 1021-335X
EI 1791-2431
J9 ONCOL REP
JI Oncol. Rep.
PD SEP
PY 2017
VL 38
IS 3
BP 1597
EP 1604
DI 10.3892/or.2017.5796
PG 8
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA FB7CM
UT WOS:000406298700029
PM 28714027
OA Bronze
DA 2022-04-25
ER

PT J
AU Sklirou, A
   Papanagnou, ED
   Fokialakis, N
   Trougakos, IP
AF Sklirou, Aimilia
   Papanagnou, Eleni-Dimitra
   Fokialakis, Nikolas
   Trougakos, Ioannis P.
TI Cancer chemoprevention via activation of proteostatic modules
SO CANCER LETTERS
LA English
DT Review
DE Cancer prevention; Proteostasis network; Natural products; Nrf2;
   Chemopreventive agents
ID UNFOLDED PROTEIN RESPONSE; LIFE-SPAN; INCREASED SUSCEPTIBILITY;
   OXIDOREDUCTASE-1 DEFICIENCY; MOLECULAR CHAPERONES; COLON CARCINOGENESIS;
   PROTEASOME ACTIVITY; SIGNALING PATHWAYS; DIETARY CURCUMIN; MOUSE SKIN
AB Proteins carry out the majority of cellular functions and maintain cellular homeodynamics mostly by participating in multimeric assemblies that operate as protein machines. Proteome quality control is thus critical for cellular functionality, and it is carried out through the curating activity of the proteostasis network (PN). Key components of the PN are the protein synthesis and trafficking modules, the endoplasmic reticulum unfolded protein response, molecular chaperones, and the two main degradation machineries, namely the ubiquitin proteasome and autophagy lysosome pathways. Part of the PN are also several stress responsive pathways, including nuclear factor erythroid 2-related factor 2 (Nrf2), which mobilises genomic responses against oxidative and/or xenobiotic damage. Nevertheless, the gradual accumulation of stressors during ageing or earlier due to lifestyle results in an increasingly damaged and unstable proteome. This outcome may then increase genomic instability due to reduced DNA replication fidelity or repair, leading to various age-related diseases such as cancer. Considering that the activation of proteostatic modules exerts anti-ageing effects in model organisms, we present herein a synopsis of studies showing that proteostatic modules activation (e.g. by natural products) represents a promising tumour-chemopreventive approach. (C) 2017 Elsevier B.V. All rights reserved.
C1 [Sklirou, Aimilia; Papanagnou, Eleni-Dimitra; Trougakos, Ioannis P.] Univ Athens, Dept Cell Biol & Biophys, Fac Biol, Panepistimiopolis, Athens 15784, Greece.
   [Fokialakis, Nikolas] Univ Athens, Dept Pharmacognosy & Nat Prod Chem, Fac Pharm, Athens 15771, Greece.
RP Trougakos, IP (corresponding author), Univ Athens, Dept Cell Biol & Biophys, Fac Biol, Panepistimiopolis, Athens 15784, Greece.
EM itrougakos@biol.uoa.gr
RI Trougakos, Ioannis/R-6149-2018; Fokialakis, Nikolas/AAD-1498-2020
OI Trougakos, Ioannis/0000-0002-6179-2772; Fokialakis,
   Nikolas/0000-0001-7028-1870
FU EU grant TASCMAR (EU-H) [GA 634674]; EU grant MICROSMETICS
   (FP7-PEOPLE-IAPP) [GA 612276]
FX The authors apologise to those authors whose work was not cited due to
   space limitations. NF and IPT acknowledge funding from the EU grants
   TASCMAR (EU-H2020, GA 634674) and MICROSMETICS (FP7-PEOPLE-IAPP 2013, GA
   612276).
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NR 156
TC 26
Z9 25
U1 0
U2 19
PU ELSEVIER IRELAND LTD
PI CLARE
PA ELSEVIER HOUSE, BROOKVALE PLAZA, EAST PARK SHANNON, CO, CLARE, 00000,
   IRELAND
SN 0304-3835
EI 1872-7980
J9 CANCER LETT
JI Cancer Lett.
PD JAN 28
PY 2018
VL 413
BP 110
EP 121
DI 10.1016/j.canlet.2017.10.034
PG 12
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA FQ1ID
UT WOS:000418109300011
PM 29107114
DA 2022-04-25
ER

PT J
AU Nagakannan, P
   Tabeshmehr, P
   Eftekharpour, E
AF Nagakannan, Pandian
   Tabeshmehr, Parisa
   Eftekharpour, Eftekhar
TI Oxidative damage of lysosomes in regulated cell death systems:
   Pathophysiology and pharmacologic interventions
SO FREE RADICAL BIOLOGY AND MEDICINE
LA English
DT Article
ID AUTOPHAGY-DEPENDENT APOPTOSIS; COLON-CANCER CELLS; CASPASE-INDEPENDENT
   APOPTOSIS; CATHEPSIN-B CONTRIBUTES; ALPHA INDUCED APOPTOSIS;
   CYTOCHROME-C RELEASE; MEMBRANE PERMEABILIZATION; IN-VITRO; ACID
   SPHINGOMYELINASE; CYSTEINE CATHEPSINS
AB Lysosomes are small specialized organelles containing a variety of different hydrolase enzymes that are responsible for degradation of all macromolecules, entering the cells through the endosomal system or originated from the internal sources. This allows for transport and recycling of nutrients and internalization of surface proteins for antigen presentation as well as maintaining cellular homeostasis. Lysosomes are also important storage compartments for metal ions and nutrients. The integrity of lysosomal membrane is central to maintaining their normal function, but like other cellular membranes, lysosomal membrane is subject to damage mediated by reactive oxygen species. This results in spillage of lysosomal enzymes into the cytoplasm, leading to proteolytic damage to cellular systems and organelles. Several forms of lysosomal dependent cell death have been identified in diseases. Examination of these events are important for finding treatment strategies relevant to cancer or neurodegenerative diseases as well as autoimmune deficiencies. In this review, we have examined the current literature on involvement of lysosomes in induction of programed cell death and have provided an extensive list of therapeutic approaches that can modulate cell death. Exploitation of these mechanisms can lead to novel therapies for cancer and neurodegenerative diseases.
C1 Univ Manitoba, Dept Physiol & Pathophysiol, Regenerat Med Program, Winnipeg, MB, Canada.
   Univ Manitoba, Dept Physiol & Pathophysiol, Spinal Cord Res Ctr, Winnipeg, MB, Canada.
RP Eftekharpour, E (corresponding author), Univ Manitoba, 631-BMSB,745 Bannatyne Ave, Winnipeg, MB R3E 0J9, Canada.
EM eftekhar.eftekharpour@umanitoba.ca
OI Pandian, Nagakannan/0000-0002-6791-0661
FU Will-to-Win foundation - Wings for Life Foundation; Natural Sciences and
   Engineering Research Council of CanadaNatural Sciences and Engineering
   Research Council of Canada (NSERC)CGIAR
FX PN is supported by a studentship from Will-to-Win foundation. EE is
   currently funded by Wings for Life Foundation, and Natural Sciences and
   Engineering Research Council of Canada.
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NR 374
TC 5
Z9 5
U1 0
U2 6
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA STE 800, 230 PARK AVE, NEW YORK, NY 10169 USA
SN 0891-5849
EI 1873-4596
J9 FREE RADICAL BIO MED
JI Free Radic. Biol. Med.
PD SEP
PY 2020
VL 157
SI SI
BP 94
EP 127
DI 10.1016/j.freeradbiomed.2020.04.001
PG 34
WC Biochemistry & Molecular Biology; Endocrinology & Metabolism
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Endocrinology & Metabolism
GA NA9GR
UT WOS:000560125700009
PM 32259579
DA 2022-04-25
ER

PT J
AU Ashrafizadeh, M
   Zarrabi, A
   Orouei, S
   Hushmandi, K
   Hakimi, A
   Zabolian, A
   Daneshi, S
   Samarghandian, S
   Baradaran, B
   Najafi, M
AF Ashrafizadeh, Milad
   Zarrabi, Ali
   Orouei, Sima
   Hushmandi, Kiavash
   Hakimi, Azadeh
   Zabolian, Amirhossein
   Daneshi, Salman
   Samarghandian, Saeed
   Baradaran, Behzad
   Najafi, Masoud
TI MicroRNA-mediated autophagy regulation in cancer therapy: The role in
   chemoresistance/chemosensitivity
SO EUROPEAN JOURNAL OF PHARMACOLOGY
LA English
DT Review
DE MicroRNA; Autophagy; Chemoresistance; Chemosensitivity; Cancer therapy
ID EPITHELIAL-MESENCHYMAL TRANSITION; HYPOXIA-INDUCED AUTOPHAGY;
   HEPATOCELLULAR-CARCINOMA CELLS; CISPLATIN-INDUCED AUTOPHAGY;
   LUNG-CANCER; INHIBITING AUTOPHAGY; COLORECTAL-CANCER; OVARIAN-CANCER;
   GEMCITABINE RESISTANCE; DOWN-REGULATION
AB Chemoresistance has doubled the effort needed to reach an effective treatment for cancer. Now, scientists should consider molecular pathways and mechanisms involved in chemoresistance to overcome cancer. Autophagy is a "self-digestion" mechanism in which potentially toxic and aged organelles and macromolecules are degraded. Increasing evidence has shown that autophagy possesses dual role in cancer cells (onco-suppressor or oncogene). So, it is vital to identify its role in cancer progression and malignancy. MicroRNAs (miRs) are epigenetic factors capable of modulation of autophagy in cancer cells. In the current review, we emphasize on the relationship between miRs and autophagy in cancer chemotherapy. Besides, we discuss upstream mediators of miR/autophagy axis in cancer chemotherapy including long non-coding RNAs, circular RNAs, Nrf2 c-Myc, and HIF-1 alpha. At the final section, we provide a discussion about how anti-tumor compounds affect miR/autophagy axis in ensuring chemosensitivity. These topics are described in this review to show how autophagy inhibition/induction can lead to chemosensitivity/chemoresistance, and miRs are considered as key players in these discussions.
C1 [Ashrafizadeh, Milad] Univ Tabriz, Fac Vet Med, Tabriz, Iran.
   [Zarrabi, Ali] Sabanci Univ, Nanotechnol Res & Applicat Ctr SUNUM, TR-34956 Istanbul, Turkey.
   [Orouei, Sima] Islamic Azad Univ, Dept Genet, Tehran Med Sci, Tehran, Iran.
   [Hushmandi, Kiavash] Univ Tehran, Fac Vet Med, Div Epidemiol & Zoonoses, Dept Food Hyg & Qual Control, Tehran, Iran.
   [Hakimi, Azadeh] Shiraz Univ Med Sci, Student Res Comm, Sch Med, Dept Anat Sci, Shiraz, Iran.
   [Zabolian, Amirhossein] Islamic Azad Univ, Tehran Med Sci, Young Researchers & Elite Club, Tehran, Iran.
   [Daneshi, Salman] Jiroft Univ Med Sci, Sch Hlth, Dept Publ Hlth, Jiroft, Iran.
   [Samarghandian, Saeed] Neyshabur Univ Med Sci, Dept Basic Med Sci, Neyshabur, Iran.
   [Baradaran, Behzad] Tabriz Univ Med Sci, Immunol Res Ctr, Tabriz, Iran.
   [Najafi, Masoud] Kermanshah Univ Med Sci, Inst Hlth Technol, Med Technol Res Ctr, Kermanshah, Iran.
   [Najafi, Masoud] Kermanshah Univ Med Sci, Sch Paramed Sci, Radiol & Nucl Med Dept, Kermanshah, Iran.
RP Baradaran, B (corresponding author), Tabriz Univ Med Sci, Immunol Res Ctr, Tabriz, Iran.; Najafi, M (corresponding author), Kermanshah Univ Med Sci, Inst Hlth Technol, Med Technol Res Ctr, Kermanshah, Iran.
EM baradaranb@tbzmed.ac.ir; najafi_ma@yahoo.com
RI Baradaran, Behzad/AAQ-5177-2020; najafi, masoud/L-8434-2019; Zarrabi,
   Ali/U-2602-2019
OI Baradaran, Behzad/0000-0002-8642-6795; najafi,
   masoud/0000-0002-6341-9007; Zarrabi, Ali/0000-0003-0391-1769
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NR 293
TC 16
Z9 16
U1 7
U2 13
PU ELSEVIER
PI AMSTERDAM
PA RADARWEG 29, 1043 NX AMSTERDAM, NETHERLANDS
SN 0014-2999
EI 1879-0712
J9 EUR J PHARMACOL
JI Eur. J. Pharmacol.
PD FEB 5
PY 2021
VL 892
AR 173660
DI 10.1016/j.ejphar.2020.173660
PG 16
WC Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA PQ8NJ
UT WOS:000606799900001
PM 33310181
HC Y
HP N
DA 2022-04-25
ER

PT J
AU Hu, WY
   Hu, DP
   Xie, LS
   Li, Y
   Majumdar, S
   Nonn, L
   Hu, H
   Shioda, T
   Prins, GS
AF Hu, Wen-Yang
   Hu, Dan-Ping
   Xie, Lishi
   Li, Ye
   Majumdar, Shyama
   Nonn, Larisa
   Hu, Hong
   Shioda, Toshi
   Prins, Gail S.
TI Isolation and functional interrogation of adult human prostate
   epithelial stem cells at single cell resolution
SO STEM CELL RESEARCH
LA English
DT Article
DE Prostate Stem cell; Progenitor cell; Prostasphere; Prostate cancer
ID PROGENITOR CELLS; SELF-RENEWAL; CANCER; BASAL; IDENTIFICATION; LINEAGE;
   FATE; MAINTENANCE; HOMEOSTASIS; EXPRESSION
AB Using primary cultures of normal human prostate epithelial cells, we developed a novel prostasphere-based, label-retention assay that permits identification and isolation of stem cells at a single cell level. Their bona fide stem cell nature was corroborated using in vitro and in vivo regenerative assays and documentation of symmetric/ asymmetric division. Robust WNT10B and KRT13 levels without E-cadherin or KRT14 staining distinguished individual stem cells from daughter progenitors in spheroids. Following FACS to isolate label-retaining stem cells from label-free progenitors, RNA-seq identified unique gene signatures for the separate populations which may serve as useful biomarkers. Knockdown of KRT13 or PRAC1 reduced sphere formation and symmetric self-renewal highlighting their role in stem cell maintenance. Pathways analysis identified ribosome biogenesis and membrane estrogen-receptor signaling enriched in stem cells with NF-.B signaling enriched in progenitors; activities that were biologically confirmed. Further, bioassays identified heightened autophagy flux and reduced metabolismin stemcells relative to progenitors. These approaches similarly identified stem-like cells from prostate cancer specimens and prostate, breast and colon cancer cell lines suggesting wide applicability. Together, the present studies isolate and identify unique characteristics of normal human prostate stem cells and uncover processes that maintain stem cell homeostasis in the prostate gland. (C) 2017 The Authors. Published by Elsevier B.V.
C1 [Hu, Wen-Yang; Hu, Dan-Ping; Xie, Lishi; Li, Ye; Majumdar, Shyama; Prins, Gail S.] Univ Illinois, Coll Med, Dept Urol, Chicago, IL 60612 USA.
   [Nonn, Larisa; Prins, Gail S.] Univ Illinois, Coll Med, Dept Pathol, Chicago, IL 60612 USA.
   [Nonn, Larisa; Prins, Gail S.] Univ Illinois, Coll Med, Ctr Canc, Chicago, IL 60612 USA.
   [Hu, Hong] Univ Illinois, Res Resources Ctr, Chicago, IL 60612 USA.
   [Shioda, Toshi] Massachusetts Gen Hosp, Ctr Canc Res, Charlestown, MA 02129 USA.
   [Shioda, Toshi] Harvard Med Sch, Charlestown, MA 02129 USA.
RP Prins, GS (corresponding author), Univ Illinois, Dept Urol, 820 South Wood St,M-C 955, Chicago, IL USA.
EM gprins@uic.edu
RI HU, WENYANG/L-2026-2019; Xie, Lishi/C-2334-2019
OI Xie, Lishi/0000-0003-2376-6685; Prins, Gail/0000-0002-9044-4734
FU National Cancer InstituteUnited States Department of Health & Human
   ServicesNational Institutes of Health (NIH) - USANIH National Cancer
   Institute (NCI) [R01-CA172220, R01-ES02207, R01CA166588]; Michael Reese
   Research and Education Foundation; NATIONAL CANCER INSTITUTEUnited
   States Department of Health & Human ServicesNational Institutes of
   Health (NIH) - USANIH National Cancer Institute (NCI) [R01CA172220,
   R01CA166588] Funding Source: NIH RePORTER; NATIONAL INSTITUTE OF
   ENVIRONMENTAL HEALTH SCIENCESUnited States Department of Health & Human
   ServicesNational Institutes of Health (NIH) - USANIH National Institute
   of Environmental Health Sciences (NIEHS) [P30ES027792, R01ES022071]
   Funding Source: NIH RePORTER
FX This study was supported by grants from the National Cancer Institute
   R01-CA172220 (GSP, WYH, LN), R01-ES02207 (GSP, WYH), R01CA166588, (LN,
   GSP), and the Michael Reese Research and Education Foundation (GSP, WYH,
   TS). The authors wish to thank the services of the University of
   Illinois/ Chicago (UIC) Biorepository, Dr. Mark Maienschein-Cline for
   assistance with bioinformatics analysis, Dr. Alan M. Diamond for
   providing HCT116 cells, Dr. Marcelo G. Bonini for assistancewith
   Seahorse mito-stress assay, Dr. Susan Kasper, Dr. Hung-Ming Lam and Lynn
   Birch for assistance in the editing of the manuscript.
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PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 1873-5061
EI 1876-7753
J9 STEM CELL RES
JI Stem Cell Res.
PD AUG
PY 2017
VL 23
BP 1
EP 12
DI 10.1016/j.scr.2017.06.009
PG 12
WC Cell & Tissue Engineering; Biotechnology & Applied Microbiology; Cell
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WE Science Citation Index Expanded (SCI-EXPANDED)
SC Cell Biology; Biotechnology & Applied Microbiology
GA FH2GW
UT WOS:000410958100001
PM 28651114
OA Green Accepted, gold
DA 2022-04-25
ER

PT J
AU Pal, RR
   Rajpal, V
   Singh, P
   Saraf, SA
AF Pal, Ravi Raj
   Rajpal, Vasundhara
   Singh, Priya
   Saraf, Shubhini A.
TI Recent Findings on Thymoquinone and Its Applications as a Nanocarrier
   for the Treatment of Cancer and Rheumatoid Arthritis
SO PHARMACEUTICS
LA English
DT Review
DE thymoquinone; cancer; arthritis; nanotechnology; synovial delivery;
   toxicity reduction
ID NIGELLA-SATIVA L.; EPITHELIAL-MESENCHYMAL TRANSITION; NEGATIVE
   BREAST-CANCER; COLON-CANCER; IN-VITRO; ANTICANCER ACTIVITY;
   ANTIINFLAMMATORY PROPERTIES; SIGNALING PATHWAYS; PLGA NANOPARTICLES;
   CELL CARCINOMA
AB Cancer causes a considerable amount of mortality in the world, while arthritis is an immunological dysregulation with multifactorial pathogenesis including genetic and environmental defects. Both conditions have inflammation as a part of their pathogenesis. Resistance to anticancer and disease-modifying antirheumatic drugs (DMARDs) happens frequently through the generation of energy-dependent transporters, which lead to the expulsion of cellular drug contents. Thymoquinone (TQ) is a bioactive molecule with anticancer as well as anti-inflammatory activities via the downregulation of several chemokines and cytokines. Nevertheless, the pharmacological importance and therapeutic feasibility of thymoquinone are underutilized due to intrinsic pharmacokinetics, including short half-life, inadequate biological stability, poor aqueous solubility, and low bioavailability. Owing to these pharmacokinetic limitations of TQ, nanoformulations have gained remarkable attention in recent years. Therefore, this compilation intends to critically analyze recent advancements in rheumatoid arthritis and cancer delivery of TQ. This literature search revealed that nanocarriers exhibit potential results in achieving targetability, maximizing drug internalization, as well as enhancing the anti-inflammatory and anticancer efficacy of TQ. Additionally, TQ-NPs (thymoquinone nanoparticles) as a therapeutic payload modulated autophagy as well as enhanced the potential of other drugs when given in combination. Moreover, nanoformulations improved pharmacokinetics, drug deposition, using EPR (enhanced permeability and retention) and receptor-mediated delivery, and enhanced anti-inflammatory and anticancer properties. TQ's potential to reduce metal toxicity, its clinical trials and patents have also been discussed.
C1 [Pal, Ravi Raj; Singh, Priya; Saraf, Shubhini A.] Babasaheb Bhimrao Ambedkar Univ, Dept Pharmaceut Sci, Raebareli Rd, Lucknow 226025, Uttar Pradesh, India.
   [Rajpal, Vasundhara] Babasaheb Bhimrao Ambedkar Univ, Dept Biotechol, Raebareli Rd, Lucknow 226025, Uttar Pradesh, India.
RP Saraf, SA (corresponding author), Babasaheb Bhimrao Ambedkar Univ, Dept Pharmaceut Sci, Raebareli Rd, Lucknow 226025, Uttar Pradesh, India.
EM ravirajpal.rs@bbau.ac.in; vasundhararaj05@gmail.com;
   priyas.rs@bbau.ac.in; sasaraf@bbau.ac.in
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   raviraj/0000-0001-6798-5009; Saraf, Shubhini/0000-0002-4180-0931; Singh,
   Priya/0000-0002-1352-2188
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NR 241
TC 3
Z9 3
U1 6
U2 9
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 1999-4923
J9 PHARMACEUTICS
JI Pharmaceutics
PD JUN
PY 2021
VL 13
IS 6
AR 775
DI 10.3390/pharmaceutics13060775
PG 37
WC Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA SZ4QY
UT WOS:000666552800001
PM 34067322
OA gold, Green Published
DA 2022-04-25
ER

PT J
AU Li, X
   Chen, FY
   Kang, JW
   Zhou, J
   Peng, C
   Huang, W
   Zhou, MK
   He, G
   Han, B
AF Li, Xiang
   Chen, Fei-Yu
   Kang, Jing-Wen
   Zhou, Jin
   Peng, Cheng
   Huang, Wei
   Zhou, Mu-Ke
   He, Gu
   Han, Bo
TI Stereoselective Assembly of Multifunctional Spirocyclohexene Pyrazolones
   That Induce Autophagy-Dependent Apoptosis in Colorectal Cancer Cells
SO JOURNAL OF ORGANIC CHEMISTRY
LA English
DT Article
ID ORGANOCATALYTIC ASYMMETRIC-SYNTHESIS; CATALYZED 4+2 CYCLOADDITION;
   ENANTIOSELECTIVE SYNTHESIS; CASCADE REACTION; UNSATURATED PYRAZOLONES;
   ANTIMICROBIAL ACTIVITY; CONSTRUCTION; SCAFFOLD; SPIROPYRAZOLONES;
   PROLIFERATION
AB Enantio- and diastereoselective synthesis of multifunctional spiropyrazolone scaffolds has been achieved using secondary amine-catalyzed [4 + 2] annulations of alpha,beta,gamma,delta,-unsaturated pyrazolones with aldehydes. The pyrazolone substrates serve as C4 synthons to produce 6-membered, carbocycle-based, chiral spiropyrazolone derivatives. The synthesized chiral compounds showed potent toxicity against a panel of cancer cell lines. The most potent compound 3h-induced cell cycle arrest and macroautophagy in HCT116 colorectal cancer cells, triggering autophagy-dependent apoptotic cell death.
C1 [Li, Xiang; Chen, Fei-Yu; Kang, Jing-Wen; Zhou, Jin; Peng, Cheng; Huang, Wei; Han, Bo] Chengdu Univ Tradit Chinese Med, Sch Pharm, State Key Lab Southwestern Chinese Med Resources, Chengdu 611137, Sichuan, Peoples R China.
   [Zhou, Mu-Ke; He, Gu] Sichuan Univ, West China Hosp, State Key Lab Biotherapy, Chengdu 610041, Sichuan, Peoples R China.
   [Zhou, Mu-Ke; He, Gu] Sichuan Univ, West China Hosp, Dept Dermatol, Chengdu 610041, Sichuan, Peoples R China.
   [Zhou, Mu-Ke; He, Gu] Collaborat Innovat Ctr Biotherapy, Chengdu 610041, Sichuan, Peoples R China.
RP Peng, C; Han, B (corresponding author), Chengdu Univ Tradit Chinese Med, Sch Pharm, State Key Lab Southwestern Chinese Med Resources, Chengdu 611137, Sichuan, Peoples R China.; He, G (corresponding author), Sichuan Univ, West China Hosp, State Key Lab Biotherapy, Chengdu 610041, Sichuan, Peoples R China.; He, G (corresponding author), Sichuan Univ, West China Hosp, Dept Dermatol, Chengdu 610041, Sichuan, Peoples R China.; He, G (corresponding author), Collaborat Innovat Ctr Biotherapy, Chengdu 610041, Sichuan, Peoples R China.
EM pengcheng@cdutcm.edu.cn; hegu@scu.edu.cn; hanbo@cdutcm.edu.cn
RI He, Gu/G-5446-2015
OI He, Gu/0000-0002-1536-8882; Han, Bo/0000-0003-3200-4682
FU National Natural Science Foundation of ChinaNational Natural Science
   Foundation of China (NSFC) [81573588, 81773889, 21772131]; Science &
   Technology Department of Sichuan Province [2017JZYD0001, 2017JQ0002,
   2017JY0323]
FX We are grateful for financial support from the National Natural Science
   Foundation of China (81573588, 81773889, and 21772131) and the Science &
   Technology Department of Sichuan Province (2017JZYD0001, 2017JQ0002, and
   2017JY0323).
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Z9 17
U1 5
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PU AMER CHEMICAL SOC
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PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA
SN 0022-3263
EI 1520-6904
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BP 9138
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PG 13
WC Chemistry, Organic
WE Science Citation Index Expanded (SCI-EXPANDED); Index Chemicus (IC); Current Chemical Reactions (CCR-EXPANDED)
SC Chemistry
GA IK9ZY
UT WOS:000476957000030
PM 31267754
DA 2022-04-25
ER

PT J
AU Chatterjee, I
   Zhang, YG
   Zhang, JL
   Lu, R
   Xia, YL
   Sun, J
AF Chatterjee, Ishita
   Zhang, Yongguo
   Zhang, Jilei
   Lu, Rong
   Xia, Yinglin
   Sun, Jun
TI Overexpression of Vitamin D Receptor in Intestinal Epithelia Protects
   Against Colitis via Upregulating Tight Junction Protein Claudin 15
SO JOURNAL OF CROHNS & COLITIS
LA English
DT Article
DE Claudin; Crohn's disease; colonoids; IBD; inflammation; Salmonella;
   tight junction; VDR; ulcerative colitis
ID INFLAMMATORY-BOWEL-DISEASE; ULCERATIVE-COLITIS; GUT; EXPRESSION; LEADS;
   ACTIVATION; DEFECTS; PATHWAY; BARRIER; CANCER
AB Background and Aims: Dysfunction of the vitamin D receptor [VDR] contributes to the aetiology of IBD by regulating autophagy, immune response, and mucosal permeability. VDR directly controls the paracellular tight junction protein Claudin-2. Claudin-2 and Claudin-15 are unique in maintaining paracellular permeability. Interestingly, claudin-15 mRNA was downregulated in patients with ulcerative colitis. However, the exact mechanism of Claudin-15 regulation in colitis is still unknown. Here, we investigated the protective role of VDR against intestinal inflammation via upregulating Claudin-15.
   Methods: We analysed the correlation of Claudin-15 with the reduction of VDR in human colitis. We generated intestinal epithelial overexpression of VDR [O-VDR] mice to study the gain of function of VDR in colitis. Intestinal epithelial VDR knockout [VDRIEC] mice were used for the loss of function study. Colonoids and SKCO15 cells were used as in vitro models.
   Results: Reduced Claudin-15 was significantly correlated with decreased VDR along the colonic epithelium of human IBD. O-VDR mice showed decreased susceptibility to chemically and bacterially induced colitis and marked increased Claudin-15 expression [both mRNA and protein] in the colon. Correspondingly, colonic Claudin-15 was reduced in VDRIEC mice, which were susceptible to colitis. Overexpression of intestinal epithelial VDR and vitamin D treatment resulted in a significantly increased Claudin-15. ChIP assays identified the direct binding of VDR to the claudin-15 promoter, suggesting that claudin-15 is a target gene of VDR.
   Conclusion: We demonstrated the mechanism of VDR upregulation of Claudin-15 to protect against colitis. This might enlighten the mechanism of barrier dysfunction in IBD and potential therapeutic strategies to inhibit inflammation.
C1 [Chatterjee, Ishita; Zhang, Yongguo; Zhang, Jilei; Lu, Rong; Xia, Yinglin; Sun, Jun] Univ Illinois, Dept Med, Div Gastroenterol & Hepatol, 840 S Wood St,Room 704 CSB,MC716, Chicago, IL 60612 USA.
   [Sun, Jun] Univ Illinois, UIC Canc Ctr, Chicago, IL USA.
   [Sun, Jun] Univ Illinois, Dept Microbiol & Immunol, Chicago, IL 60680 USA.
   [Sun, Jun] Jesse Brown VA Med Ctr, Chicago, IL USA.
RP Sun, J (corresponding author), Univ Illinois, Dept Med, Div Gastroenterol & Hepatol, 840 S Wood St,Room 704 CSB,MC716, Chicago, IL 60612 USA.
EM junsun@uic.edu
RI Sun, Jun/S-7440-2019
OI Sun, Jun/0000-0001-7465-3133
FU NIDDK (National Institute of Diabetes and Digestive and Kidney
   Diseases)United States Department of Health & Human ServicesNational
   Institutes of Health (NIH) - USANIH National Institute of Diabetes &
   Digestive & Kidney Diseases (NIDDK) [R01 DK105118, R01DK114126]; DOD
   (The Department of Defense) CDMRP (Congressionally Directed Medical
   Research Programs) [BC160450P1]; VA (Veterans Affairs) Merit Award [1
   I01BX004824-01]
FX This work was supported by the NIDDK (National Institute of Diabetes and
   Digestive and Kidney Diseases) grant R01 DK105118, R01DK114126, and DOD
   (The Department of Defense) CDMRP (Congressionally Directed Medical
   Research Programs) log No BC160450P1, and the VA (Veterans Affairs)
   Merit Award 1 I01BX004824-01to JS (Prof. Jun Sun). The contents do not
   represent the views of the United States Department of Veterans Affairs
   or the United States Government.
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NR 53
TC 5
Z9 5
U1 9
U2 9
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 1873-9946
EI 1876-4479
J9 J CROHNS COLITIS
JI J. Crohns Colitis
PD OCT
PY 2021
VL 15
IS 10
BP 1720
EP 1736
DI 10.1093/ecco-jcc/jjab044
EA MAR 2021
PG 17
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA WM9IT
UT WOS:000711392000011
PM 33690841
OA Green Published
DA 2022-04-25
ER

PT J
AU Zhong, WW
   Dai, QQ
   Huang, QH
AF Zhong, Weiwei
   Dai, Qianqian
   Huang, Qionghui
TI Effect of lncRNA KCNQ1OT1 on autophagy and drug resistance of
   hepatocellular carcinoma cells by targeting miR-338-3p
SO CELLULAR AND MOLECULAR BIOLOGY
LA English
DT Article
DE Hepatocellular carcinoma; lncRNA KCNQ1OT1; miR-338-3p; Survival rate;
   Autophagy; Cisplatin sensitivity
ID CANCER CELLS; COLON-CANCER
AB The current experiment aimed to investigate the effects of lncRNA KCNQ1OT1 on the proliferation, autophagy and drug resistance of hepatocellular carcinoma cells, as well as the potential molecular mechanism. Hepatocellular carcinoma SK-HEP-1 cells and DDP resistant SK-HEP-1/DDP cells were treated with cisplatin (DDP) of different concentrations (1 nmol/L 2 nmol/L, 4 nmol/L, 8 nmol/L, 16 nmol/L,). The survival rate 01 SK-HEP-1 and SK-HEP-TDDP cells vas determined by the CCK8 method. QRT-PCR was used to detect the levels of lncRNAKCNQ1OT1 and miR-338-3p in normal hepatocyte HH01, hepatocellular ell SK-HEP-1 and hepatoma cisplatin-resistant cell SK-HEP-1/DDP. Western blot was carried out to detect the expression levels of autophagy-related protein Beclin1 and proliferation-related protein P21 in cells. A dual-luciferase reporter assay system was performed to validate the relationship between KCNQ1OT1 and miR-338-3p. After the treatment of 1 nmol/L, 2 nmol/L, 8nmol/L, and 16nmol/L cisplatin (DDP), the survival rate or SK-HEP-FDDP cells is higher than that of SK-HEP-1 cells. The level or lncRNA KCNQ1OT1 was increased successively in HH01, SK-HEP-1 and SK-HEP-1/DDP cells, while miR-338-3p was decreased successively. Silencing lncRNA KCNQ1OT1 or over-expressing miR-338-3p combined with 16 nmol/L DDP treatment reduced the survival rate of SK-HEP-1/DDP cells and up-regulate levels of P21 and Beclin1 proteins. LncRNA KCNQ1OT1 targeted and negatively regulated the expression of miR-338-3p. Inhibition or miR-338-3p reversed the effect of silencing lncRNA KCNQ1OT1 on survival, autophagy and cisplatin sensitivity of SK-HEP-1/DDP cell. LncRNA KCNQ1OT1 targets miR-338-3p to regulate the survival rate and autophagy or SK-HEP-1/DDP cells and improve the cisplatin sensitivity of SK-HEP-1/DDP cells. LncRNA KCNQ1OT1 is a potential molecular target for hepatocellular carcinoma.
C1 [Zhong, Weiwei] Jingmen 1 Peoples Hosp, GI Med, Jingmen 448000, Peoples R China.
   [Dai, Qianqian] Jingmen 1 Peoples Hosp, Infect Dis Dept, Jingmen 448000, Peoples R China.
   [Huang, Qionghui] Jingmen 2 Peoples Hosp, Psychiat Dept, Jingmen 448000, Peoples R China.
RP Dai, QQ (corresponding author), Jingmen 1 Peoples Hosp, Infect Dis Dept, Jingmen 448000, Peoples R China.
EM dq_1005@126.com
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NR 20
TC 2
Z9 2
U1 0
U2 2
PU C M B  ASSOC
PI POITIERS
PA 34 BOULEVARD SOLFERINO, 86000 POITIERS, FRANCE
SN 0145-5680
EI 1165-158X
J9 CELL MOL BIOL
JI Cell. Mol. Biol.
PY 2020
VL 66
IS 3
BP 191
EP 196
DI 10.14715/cmb/2020.66.3.31
PG 6
WC Biochemistry & Molecular Biology; Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Cell Biology
GA LY3EW
UT WOS:000540410000031
PM 32538770
DA 2022-04-25
ER

PT J
AU Sakanashi, F
   Shintani, M
   Tsuneyoshi, M
   Ohsaki, H
   Kamoshida, S
AF Sakanashi, Fuminori
   Shintani, Michiko
   Tsuneyoshi, Masazumi
   Ohsaki, Hiroyuki
   Kamoshida, Shingo
TI Apoptosis, necroptosis and autophagy in colorectal cancer: Associations
   with tumor aggressiveness and p53 status
SO PATHOLOGY RESEARCH AND PRACTICE
LA English
DT Article
DE Cleaved caspase-3; Colorectal cancer; Microtubule-associated protein-1
   light chain-3; Phosphorylated-mixed-lineage kinase domain-like protein;
   p53; Pathological aggressiveness
ID CELL-DEATH; MUTATIONS; CARCINOMA; PATHWAYS; SURVIVAL; NECROSIS; BIOLOGY;
   MARKER; KINASE; LC3
AB Objective: Cleaved caspase-3 (CC3), phosphorylated-mixed-lineage kinase domain-like protein (p-MLKL), and microtubule-associated protein-1 light chain-3B (LC3B) have pivotal functions in apoptosis, necroptosis, and autophagy, respectively. In vitro studies have shown that interaction of these proteins are complex and their roles in cancer can be influenced by many factors. However, these findings are not adequately assessed in human tissues. Here, we determined CC3, p-MLKL, and LC3B expression in colorectal cancers (CRCs), and assessed their associations with clinicopathological parameters, and with KRAS and p53 status.
   Methods: We immunohistochemically assessed 113 CRC specimens for levels of CC3, p-MLKL, LC3B, and p53. KRAS gene status was analyzed using the Scorpion-amplification refractory mutation system.
   Results: High levels of CC3 (CC3(High)) and LC3B (LC3B(High)) were detected in 38% and 35% of the 113 CRCs, respectively, but no or only a few p-MLKL-positive cells were observed in any of the tumors. CC3(High) was significantly associated with high pT status (P = 0.03), vascular invasion (P = 0.03) and high pStage (P = 0.04) and was marginally associated with lymph node (P = 0.06) and distant metastases (P = 0.06). LC3B(High) was also significantly associated with high pT status (P = 0.02) and lymphatic invasion (P = 0.002), and was marginally associated with nerve plexus invasion (P = 0.06). In combined analysis, compared with CC3(Low)/LC3B(Low) tumors, tumors that were either CC3(High), LC3B(High), or both were significantly associated with high pT status (P = 0.0007), lymphatic invasion (P = 0.03), vascular invasion (P = 0.003), distant metastasis (P = 0.04) and high pStage (P = 0.04). LC3B(High) was significantly associated with a mutant-type expression pattern of p53 (P = 0.003).
   Conclusion: To the best of our knowledge, this is the first study to examine the combination of CC3/LC3B and p-MLKL expression in clinical CRC samples and to correlate these expression data with clinicopathological parameters and EGFR and p53 status. Our results suggest that necroptosis is a rare process in CRC, apoptosis and autophagy are upregulated in aggressive CRCs, and p53 mutation may lead to the upregulation of autophagy.
C1 [Sakanashi, Fuminori; Ohsaki, Hiroyuki; Kamoshida, Shingo] Kobe Univ, Grad Sch Hlth Sci, Dept Med Biophys, Lab Pathol,Suma Ku, 7-10-2 Tomogaoka, Kobe, Hyogo 6540142, Japan.
   [Sakanashi, Fuminori; Tsuneyoshi, Masazumi] Fukuoka Sanno Hosp, Dept Diagnost Pathol, 3-6-45 Momochihama, Sawara, Fukuoka 8140001, Japan.
   [Shintani, Michiko] Kobe Tokiwa Univ, Dept Med Technol, 2-6-2 Ohtani, Kobe, Hyogo 6530838, Japan.
RP Sakanashi, F (corresponding author), Kobe Univ, Grad Sch Hlth Sci, Dept Med Biophys, Lab Pathol,Suma Ku, 7-10-2 Tomogaoka, Kobe, Hyogo 6540142, Japan.
EM sakanashi@kouhoukai.or.jp
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NR 41
TC 9
Z9 10
U1 0
U2 10
PU ELSEVIER GMBH
PI MUNICH
PA HACKERBRUCKE 6, 80335 MUNICH, GERMANY
SN 0344-0338
J9 PATHOL RES PRACT
JI Pathol. Res. Pract.
PD JUL
PY 2019
VL 215
IS 7
AR 152425
DI 10.1016/j.prp.2019.04.017
PG 6
WC Pathology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pathology
GA IH7HH
UT WOS:000474674200022
PM 31097354
OA Green Published
DA 2022-04-25
ER

PT J
AU Voloshin, T
   Kaynan, N
   Davidi, S
   Porat, Y
   Shteingauz, A
   Schneiderman, RS
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   Kirson, ED
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AF Voloshin, Tali
   Kaynan, Noa
   Davidi, Shiri
   Porat, Yaara
   Shteingauz, Anna
   Schneiderman, Rosa S.
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   Munster, Mijal
   Blat, Roni
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   Cahal, Shay
   Itzhaki, Aviran
   Giladi, Moshe
   Kirson, Eilon D.
   Weinberg, Uri
   Kinzel, Adrian
   Palti, Yoram
TI Tumor-treating fields (TTFields) induce immunogenic cell death resulting
   in enhanced antitumor efficacy when combined with anti-PD-1 therapy
SO CANCER IMMUNOLOGY IMMUNOTHERAPY
LA English
DT Article
DE Tumor-treating fields; Anti-PD-1; ER stress; Immunogenic cell death;
   Autophagy
ID CALRETICULIN EXPOSURE; ATP SECRETION; AUTOPHAGY; BLOCKADE; CHEMOTHERAPY;
   PROGRESSION; MECHANISMS; RESPONSES; RELEASE; MODELS
AB Tumor-treating fields (TTFields) are alternating electric fields in a specific frequency range (100-300 kHz) delivered to the human body through transducer arrays. In this study, we evaluated whether TTFields-mediated cell death can elicit antitumoral immunity and hence would be effectively combined with anti-PD-1 therapy. We demonstrate that in TTFields-treated cancer cells, damage-associated molecular patterns including high-mobility group B1 and adenosine triphosphate are released and calreticulin is exposed on the cell surface. Moreover, we show that TTFields treatment promotes the engulfment of cancer cells by dendritic cells (DCs) and DCs maturation in vitro, as well as recruitment of immune cells in vivo. Additionally, our study demonstrates that the combination of TTFields with anti-PD-1 therapy results in a significant decline of tumor volume and increase in the percentage of tumor-infiltrating leukocytes in two tumor models. In orthotopic lung tumors, these infiltrating leukocytes, specifically macrophages and DCs, showed elevated expression of PD-L1. Compatibly, cytotoxic T-cells isolated from these tumors demonstrated increased production of IFN-gamma. In colon cancer tumors, T-cells infiltration was significantly increased following long treatment duration with TTFields plus anti-PD-1. Collectively, our results suggest that TTFields therapy can induce anticancer immune response. Furthermore, we demonstrate robust efficacy of concomitant application of TTFields and anti-PD-1 therapy. These data suggest that integrating TTFields with anti-PD-1 therapy may further enhance antitumor immunity, hence achieve better tumor control.
C1 [Voloshin, Tali; Kaynan, Noa; Davidi, Shiri; Porat, Yaara; Shteingauz, Anna; Schneiderman, Rosa S.; Zeevi, Einav; Munster, Mijal; Blat, Roni; Tempel Brami, Catherine; Cahal, Shay; Itzhaki, Aviran; Giladi, Moshe; Kirson, Eilon D.; Weinberg, Uri; Palti, Yoram] Novocure Ltd, MATAM Ctr, Topaz Bldg, IL-31905 Haifa, Israel.
   [Kinzel, Adrian] Novocure GmbH, Munich, Germany.
RP Giladi, M (corresponding author), Novocure Ltd, MATAM Ctr, Topaz Bldg, IL-31905 Haifa, Israel.
EM mosheg@novocure.com
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NR 43
TC 22
Z9 27
U1 3
U2 20
PU SPRINGER
PI NEW YORK
PA ONE NEW YORK PLAZA, SUITE 4600, NEW YORK, NY, UNITED STATES
SN 0340-7004
EI 1432-0851
J9 CANCER IMMUNOL IMMUN
JI Cancer Immunol. Immunother.
PD JUL
PY 2020
VL 69
IS 7
BP 1191
EP 1204
DI 10.1007/s00262-020-02534-7
PG 14
WC Oncology; Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Immunology
GA LZ2QV
UT WOS:000541074000005
PM 32144446
OA Green Published, hybrid
DA 2022-04-25
ER

PT J
AU Lu, CL
   Qin, LL
   Liu, HC
   Candas, D
   Fan, M
   Li, JJ
AF Lu, Chung-Ling
   Qin, Lili
   Liu, Hsin-Chen
   Candas, Demet
   Fan, Ming
   Li, Jian Jian
TI Tumor Cells Switch to Mitochondrial Oxidative Phosphorylation under
   Radiation via mTOR-Mediated Hexokinase II Inhibition - A
   Warburg-Reversing Effect
SO PLOS ONE
LA English
DT Article
ID MAMMALIAN TARGET; CANCER-CELLS; UP-REGULATION; RAPAMYCIN; PATHWAY;
   GROWTH; METABOLISM; NVP-BEZ235; AUTOPHAGY; STRESS
AB A unique feature of cancer cells is to convert glucose into lactate to produce cellular energy, even under the presence of oxygen. Called aerobic glycolysis [The Warburg Effect] it has been extensively studied and the concept of aerobic glycolysis in tumor cells is generally accepted. However, it is not clear if aerobic glycolysis in tumor cells is fixed, or can be reversed, especially under therapeutic stress conditions. Here, we report that mTOR, a critical regulator in cell proliferation, can be relocated to mitochondria, and as a result, enhances oxidative phosphorylation and reduces glycolysis. Three tumor cell lines (breast cancer MCF-7, colon cancer HCT116 and glioblastoma U87) showed a quick relocation of mTOR to mitochondria after irradiation with a single dose 5 Gy, which was companied with decreased lactate production, increased mitochondrial ATP generation and oxygen consumption. Inhibition of mTOR by rapamycin blocked radiation-induced mTOR mitochondrial relocation and the shift of glycolysis to mitochondrial respiration, and reduced the clonogenic survival. In irradiated cells, mTOR formed a complex with Hexokinase II [HK II], a key mitochondrial protein in regulation of glycolysis, causing reduced HK II enzymatic activity. These results support a novel mechanism by which tumor cells can quickly adapt to genotoxic conditions via mTOR-mediated reprogramming of bioenergetics from predominantly aerobic glycolysis to mitochondrial oxidative phosphorylation. Such a "waking-up" pathway for mitochondrial bioenergetics demonstrates a flexible feature in the energy metabolism of cancer cells, and may be required for additional cellular energy consumption for damage repair and survival. Thus, the reversible cellular energy metabolisms should be considered in blocking tumor metabolism and may be targeted to sensitize them in anti-cancer therapy.
C1 [Lu, Chung-Ling; Qin, Lili; Liu, Hsin-Chen; Candas, Demet; Fan, Ming; Li, Jian Jian] Univ Calif Davis, Sch Med, Dept Radiat Oncol, Sacramento, CA 95817 USA.
RP Li, JJ (corresponding author), Univ Calif Davis, Sch Med, Dept Radiat Oncol, Sacramento, CA 95817 USA.
EM jijli@ucdavis.edu
RI Qin, Lili/J-7481-2016
OI Li, Jian Jian/0000-0003-3694-9675
FU National Institutes of Health RO1United States Department of Health &
   Human ServicesNational Institutes of Health (NIH) - USA [CA133402,
   CA152313]; NATIONAL CANCER INSTITUTEUnited States Department of Health &
   Human ServicesNational Institutes of Health (NIH) - USANIH National
   Cancer Institute (NCI) [R01CA133402, R01CA152313, P30CA093373] Funding
   Source: NIH RePORTER
FX This study was supported by National Institutes of Health RO1 Grants
   CA133402 and CA152313 to JL. The funders had no role in study design,
   data collection and analysis, decision to publish, or preparation of the
   manuscript.
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NR 58
TC 99
Z9 101
U1 1
U2 34
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 1160 BATTERY STREET, STE 100, SAN FRANCISCO, CA 94111 USA
SN 1932-6203
J9 PLOS ONE
JI PLoS One
PD MAR 25
PY 2015
VL 10
IS 3
AR e0121046
DI 10.1371/journal.pone.0121046
PG 20
WC Multidisciplinary Sciences
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Science & Technology - Other Topics
GA CE5MO
UT WOS:000351880000126
PM 25807077
OA Green Published, gold, Green Submitted
DA 2022-04-25
ER

PT J
AU Bialy, LP
   Kuckelkorn, U
   Henklein, P
   Fayet, J
   Wilczynski, GM
   Kaminski, A
   Mlynarczuk-Bialy, I
AF Bialy, L. P.
   Kuckelkorn, U.
   Henklein, P.
   Fayet, J.
   Wilczynski, G. M.
   Kaminski, A.
   Mlynarczuk-Bialy, I
TI Changes in spatio-temporal localization of tripeptidyl peptidase II
   (TPPII) in murine colon adenocarcinoma cells during aggresome formation:
   a microscopy study based on a novel fluorescent proteasome inhibitor
SO HISTOLOGY AND HISTOPATHOLOGY
LA English
DT Article
DE TPPII; Proteasome; Ubiquitin; Aggresome; Proteasome inhibitor BSc2118
ID CHYMOTRYPSIN-LIKE ACTIVITY; BSC2118; DEGRADATION; BORTEZOMIB; AUTOPHAGY;
   UBIQUITIN; PROTEOLYSIS; APOPTOSIS; CASPASES; PROTEINS
AB Extralysosomal proteolysis is a multistep process involving the Ubiquitin- Proteasome System (UPS) and supplementary peptidases. Tripeptidyl peptidase II (TPPII) is the most extensively characterized enzyme, supplementing and sometimes substituting for proteasomal functions. In response to proteasome inhibition, polyubiquitinated proteins acting as proteasome substrates aggregate with proteasomes and form aggresomes. Several proteasome inhibitors are used as anti-cancer drugs.
   Thus, in our study, we used a novel fluorescent-tagged proteasome inhibitor BSc2118 to induce aggresome formation in C26 murine colon adenocarcinoma cells. It allowed us to obtain effective, inhibitor-based, proteasome staining in vivo. This method has been validated by standard post-fixed indirect immunostaining and also allowed co-immunodetection of TPPII and polyubiquitinated proteins under laser scanning confocal microscopy.
   We found that in the absence of the inhibitor, TPPH is diffusely dispersed within the cytoplasm of C26 cells. The proteasome and ubiquitin-rich perinuclear region failed to display enhanced TPPII staining. However, when proteasome function was impaired by the inhibitor, TPPII associated more closely with both the proteasome and polyubiquitinated proteins via TPPII recruitment to the perinuclear region and subsequently into emerging aggresomal structures. Furthermore, we have demonstrated the dynamic recruitment of TPPII into the developing aggresome: TPPII in the early aggresome was dispersed within the central part but subsequently aggregated on the surface of this structure. In the mature aggresome of C26 cells TPPII formed a spherical mantle, which surrounded the round core containing proteasomes and polyubiquitinated proteins.
   Our morphological data indicate that TPPII displays spatial localization with proteasomes especially upon proteasome inhibition in aggresomes of C26 cells.
C1 [Bialy, L. P.; Mlynarczuk-Bialy, I] Med Univ Warsaw, Ctr Biostruct Res, Dept Histol & Embryol, Chalubinskiego 5, PL-02004 Warsaw, Poland.
   [Kuckelkorn, U.; Henklein, P.] Charite Univ Med Berlin, Inst Biochem, Berlin, Germany.
   [Fayet, J.] Med Univ Warsaw, Med Fac 1, Dept Ophthalmol, Warsaw, Poland.
   [Wilczynski, G. M.] Nencki Inst Expt Biol PAS, Dept Neurophysiol, Lab Mol & Syst Neuromorphol, Warsaw, Poland.
   [Kaminski, A.] Med Univ Warsaw, Ctr Biostruct Res, Dept Transplantol, Warsaw, Poland.
   [Kaminski, A.] Med Univ Warsaw, Ctr Biostruct Res, Cent Tissue Bank, Warsaw, Poland.
RP Mlynarczuk-Bialy, I (corresponding author), Med Univ Warsaw, Ctr Biostruct Res, Dept Histol & Embryol, Chalubinskiego 5, PL-02004 Warsaw, Poland.
EM izamlynar@esculap.pl
RI Mlynarczuk-Bialy, Izabela/AAA-2064-2022; Biały, Lukasz/AAW-8500-2021
OI Mlynarczuk-Bialy, Izabela/0000-0002-5192-6415; Wilczynski,
   Grzegorz/0000-0001-6667-0291; Henklein, Petra/0000-0001-7468-8926;
   Bialy, Lukasz/0000-0001-6931-6431; Kuckelkorn,
   Ulrike/0000-0002-3085-9161
FU European Regional Development FundEuropean Commission [1M15/WB2/10];
   Polish National Center [POIG 01.01.02-00-008/08]; 
   [UMO-2013/08/M/NZ3/00655]
FX The work was supported by financial resources of Medical University of
   Warsaw (1M15/WB2/10) to LB and by the European Regional Development Fund
   POIG 01.01.02-00-008/08, and by the grant from Polish National Center
   no. UMO-2013/08/M/NZ3/00655 (both to GW)
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NR 61
TC 3
Z9 3
U1 0
U2 5
PU F HERNANDEZ
PI MURCIA
PA PLAZA FUENSANTA 2-7 C, 30008 MURCIA, SPAIN
SN 0213-3911
EI 1699-5848
J9 HISTOL HISTOPATHOL
JI Histol. Histopath.
PD APR
PY 2019
VL 34
IS 4
BP 359
EP 372
DI 10.14670/HH-18-042
PG 14
WC Cell Biology; Pathology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Cell Biology; Pathology
GA HM5UA
UT WOS:000459539500005
PM 30226264
DA 2022-04-25
ER

PT J
AU Jiang, Q
   Li, F
   Shi, K
   Wu, P
   An, J
   Yang, Y
   Xu, C
AF Jiang, Q.
   Li, F.
   Shi, K.
   Wu, P.
   An, J.
   Yang, Y.
   Xu, C.
TI Involvement of p38 in signal switching from autophagy to apoptosis via
   the PERK/eIF2 alpha/ATF4 axis in selenite-treated NB4 cells
SO CELL DEATH & DISEASE
LA English
DT Article
DE p38; selenite; autophagy; apoptosis; p53
ID ACUTE PROMYELOCYTIC LEUKEMIA; COLON-CANCER CELLS; ER STRESS;
   ENDOPLASMIC-RETICULUM; P53; EXPRESSION; GENE; ATF4; PHOSPHORYLATION;
   TRANSCRIPTION
AB Selenite has emerged as an optional chemotherapeutic agent for hematological malignancies. Autophagy and apoptosis are both engaged in selenite-induced cell death. In a previous report, we have identified heat shock protein 90 (Hsp90) as a critical modulator of the balance between autophagy and apoptosis in selenite-treated leukemia cells. However, the mechanisms by which selenite mediates the crosstalk between autophagy and apoptosis remain largely unknown. Herein, we demonstrate that the endoplasmic reticulum (ER) stress-related PERK/eIF2 alpha/ATF4 pathway and p38 are core modules for the selenite-induced switch to apoptosis from autophagy. We found that selenite activated PERK and eIF2 alpha/ATF4 downstream to promote apoptosis. During this progression, p38 was dissociated from PERK-inhibiting Hsp90 and became autophosphorylated. Then, activated p38 further enhanced the docking of activating transcription factor 4 (ATF4) onto the CHOP (CCAAT/enhancer-binding protein homologous protein) promoter via eIF2 alpha to enhance apoptosis. We also found that activated p38 suppressed the phosphorylation of eIF4E that directed ATF4 to bind to the MAP1LC3B (microtubule-associated protein 1 light chain 3B) promoter. Because of the deactivation of eIF4E, the association of ATF4 with the MAP1LC3B promoter was inhibited, and autophagy was compromised. Intriguingly, p53 played important roles in mediating the p38-mediated regulation of eIF2 alpha and eIF4E. When activated by p38, p53 induced the phosphorylation of eIF2 alpha and the dephosphorylation of eIF4E, particularly in the nucleus where the ATF4 transcription factor was modulated, ultimately resulting in differential expression of CHOP and LC3. Moreover, selenite exhibited potent antitumor effects in vivo. In an NB4 cell xenograft model, selenite induced apoptosis and hampered autophagy. In addition, related signaling proteins demonstrated similar changes to those observed in vitro. These data suggest that selenite may be a candidate drug for leukemia therapy.
C1 [Jiang, Q.; Li, F.; Shi, K.; Wu, P.; An, J.; Yang, Y.; Xu, C.] PUMC, Inst Basic Med Sci, Natl Lab Med Mol Biol, Beijing 100005, Peoples R China.
   [Jiang, Q.; Li, F.; Shi, K.; Wu, P.; An, J.; Yang, Y.; Xu, C.] PUMC, Sch Basic Med, Beijing 100005, Peoples R China.
   [Jiang, Q.; Li, F.; Shi, K.; Wu, P.; An, J.; Yang, Y.; Xu, C.] CAMS, Beijing 100005, Peoples R China.
RP Xu, C (corresponding author), CAMS, Inst Basic Med Sci, Dept Biochem & Mol Biol, 5 DongdanSantiao, Beijing 100005, Peoples R China.
EM cmxu@ibms.pumc.edu.cn
OI Wu, Pa/0000-0002-7269-0683
FU National Natural Sciences Foundation of ChinaNational Natural Science
   Foundation of China (NSFC) [31170788, 30970655]; National Natural
   Science Foundation for Young Scholars of ChinaNational Natural Science
   Foundation of China (NSFC)National Science Fund for Distinguished Young
   Scholars [31101018]; Natural Science Foundation of BeijingBeijing
   Natural Science Foundation [5082015]; State Key Laboratory Special Fund
   [2060204]; Ministry of Education, China, for Doctor-training
   UniteMinistry of Education, China [20091106110025]
FX We thank Dr. L Pan (China-Japan Friendship Hospital) for her expertise
   in immunocytochemistry assay. This work was supported by grants from the
   National Natural Sciences Foundation of China (No. 31170788 and No.
   30970655), the National Natural Science Foundation for Young Scholars of
   China (No. 31101018), the Natural Science Foundation of Beijing (No.
   5082015), the State Key Laboratory Special Fund (No. 2060204) and the
   Ministry of Education, China, for Doctor-training Unite (No.
   20091106110025).
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NR 42
TC 53
Z9 56
U1 0
U2 26
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 2041-4889
J9 CELL DEATH DIS
JI Cell Death Dis.
PD MAY
PY 2014
VL 5
SI SI
AR e1270
DI 10.1038/cddis.2014.200
PG 13
WC Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Cell Biology
GA AI9DN
UT WOS:000337229300070
PM 24874742
OA Green Published, gold
DA 2022-04-25
ER

PT J
AU Yang, KM
   Kim, BM
   Park, JB
AF Yang, Kyung Mi
   Kim, Byeong Mo
   Park, Jin-Byung
TI omega-Hydroxyundec-9-enoic acid induces apoptosis through ROS-mediated
   endoplasmic reticulum stress in non-small cell lung cancer cells
SO BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
LA English
DT Article
DE omega-Hydroxyundec-9-enoic acid (omega-HUA); Non-small cell lung cancer
   (NSCLC); Apoptosis; Endoplasmic reticulum (ER) stress; Reactive oxygen
   species (ROS); N-Acetyl-L-cysteine (NAC)
ID FATTY-ACIDS; ER STRESS; COLON-CANCER; OXIDATIVE STRESS; LIVER-CELLS;
   INHIBITION; ACTIVATION; INDUCTION; AUTOPHAGY; ARREST
AB omega-Hydroxyundec-9-enoic acid (omega-HUA), a hydroxyl unsaturated fatty acid derivative, is involved in the antifungal activity of wild rice (Oryza officinalis). Here, we investigated the anti-cancer activity of omega-HUA on a non-small cell lung cancer (NSCLC) cell line. omega-HUA increased apoptosis and induced cleavages of caspase-6, caspase-9, and poly (ADP-ribose) polymerase (PARP). omega-HUA treatment significantly induced endoplasmic reticulum (ER) stress response. Suppression of CHOP expression and inhibiting ER stress by 4-phenylbutyrate (4-PBA) significantly attenuated the omega-HUA treatment-induced activation of caspase-6, caspase-9, and PARP, and subsequent apoptotic cell death, indicating a role for ER stress in omega-HUA-induced apoptosis. In addition, cells subjected to omega-HUA exhibited significantly increased quantity of reactive oxygen species (ROS), and the ROS scavenger N-acetyl-L-cysteine (NAC) inhibited omega-HUA-induced apoptotic cell death and ER stress signals, indicating a role for ROS in ER stress-mediated apoptosis in omega-HUA-treated cells. Taken together, these results suggest that sequential ROS generation and ER stress activation are critical in omega-HUA treatment-induced apoptosis and that omega-HUA represents a promising candidate for NSCLC treatment. (C) 2014 Elsevier Inc. All rights reserved.
C1 [Yang, Kyung Mi] Yonsei Univ, Coll Med, Dept Biochem & Mol Biol, Seoul 120749, South Korea.
   [Kim, Byeong Mo] Harvard Univ, Sch Med, Beth Israel Deaconess Med Ctr, Dept Med,Div Gerontol, Boston, MA 02215 USA.
   [Park, Jin-Byung] Ewha Womans Univ, Dept Food Sci & Engn, Seoul 120750, South Korea.
RP Park, JB (corresponding author), Ewha Womans Univ, Dept Food Sci & Engn, 52 Ewhayeodae Gil, Seoul 120750, South Korea.
EM jbpark06@ewha.ac.kr
FU Basic Science Research Program through the National Research Foundation
   of Korea (NRF) - Ministry of Education, Science and Technology
   [NRF-2012R1A1A2042157]
FX The present study was supported by the Basic Science Research Program
   through the National Research Foundation of Korea (NRF) funded by the
   Ministry of Education, Science and Technology (NRF-2012R1A1A2042157).
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NR 18
TC 21
Z9 22
U1 1
U2 17
PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 0006-291X
EI 1090-2104
J9 BIOCHEM BIOPH RES CO
JI Biochem. Biophys. Res. Commun.
PD JUN 6
PY 2014
VL 448
IS 3
BP 267
EP 273
DI 10.1016/j.bbrc.2014.04.111
PG 7
WC Biochemistry & Molecular Biology; Biophysics
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Biophysics
GA AI7KZ
UT WOS:000337070800005
PM 24796672
DA 2022-04-25
ER

PT J
AU Eom, JM
   Seo, MJ
   Baek, JY
   Chu, H
   Han, SH
   Min, TS
   Cho, CS
   Yun, CH
AF Eom, Jung-Min
   Seo, Min-Ji
   Baek, Ji-Young
   Chu, Hyuk
   Han, Seung Hyun
   Min, Tae Sun
   Cho, Chong-Su
   Yun, Cheol-Heui
TI Alpha-eleostearic acid induces autophagy-dependent cell death through
   targeting AKT/mTOR and ERK1/2 signal together with the generation of
   reactive oxygen species
SO BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
LA English
DT Article
DE Alpha-eleostearic acid; Reactive oxygen species; Apoptosis; Autophagy
ID CONJUGATED TRIENE SYSTEM; COLON-CANCER CELLS; OXIDATIVE STRESS;
   MAMMALIAN TARGET; FATTY-ACIDS; IN-VIVO; APOPTOSIS; TUMOR; PATHWAYS; AKT
AB Alpha-eleostearic acid (alpha-ESA, 9Z11E13E-18.3). a linolenic acid isomer with a conjugated triene system. is a natural and biologically-active Compound that has been shown to possess potent anti-tumor properties Herein, we demonstrate alpha-ESA induced apoptosis and autophagy with reactive oxygen species (ROS) generation in HeLa cells Treatment with alpha-ESA caused inhibition of phosphorylated (p)AKT and elongated the sub G1 phase in the cell cycle. indicating induction of apoptosis. Autophagy was also induced by alpha-ESA treatment, causing low pAKT and pP70S6K activities, increasing pERK1/2 and leading to a higher conversion rate of LC3 I to LC3 II compared to that of the control. The autophagy was further confirmed by fluorescence microscopy and flow cytometry through monodansylcadavarine (MDC) staining It appears that the role of autophagy is a protective mechanism against cell death in alpha-ESA-treated HeLa cells. Subsequently, we found that treating HeLa cells with alpha-ESA induced the generation of reactive oxygen species (ROS) The phosphorylation of P70S6K. downstream of mTOR signaling, and AKT were further reduced by pretreatment with N-acetyl-L-cysteine (NAC), an ROS scavenger, whereas the phosphorylation of ERK1/2 and the conversion of LC3 I to LC3 II were further enhanced As a result, the blocking of the action of ROS promoted alpha-ESA-induced apoptosis and autophagy. Taken together, our results indicate that the generation of ROS by alpha-ESA treatment impedes the progress of apoptosis and excessive autophagy formation which takes part in cell death, thus impeding death promotion. (C) 2009 Elsevier Inc All rights reserved
C1 [Yun, Cheol-Heui] Seoul Natl Univ, Dept Agr Biotechnol & Res, Inst Agr & Life Sci, Lab Prot Engn & Comparat Immunol, Seoul 151921, South Korea.
   [Min, Tae Sun] Natl Res Fdn Korea, Taejon 305350, South Korea.
   [Han, Seung Hyun] Seoul Natl Univ, Sch Dent, Dept Oral Microbiol & Immunol, Seoul 151921, South Korea.
   [Han, Seung Hyun] Seoul Natl Univ, Sch Dent, Dent Res Inst, Seoul 151921, South Korea.
   [Chu, Hyuk] Korea Ctr Dis Control & Prevent, Natl Inst Hlth, Div Zoonoses, Ctr Immunol & Pathol, Seoul, South Korea.
RP Yun, CH (corresponding author), Seoul Natl Univ, Dept Agr Biotechnol & Res, Inst Agr & Life Sci, Lab Prot Engn & Comparat Immunol, 599 Gwanakro, Seoul 151921, South Korea.
RI YUN, Cheol-Heui/AAR-2775-2020
OI YUN, Cheol-Heui/0000-0002-0041-2887
FU Rural Development AdministrationRural Development Administration (RDA)
   [20080401 034054]; Ministry of Education, Science and TechnologyMinistry
   of Education, Science and Technology, Republic of Korea [2008-01571]
FX This work was Supported by the Biogreen 21 program (20080401 034054),
   Rural Development Administration and by the Expansion of Nuclear R&D
   Infrastructure Program through the Korea Science and Engineering
   Foundation funded by the Ministry of Education, Science and Technology
   (2008-01571). We thank the National Instrumentation Center for
   Environmental Management (NICEM), Seoul National University for
   providing the transmission electron microscope.
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NR 31
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Z9 39
U1 0
U2 7
PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 0006-291X
EI 1090-2104
J9 BIOCHEM BIOPH RES CO
JI Biochem. Biophys. Res. Commun.
PD JAN 1
PY 2010
VL 391
IS 1
BP 903
EP 908
DI 10.1016/j.bbrc.2009.11.161
PG 6
WC Biochemistry & Molecular Biology; Biophysics
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Biophysics
GA 544AV
UT WOS:000273624500159
PM 19951696
DA 2022-04-25
ER

PT J
AU Dorsam, B
   Seiwert, N
   Foersch, S
   Stroh, S
   Nagel, G
   Begaliew, D
   Diehl, E
   Kraus, A
   McKeague, M
   Minneker, V
   Roukos, V
   Reissig, S
   Waisman, A
   Moehler, M
   Stier, A
   Mangerich, A
   Dantzer, F
   Kaina, B
   Fahrer, J
AF Doersam, Bastian
   Seiwert, Nina
   Foersch, Sebastian
   Stroh, Svenja
   Nagel, Georg
   Begaliew, Diana
   Diehl, Erika
   Kraus, Alexander
   McKeague, Maureen
   Minneker, Vera
   Roukos, Vassilis
   Reissig, Sonja
   Waisman, Ari
   Moehler, Markus
   Stier, Anna
   Mangerich, Aswin
   Dantzer, Francoise
   Kaina, Bernd
   Fahrer, Joerg
TI PARP-1 protects against colorectal tumor induction, but promotes
   inflammation-driven colorectal tumor progression
SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF
   AMERICA
LA English
DT Article
DE DNA repair; PARP-1; colorectal carcinogenesis; mouse models; intestinal
   inflammation
ID ADP-RIBOSE POLYMERASE-1; DNA-DAMAGE; POLY(ADP-RIBOSE) POLYMERASE;
   O-6-METHYLGUANINE-DNA METHYLTRANSFERASE; MUCOSAL INJURY; DEFICIENT MICE;
   CANCER CELLS; IN-VIVO; REPAIR; INHIBITION
AB Colorectal cancer (CRC) is one of the most common tumor entities, which is causally linked to DNA repair defects and inflammatory bowel disease (IBD). Here, we studied the role of the DNA repair protein poly(ADP-ribose) polymerase-1 (PARP-1) in CRC. Tissue microarray analysis revealed PARP-1 overexpression in human CRC, correlating with disease progression. To elucidate its function in CRC, PARP-1 deficient (PARP-1(-/-)) and wild-type animals (WT) were subjected to azoxymethane (AOM)/dextran sodium sulfate (DSS)-induced colorectal carcinogenesis. Miniendoscopy showed significantly more tumors in WT than in PARP-1(-/-) mice. Although the lack of PARP-1 moderately increased DNA damage, both genotypes exhibited comparable levels of AOM-induced autophagy and cell death. Interestingly, miniendoscopy revealed a higher AOM/DSS-triggered intestinal inflammation in WT animals, which was associated with increased levels of innate immune cells and proinflammatory cytokines. Tumors in WT animals were more aggressive, showing higher levels of STAT3 activation and cyclin D1 up-regulation. PARP-1(-/-) animals were then crossed with O(6-)methylguanine-DNA methyltransferase (MGMT)-deficient animals hypersensitive to AOM. Intriguingly, PARP-1(-/-)/MGMT(-/-)double knockout (DKO) mice developed more, but much smaller tumors than MGMT(-/-) animals. In contrast to MGMT-deficient mice, DKO animals showed strongly reduced AOM-dependent colonic cell death despite similar O-6-methylguanine levels. Studies with PARP-1(-/-) cells provided evidence for increased alkylation-induced DNA strand break formation when MGMT was inhibited, suggesting a role of PARP-1 in the response to O-6-methylguanine adducts. Our findings reveal PARP-1 as a double-edged sword in colorectal carcinogenesis, which suppresses tumor initiation following DNA alkylation in a MGMT-dependent manner, but promotes inflammation-driven tumor progression.
C1 [Doersam, Bastian; Seiwert, Nina; Stroh, Svenja; Nagel, Georg; Begaliew, Diana; Diehl, Erika; Kraus, Alexander; Kaina, Bernd; Fahrer, Joerg] Univ Med Ctr Mainz, Dept Toxicol, D-55131 Mainz, Germany.
   [Seiwert, Nina; Fahrer, Joerg] Justus Liebig Univ Giessen, Rudolf Buchheim Inst Pharmacol, D-35392 Giessen, Germany.
   [Foersch, Sebastian] Univ Med Ctr Mainz, Inst Pathol, D-55131 Mainz, Germany.
   [McKeague, Maureen] ETH, Dept Hlth Sci & Technol, CH-8092 Zurich, Switzerland.
   [Minneker, Vera; Roukos, Vassilis] Inst Mol Biol, D-55128 Mainz, Germany.
   [Reissig, Sonja; Waisman, Ari] Univ Med Ctr Mainz, Inst Mol Med, D-55131 Mainz, Germany.
   [Moehler, Markus] Univ Med Ctr Mainz, Dept Internal Med 1, D-55131 Mainz, Germany.
   [Stier, Anna; Mangerich, Aswin] Univ Konstanz, Dept Biol, Mol Toxicol Grp, D-78457 Constance, Germany.
   [Dantzer, Francoise] Ecole Biotechnol Strasbourg, Inst Rech, F-67412 Illkirch Graffenstaden, France.
   [Doersam, Bastian] Philipps Univ, Ctr Tumor Biol & Immunol, Clin Hematol Oncol & Immunol, Expt Tumor Res, D-35043 Marburg, Germany.
RP Fahrer, J (corresponding author), Univ Med Ctr Mainz, Dept Toxicol, D-55131 Mainz, Germany.; Fahrer, J (corresponding author), Justus Liebig Univ Giessen, Rudolf Buchheim Inst Pharmacol, D-35392 Giessen, Germany.
EM Joerg.Fahrer@pharma.med.uni-giessen.de
RI Mangerich, Aswin/K-1197-2019; Kaina, Bernd/AAE-4692-2020; Roukos,
   Vassilis/AAC-4827-2020; McKeague, Maureen/AAP-4667-2020
OI Mangerich, Aswin/0000-0001-9742-2338; Dantzer,
   Francoise/0000-0003-0945-8483; Seiwert, Nina/0000-0003-2169-3670;
   Roukos, Vassilis/0000-0002-5065-3937; , Markus/0000-0003-2490-9131;
   McKeague, Maureen/0000-0002-3750-6027
FU University Medical Center, Mainz (MAIFOR); German Research
   FoundationGerman Research Foundation (DFG) [DFG-FA1034/3-1,
   DFG-KA724/29-1, INST 38/537-1]; UCT (Universitaeres Centrum fuer
   Tumorerkrankungen) Mainz
FX We thank Dr. Alexander Burkle (University of Konstanz) for the kind gift
   of PARP-1 and PAR antibodies, Dr. Leona D. Samson (Massachusetts
   Institute of Technology) for providing MGMT knockout animals, and Dr.
   Shana J Sturla (ETH Zurich) for providing support with mass
   spectrometry-based O<SUP>6</SUP>-MeG analysis. This work was supported
   by the University Medical Center, Mainz (MAIFOR), and the German
   Research Foundation (DFG-FA1034/3-1, DFG-KA724/29-1, and INST 38/537-1).
   S.F. was supported by a TransMed Fellowship of the UCT (Universitaeres
   Centrum fuer Tumorerkrankungen) Mainz. Tissue samples were provided by
   the tissue bank of the University Medical Center, Mainz, in accordance
   with the regulations of the tissue bank.
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NR 50
TC 37
Z9 42
U1 0
U2 5
PU NATL ACAD SCIENCES
PI WASHINGTON
PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 USA
SN 0027-8424
J9 P NATL ACAD SCI USA
JI Proc. Natl. Acad. Sci. U. S. A.
PD APR 24
PY 2018
VL 115
IS 17
BP E4061
EP E4070
DI 10.1073/pnas.1712345115
PG 10
WC Multidisciplinary Sciences
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Science & Technology - Other Topics
GA GD7MZ
UT WOS:000430697500026
PM 29632181
OA Green Published
DA 2022-04-25
ER

PT J
AU Guan, YJ
   Wang, YF
   Li, B
   Shen, K
   Li, QF
   Ni, YY
   Huang, L
AF Guan, Yanjie
   Wang, Yifei
   Li, Bo
   Shen, Kai
   Li, Quanfu
   Ni, Yingyin
   Huang, Lei
TI Mitophagy in carcinogenesis, drug resistance and anticancer therapeutics
SO CANCER CELL INTERNATIONAL
LA English
DT Review
DE Mitophagy; Mechanism; Carcinogenesis; Drug resistance; Anticancer
   therapeutics
ID SELECTIVE MITOCHONDRIAL AUTOPHAGY; COLORECTAL-CANCER;
   OXIDATIVE-PHOSPHORYLATION; BNIP3 PROTEIN; PARKIN; PINK1; NIX; APOPTOSIS;
   CELLS; MUTATIONS
AB The mitochondrion is an organelle that plays a vital role in energy production, cytoplasmic protein degradation and cell death. Mitophagy is an autophagic procedure that specifically clears damaged mitochondria and maintains its homeostasis. Emerging evidence indicates that mitophagy is involved in many physiological processes, including cellular homeostasis, cellular differentiation and nerve protection. In this review, we describe the regulatory mechanisms of mitophagy in mammals and yeasts and highlight the recent advances relevant to its function in carcinogenesis and drug resistance. Finally, a section has been dedicated to describing the role of mitophagy in anticancer therapeutics, which is a new frontier that offers a precise and promising strategy.
C1 [Guan, Yanjie; Wang, Yifei; Li, Bo; Shen, Kai; Li, Quanfu; Ni, Yingyin; Huang, Lei] Shanghai Jiao Tong Univ, Dept Histoembryol Genet & Dev Biol, Key Lab Cell Differentiat & Apoptosis,Sch Med, Chinese Minist Educ,Shanghai Key Lab Reprod Med, 280 South Chongqing Rd, Shanghai 200025, Peoples R China.
   [Li, Quanfu; Ni, Yingyin; Huang, Lei] Innovat Res Team High Level Local Univ Shanghai, Shanghai, Peoples R China.
RP Ni, YY; Huang, L (corresponding author), Shanghai Jiao Tong Univ, Dept Histoembryol Genet & Dev Biol, Key Lab Cell Differentiat & Apoptosis,Sch Med, Chinese Minist Educ,Shanghai Key Lab Reprod Med, 280 South Chongqing Rd, Shanghai 200025, Peoples R China.; Ni, YY; Huang, L (corresponding author), Innovat Res Team High Level Local Univ Shanghai, Shanghai, Peoples R China.
EM niyingyin@126.com; leihuang@shsmu.edu.cn
OI Huang, Lei/0000-0002-4851-4807
FU National Natural Science Foundation of ChinaNational Natural Science
   Foundation of China (NSFC) [82073111, 81874197]; Science and Technology
   Commission of Shanghai MunicipalityScience & Technology Commission of
   Shanghai Municipality (STCSM) [21S11901600]
FX The authors acknowledge financial support from National Natural Science
   Foundation of China (Grant Numbers 82073111, 81874197) and Science and
   Technology Commission of Shanghai Municipality (Grant Number
   21S11901600) to L.H.
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NR 89
TC 6
Z9 7
U1 6
U2 12
PU BMC
PI LONDON
PA CAMPUS, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
EI 1475-2867
J9 CANCER CELL INT
JI Cancer Cell Int.
PD JUL 5
PY 2021
VL 21
IS 1
AR 350
DI 10.1186/s12935-021-02065-w
PG 9
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA TI0HN
UT WOS:000672462300004
PM 34225732
OA gold, Green Published
DA 2022-04-25
ER

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   Guefack, Michel-Gael F.
   Tankeo, Simplice Beaudelaire
   Abdelfatah, Sara
   Bitchagno, Gabin T. M.
   Celik, Ilhami
   Kuete, Victor
   Efferth, Thomas
TI 8,8-bis-(Dihydroconiferyl)-diferulate displayed impressive cytotoxicity
   towards a panel of human and animal cancer cells
SO PHYTOMEDICINE
LA English
DT Article
DE 8, 8-bis-(dihydroconiferyl)-diferulate; Diferulic acid; Cell death;
   Multi-drug resistance; Natural product
ID BREAST-CANCER; MULTIDRUG-RESISTANCE; MEDICINAL-PLANTS; FERULIC ACID;
   MODES; TRANSPORTER; FERROPTOSIS; FLAVONOIDS; DEATH
AB Background: Recalcitrant cancers appear as a major obstacle to chemotherapy, prompting scientists to intensify the search for novel drugs to tackle the cell lines expressing multi-drug resistant (MDR) phenotypes.
   Purpose: The purpose of this study was to evaluate the antiproliferative potential of a ferrulic acid derivative, 8,8-bis-(dihydroconiferyl)-diferulate (DHCF2) on a panel of 18 cancer cell lines, including various sensitive and drug-resistant phenotypes, belonging to human and animals. The mode of induction of cell death by this compound was further studied.
   Methods: The antiproliferative activity, autophagy, ferroptotic and necroptotic cell death were evaluated by the resazurin reduction assay (RRA). CCRF-CEM leukemia cells were used for all mechanistic studies. A caspase-Glo assay was applied to evaluate the activity of caspases. Cell cycle analysis (PI staining), apoptosis (annexin V/PI staining), mitochondrial membrane potential (MMP) (JC-1) and reactive oxygen species (ROS) (H2DCFH-DA) were assessed by flow cytometry.
   Results: DHCF2 demonstrated impressive cytotoxic effects towards the 18 cancer cell lines tested, with IC50, values all below 6.5 mu M. The obtained IC50 values were in the range of 1.17 mu M (towards CCRF-CEM leukemia cells) to 6.34 mu M (towards drug-resistant HCT116 p53(-/- )human colon adenocarcinoma cells) for DHCF2 and from 0.02 mu M (against CCRF-CEM cells) to 122.96 mu M (against multidrug-resistant CEM/ADR5000 leukemia cells) for the reference drug, doxorubicin. DHCF2 had IC50, values lower than those of doxorubicin, against CEM/ADR5000 cells and on some melanoma cell lines, such as MaMel-80a cells, Mel-2a cells, MV3 cells and SKMel-505 cells. DHCF2 induced autophagy as well as apoptosis in CCRF-CEM cells though caspases activation, MMP alteration and increase of ROS production.
   Conclusion: The studied diferulic acid, DHCF2, is a promising antiproliferative compound. It deserves further indepth investigations with the ultimate aim to develop a novel drug to fight cancer drug resistance.
C1 [Mbaveng, Armelle T.; Tankeo, Simplice Beaudelaire; Abdelfatah, Sara; Kuete, Victor; Efferth, Thomas] Johannes Gutenberg Univ Mainz, Inst Pharm & Biochem, Dept Pharmaceut Biol, Staudinger Weg 5, D-55128 Mainz, Germany.
   [Mbaveng, Armelle T.; Guefack, Michel-Gael F.; Tankeo, Simplice Beaudelaire; Kuete, Victor] Univ Dschang, Fac Sci, Dept Biochem, POB 67, Dschang, Cameroon.
   [Damen, Francois; Bitchagno, Gabin T. M.] Univ Dschang, Fac Sci, Dept Chem, POB 67, Dschang, Cameroon.
   [Celik, Ilhami] Eskisehir Tech Univ, Fac Sci, Dept Chem, TR-26470 Eskisehir, Turkey.
RP Efferth, T (corresponding author), Johannes Gutenberg Univ Mainz, Inst Pharm & Biochem, Dept Pharmaceut Biol, Staudinger Weg 5, D-55128 Mainz, Germany.; Kuete, V (corresponding author), POB 1499, Bafoussam, Cameroon.
EM kuetevictor@yahoo.fr; efferth@uni-mainz.de
RI Mbahbou, Gabin T. Bitchagno/AAE-3745-2021; Bitchagno,
   Gabin/AAN-2538-2020
OI Bitchagno Mbahbou, Gabin Thierry/0000-0001-5506-451X; Kuete,
   Victor/0000-0002-1070-1236; Mbaveng, Armelle/0000-0003-4178-4967;
   Abdelfatah, Sara/0000-0002-9186-2516
FU Alexander von Humboldt FoundationAlexander von Humboldt Foundation;
   Scientific Research Projects Commission of Anadolu University,
   Eskisehir, Turkey [1306F110]
FX ATM is thankful to Alexander von Humboldt Foundation for an 18 months
   fellowship in Prof. Dr. Thomas Efferth's laboratory in Mainz, Germany
   through the ''Georg Foster Research Fellowship for Experienced
   Researcher'' program. VK and SBT are very grateful to the Alexander von
   Humboldt Foundation for the 6 months further research stay fellowship in
   Mainz. Authors are also thankful to the Institute of Molecular Biology
   gGmbH (IMB) (Mainz, Germany), where the flow cytometry measurements of
   MMP were performed. Authors acknowledge the Scientific Research Projects
   Commission of Anadolu University, Eskisehir, Turkey for the funding
   grant (1306F110).
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NR 49
TC 11
Z9 11
U1 0
U2 10
PU ELSEVIER GMBH
PI MUNICH
PA HACKERBRUCKE 6, 80335 MUNICH, GERMANY
SN 0944-7113
EI 1618-095X
J9 PHYTOMEDICINE
JI Phytomedicine
PD APR 15
PY 2020
VL 70
AR 153215
DI 10.1016/j.phymed.2020.153215
PG 10
WC Plant Sciences; Chemistry, Medicinal; Integrative & Complementary
   Medicine; Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Plant Sciences; Pharmacology & Pharmacy; Integrative & Complementary
   Medicine
GA LM1XQ
UT WOS:000532046800002
PM 32388040
DA 2022-04-25
ER

PT J
AU Ni, BB
   Shen, H
   Wang, W
   Lu, H
   Jiang, LS
AF Ni, Binbin
   Shen, Hao
   Wang, Wei
   Lu, Hua
   Jiang, Leisheng
TI TGF-beta 1 reduces the oxidative stress-induced autophagy and apoptosis
   in rat annulus fibrosus cells through the ERK signaling pathway
SO JOURNAL OF ORTHOPAEDIC SURGERY AND RESEARCH
LA English
DT Article
DE Hydrogen peroxide; Autophagy; Apoptosis; ERK; Annulus fibrosus cells;
   Glutathion peroxidase-1; Intervertebral disc degeneration
ID NUCLEUS PULPOSUS CELLS; COLON-CANCER CELLS; DEPENDENT APOPTOSIS;
   CELLULAR SENESCENCE; CROSS-TALK; IN-VITRO; MITOCHONDRIAL; DEATH;
   INVOLVEMENT; ACTIVATION
AB BackgroundThe aim of this study is to explore the effects of TGF-beta 1 on autophagy and apoptosis induced by exogenous hydrogen peroxide (H2O2) in annulus fibrosus (AF) cells and possible signal pathways involved in this process.MethodsAF cells were isolated from rat lumbar discs and subjected to different concentrations of exogenous H2O2 (50, 100, 200 mu mol/L) for different time periods (0.5, 1, 2, and 4h). Cell viability was determined by CCK-8 assay, and the levels of autophagy and apoptosis were evaluated by Western blotting and caspase 3, 8, 9 activity assay. By administration with different concentrations of TGF-beta 1 (5, 10, 20ng/mL), the effects of TGF-beta 1 on autophagy and apoptosis induced by H2O2 were observed, and the possible signaling pathways were also investigated by using various apoptosis inhibitors or an autophagy inhibitor Bafilomycin A (Baf A) in AF cells.ResultsH(2)O(2) significantly impaired cell viability in a dose- and time-dependent manner. H2O2 also induced a sudden and the highest level of autophagy at 1h, and gradually increased apoptosis through ERK pathway. The mitochondrial pathway was involved in H2O2-induced apoptosis in AF cells. TGF-beta 1 reduced the expression of p-ERK and downregulated the expressions of Beclin-1, LC3 II/I, and mitochondrial-related apoptotic proteins (Bax/Bcl-2, caspase-9). Meanwhile, TGF-beta 1 downregulated the level of intracellular H2O2 through upregulating the expression level of glutathione peroxidase-1 (GPx-1).ConclusionsTGF-beta 1 reduced autophagy and apoptosis induced by exogenous H2O2 through downregulating the expression of ERK in AF cells. TGF-beta 1 could downregulate the level of ERK and intracellular H2O2 by upregulating GPx-1.
C1 [Ni, Binbin; Shen, Hao; Wang, Wei; Lu, Hua; Jiang, Leisheng] Shanghai Jiao Tong Univ, Sch Med, Xinhua Hosp, Dept Orthopaed Surg, 1665 Kongjiang Rd, Shanghai 200092, Peoples R China.
RP Lu, H; Jiang, LS (corresponding author), Shanghai Jiao Tong Univ, Sch Med, Xinhua Hosp, Dept Orthopaed Surg, 1665 Kongjiang Rd, Shanghai 200092, Peoples R China.
EM luhua@xinhuamed.com.cn; jiangleisheng@xinhuamed.com.cn
FU National Natural Science Foundation of ChinaNational Natural Science
   Foundation of China (NSFC) [81171757]
FX This work was supported by the National Natural Science Foundation of
   China (No. 81171757).
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NR 43
TC 10
Z9 11
U1 1
U2 4
PU BMC
PI LONDON
PA CAMPUS, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 1749-799X
J9 J ORTHOP SURG RES
JI J. Orthop. Surg. Res.
PD JUL 29
PY 2019
VL 14
AR 241
DI 10.1186/s13018-019-1260-4
PG 13
WC Orthopedics
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Orthopedics
GA IM3ML
UT WOS:000477897200003
PM 31358027
OA gold, Green Published
DA 2022-04-25
ER

PT J
AU Huang, YC
   Yu, HS
   Chai, CY
AF Huang, Ya-Chun
   Yu, Hsin-Su
   Chai, Chee-Yin
TI Roles of oxidative stress and the ERK1/2, PTEN and p70S6K signaling
   pathways in arsenite-induced autophagy
SO TOXICOLOGY LETTERS
LA English
DT Article
DE Arsenite; Oxidative stress; Autophagy; p70S6K; ERK1/2
ID ACTIVATING TRANSCRIPTION FACTOR; HUMAN NEUROBLASTOMA-CELLS; COLON-CANCER
   CELLS; DNA-DAMAGE; S6 KINASE; C-JUN; EXPRESSION; PROTEIN; INHIBITION;
   REPAIR
AB Studies show that arsenite induces oxidative stress and modifies cellular function via phosphorylation of proteins and inhibition of DNA repair enzymes. Autophagy, which has multiple physiological and pathological roles in cellular function, is initiated by oxidative stress and is regulated by the signaling pathways of phosphatidylinositol 3-phosphate kinase (PI3K)/mammalian target of rapamycin (mTOR)/p70S6 kinase (p70S6K) and extracellular signaling-regulated protein kinase 1/2 (ERK1/2) that play important roles in oncogenesis. However, the effects of arsenite-induced oxidative stress on autophagy and on expression of related proteins are not fully understood. This study found that cells treated with sodium arsenite had reduced 8-oxoguanine DNA glycosylase 1 (OGG1) and increased 8-hydroxy-20deoxyguanosine (8-OHdG) and activating transcription factor (ATF) 3 in SV-40 immortalized human uroepithelial (SV-HUC-1) cells. Arsenite also increased the number of autophagosomes and increased levels of the autophagy markers Beclin-1 and microtubule-associated protein 1 light chain 3B. Reactive oxygen species scavenger decreased arsenite-induced autophagy in SV-HUC-1 cells. Our previous work showed that arsenite induced phosphorylation of the ERK1/2 signaling pathway. The current study further showed that arsenite decreased phosphatase and tensin homologue (PTEN) levels and increased phospho-p70S6 kinase (p-p70S6K) in SV-HUC-1 cells. However, both kinase inhibitor U0126 and the DNA (cytosine-5-)-methyltransferase 1 (DNMT1) inhibitor 5-aza-deoxycytidine abolished the effect of arsenite on expressions of PTEN and p-p70S6K. These results show that autophagy induced by arsenite exposure is mediated by oxidative stress, which regulates activation of the PTEN, p70S6K and ERK1/2 signaling pathways. Thus, this study clarifies the role of autophagy in arsenite-induced urothelial carcinogenesis. (C) 2015 Elsevier Ireland Ltd. All rights reserved.
C1 [Huang, Ya-Chun; Chai, Chee-Yin] Kaohsiung Med Univ, Dept Pathol, Coll Med, Kaohsiung, Taiwan.
   [Yu, Hsin-Su] Kaohsiung Med Univ, Dept Dermatol, Coll Med, Kaohsiung, Taiwan.
   [Yu, Hsin-Su] Kaohsiung Med Univ, Kaohsiung Med Univ Hosp, Dept Dermatol, Kaohsiung, Taiwan.
   [Chai, Chee-Yin] Kaohsiung Med Univ, Grad Inst Med, Coll Med, Kaohsiung, Taiwan.
   [Chai, Chee-Yin] Kaohsiung Med Univ, Kaohsiung Med Univ Hosp, Dept Pathol, Kaohsiung, Taiwan.
   [Chai, Chee-Yin] Natl Sun Yat Sen Univ, Inst Biomed Sci, Kaohsiung 80424, Taiwan.
RP Chai, CY (corresponding author), Kaohsiung Med Univ Hospital, Dept Pathol, 100,Tzyou 1st Rd, Kaohsiung 807, Taiwan.
EM cychai@kmu.edu.tw
OI Chai, Chee-Yin/0000-0003-0486-9742
FU Ministry of Science and Technology, TaiwanMinistry of Science and
   Technology, Taiwan [NSC101-2320-B-037-026-MY 3]; Kaohsiung Medical
   University Hospital, Kaohsiung, Taiwan [KMUH103-3R65]
FX This work was supported by a research grants from the Ministry of
   Science and Technology, Taiwan (NSC101-2320-B-037-026-MY 3), and
   Kaohsiung Medical University Hospital, Kaohsiung, Taiwan (KMUH103-3R65).
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NR 55
TC 22
Z9 27
U1 0
U2 24
PU ELSEVIER IRELAND LTD
PI CLARE
PA ELSEVIER HOUSE, BROOKVALE PLAZA, EAST PARK SHANNON, CO, CLARE, 00000,
   IRELAND
SN 0378-4274
EI 1879-3169
J9 TOXICOL LETT
JI Toxicol. Lett.
PD DEC 15
PY 2015
VL 239
IS 3
BP 172
EP 181
DI 10.1016/j.toxlet.2015.09.022
PG 10
WC Toxicology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Toxicology
GA CU9HZ
UT WOS:000363856800004
PM 26432159
DA 2022-04-25
ER

PT J
AU Shi, L
   Yan, H
   An, SX
   Shen, MQ
   Jia, WZ
   Zhang, RX
   Zhao, L
   Huang, G
   Liu, JJ
AF Shi, Liang
   Yan, Hui
   An, Shuxian
   Shen, Mengqin
   Jia, Wenzhi
   Zhang, Ruixue
   Zhao, Li
   Huang, Gang
   Liu, Jianjun
TI SIRT5-mediated deacetylation of LDHB promotes autophagy and
   tumorigenesis in colorectal cancer
SO MOLECULAR ONCOLOGY
LA English
DT Article
DE autophagy; colorectal cancer; deacetylation; lactate dehydrogenase B;
   sirtuin 5
ID CELLULAR-METABOLISM; SIRT5 DEACETYLATES; PROTEIN; MITOCHONDRIAL;
   DESUCCINYLATION; CELLS; MALONYLATION; ACETYLATION; DEGRADATION;
   CONTRIBUTES
AB Lactate dehydrogenase B (LDHB) is a glycolytic enzyme that catalyses the conversion of lactate and NAD(+) to pyruvate, NADH and H+. Protons (H+) generated by LDHB promote lysosomal acidification and autophagy in cancer, but how this role is regulated has not been defined. In this study, we identified an important post-translational mechanism by which LDHB is regulated during autophagy in cancer cells. Mass spectrometry revealed that protein sirtuin 5 (SIRT5) is a binding partner of LDHB that deacetylated LDHB at lysine-329, thereby promoting its enzymatic activity. Deacetylated LDHB increased autophagy and accelerated the growth of colorectal cancer (CRC) cells. Notably, SIRT5 knockout or inhibition by GW5074 increased LDHB acetylation at K329 and inhibited LDHB activity, which downregulated autophagy and CRC cell growth in vitro and in vivo. Clinically, the LDHB-Ac-K329 staining score in CRC tissues was lower than that in corresponding peritumour tissues. Low LDHB-Ac-K329 status was associated with malignant progression of human CRC and served as a potential prognostic indicator for patients with CRC. Altogether, we conclude that SIRT5-induced deacetylation of LDHB triggers hyperactivation of autophagy, a key event in tumorigenesis. Thus, the SIRT5/LDHB pathway may represent a novel target for treating CRC.
C1 [Shi, Liang; Yan, Hui; An, Shuxian; Shen, Mengqin; Jia, Wenzhi; Zhang, Ruixue; Zhao, Li; Huang, Gang; Liu, Jianjun] Shanghai Jiao Tong Univ, Dept Nucl Med, Renji Hosp, Sch Med, 1630 Dongfang Rd, Shanghai 200127, Peoples R China.
   [Huang, Gang] Shanghai Univ Med & Hlth Sci, Dept Canc Metab, Shanghai, Peoples R China.
RP Huang, G; Liu, JJ (corresponding author), Shanghai Jiao Tong Univ, Dept Nucl Med, Renji Hosp, Sch Med, 1630 Dongfang Rd, Shanghai 200127, Peoples R China.
EM huanggang0710@126.com; ljjtbno@126.com
FU National Natural Science Foundation of ChinaNational Natural Science
   Foundation of China (NSFC) [81771858, 81471687, 81530053, 81471685]
FX The authors thank Dr Chaoming Mao (Department of Nuclear Medicine, The
   Affiliated Hospital of Jiangsu University) for technical assistance with
   mature autolysosome abundance analysis by the mRFP-EGFP-LC3 reporter.
   Funding was provided by the National Natural Science Foundation of China
   (Nos. 81771858, 81471687, 81530053 and 81471685).
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NR 50
TC 44
Z9 47
U1 8
U2 25
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1878-0261
J9 MOL ONCOL
JI Mol. Oncol.
PD FEB
PY 2019
VL 13
IS 2
BP 358
EP 375
DI 10.1002/1878-0261.12408
PG 18
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA HK2NA
UT WOS:000457747900015
PM 30443978
OA gold, Green Published
DA 2022-04-25
ER

PT J
AU Sun, W
   Li, JL
   Zhou, LK
   Han, JY
   Liu, R
   Zhang, HY
   Ning, T
   Gao, ZY
   Liu, BR
   Chen, X
   Ba, Y
AF Sun, Wu
   Li, Jialu
   Zhou, Likun
   Han, Jiayi
   Liu, Rui
   Zhang, Haiyang
   Ning, Tao
   Gao, Zhiying
   Liu, Baorui
   Chen, Xi
   Ba, Yi
TI The c-Myc/miR-27b-3p/ATG10 regulatory axis regulates chemoresistance in
   colorectal cancer
SO THERANOSTICS
LA English
DT Article
DE miR-27b-3p; ATG10; chemoresistance; colorectal cancer; autophagy
ID TUMOR PROGRESSION; AUTOPHAGY; PROLIFERATION; CELLS; MICRORNAS; TARGET
AB Oxaliplatin (OXA) resistance is the major obstacle to the anticancer effects of chemotherapy in colorectal cancer (CRC) patients. MicroRNAs (miRNAs) play an important role in the chemoresistance of various tumors. Our objective is to clarify the underlying mechanism of miRNAs in chemoresistance and provide a potential strategy to improve the response of CRC patients to chemotherapeutics.
   Methods: MiRNA microarray and Real-time PCR were performed to compare changes in miRNA expression between oxaliplatin-resistant and the parental cells. CCK8, apoptosis assay, immunofluorescence and xenograft studies were used to elucidate the impact of miR-27b-3p on regulating chemoresistance. Luciferase reporter assay and western blot were carried to assess the regulatory role of miR-27b-3p in ATG10 expression. The effects of miR-27b-3p and ATG10 on autophagy were investigated by GFP-LC3 fluorescence microscopy, transmission electron microscopy, and western blot. ChIP assay and luciferase assay were performed to test the c-Myc's occupancy on the miR-27B promoter.
   Results: We observed that miR-27b-3p expression was significantly downregulated in oxaliplatin-resistant cell lines (SW480-OxR and HCT116-OxR) compared to the corresponding parental cell lines and that miR-27b-3p expression was positively correlated with disease-free survival (DFS) time in colorectal cancer patients. MiR-27b-3p could sensitize colorectal cancer cells to oxaliplatin in vitro and in vivo. Under oxaliplatin treatment, chemoresistant cells showed a higher autophagy level than parental cells. Moreover, we also identified that miR-27b-3p inhibited the expression of ATG10 at the posttranscriptional level, thus inhibiting autophagy. Further study demonstrated that c-Myc can inhibit the expression of miR-27b-3p via binding to the promoter region of miR-27B gene.
   Conclusions: Our study identifies a novel c-Myc/miR-27b-3p/ATG10 signaling pathway that regulates colorectal cancer chemoresistance. These results suggest that miR-27b-3p is not only a potential indicator for evaluating efficiency of chemotherapy, but also a valuable therapeutic target for CRC, especially for patients with chemoresistance.
C1 [Sun, Wu; Zhou, Likun; Han, Jiayi; Liu, Rui; Zhang, Haiyang; Ning, Tao; Ba, Yi] Tianjin Med Univ Canc Inst & Hosp, Natl Clin Res Ctr Canc, Tianjins Clin Res Ctr Canc, Key Lab Canc Prevent & Therapy, Huan Hu Xi Rd 18, Tianjin 300060, Peoples R China.
   [Li, Jialu] Shanghai Jiao Tong Univ, Shanghai Inst Digest Dis,Div Gastroenterol & Hepa, Sch Med,Key Lab Gastroenterol & Hepatol,Minist Hl, Renji Hosp,State Key Lab Oncogenes & Related Gene, Shanghai, Peoples R China.
   [Gao, Zhiying; Chen, Xi] Nanjing Univ, NAILS, Jiangsu Engn Res Ctr MicroRNA Biol & Biotechnol, State Key Lab Pharmaceut Biotechnol,Sch Life Sci, Xianlin Rd 163, Nanjing 210046, Jiangsu, Peoples R China.
   [Liu, Baorui] Nanjing Univ, Comprehens Canc Ctr, Drum Tower Hosp, Med Sch, Zhognshan Rd 321, Nanjing 210008, Jiangsu, Peoples R China.
   [Liu, Baorui] Nanjing Univ, Clin Canc Inst, Zhognshan Rd 321, Nanjing 210008, Jiangsu, Peoples R China.
RP Ba, Y (corresponding author), Tianjin Med Univ Canc Inst & Hosp, Natl Clin Res Ctr Canc, Tianjins Clin Res Ctr Canc, Key Lab Canc Prevent & Therapy, Huan Hu Xi Rd 18, Tianjin 300060, Peoples R China.; Chen, X (corresponding author), Nanjing Univ, NAILS, Jiangsu Engn Res Ctr MicroRNA Biol & Biotechnol, State Key Lab Pharmaceut Biotechnol,Sch Life Sci, Xianlin Rd 163, Nanjing 210046, Jiangsu, Peoples R China.; Liu, BR (corresponding author), Nanjing Univ, Comprehens Canc Ctr, Drum Tower Hosp, Med Sch, Zhognshan Rd 321, Nanjing 210008, Jiangsu, Peoples R China.; Liu, BR (corresponding author), Nanjing Univ, Clin Canc Inst, Zhognshan Rd 321, Nanjing 210008, Jiangsu, Peoples R China.
EM baoruiliu07@163.com; xichen@nju.edu.cn; bayi@tjmuch.com
FU National Natural Science Foundation of ChinaNational Natural Science
   Foundation of China (NSFC) [8170243, 81772629, 81602158, 81602156,
   81702275, 81802363, 81702431, 81702437, 81772843]; Demonstrative
   Research Platform of Clinical Evaluation Technology for New Anticancer
   Drugs [2018ZX09201015]; Tianjin Science FoundationNatural Science
   Foundation of Tianjin [18JCQNJC81900, 18JCYBJC92000, 18JCYBJC25400,
   16PTSYJC00170, 18JCYBJC92900]; Science & Technology Development Fund of
   the Tianjin Education Commission for Higher Education [2018KJ046,
   2017KJ227, 2017KJ204]
FX This work was supported by grants from the National Natural Science
   Foundation of China (Nos. 8170243, 81772629, 81602158, 81602156,
   81702275, 81802363, 81702431, 81702437, 81772843) and the Demonstrative
   Research Platform of Clinical Evaluation Technology for New Anticancer
   Drugs (No. 2018ZX09201015). This work was also supported by the Tianjin
   Science Foundation (Nos. 18JCQNJC81900, 18JCYBJC92000, 18JCYBJC25400,
   16PTSYJC00170, 18JCYBJC92900) and the Science & Technology Development
   Fund of the Tianjin Education Commission for Higher Education
   (2018KJ046, 2017KJ227, 2017KJ204). The funders had no role in the study
   design, the data collection and analysis, the interpretation of the
   data, the writing of the report, and the decision to submit this article
   for publication.
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NR 46
TC 37
Z9 38
U1 4
U2 11
PU IVYSPRING INT PUBL
PI LAKE HAVEN
PA PO BOX 4546, LAKE HAVEN, NSW 2263, AUSTRALIA
SN 1838-7640
J9 THERANOSTICS
JI Theranostics
PY 2020
VL 10
IS 5
BP 1981
EP 1996
DI 10.7150/thno.37621
PG 16
WC Medicine, Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Research & Experimental Medicine
GA KD6XK
UT WOS:000508008300001
PM 32104496
OA gold, Green Published
DA 2022-04-25
ER

PT J
AU Wang, WC
   Zhang, R
   Wang, JX
   Tang, J
   Wang, MG
   Kuang, Y
AF Wang, Wencong
   Zhang, Rui
   Wang, Jinxing
   Tang, Jun
   Wang, Mingan
   Kuang, Yu
TI Antitumour Activity of Muricatacin Isomers and its Derivatives in Human
   Colorectal Carcinoma Cell HCT116
SO ANTI-CANCER AGENTS IN MEDICINAL CHEMISTRY
LA English
DT Article
DE Muricatacin; antitumour activity; colorectal carcinoma cell line HCT116;
   cell cycle arrest; apoptosis; autophagy
ID P53; 6-ACETOXY-5-HEXADECANOLIDE; ACETOGENINS; RESISTANCE; ARREST
AB Background and Purpose: Colorectal cancer is one of the leading causes of cancer-related death in elderly people. The natural product muricatacin is an important member of the gamma-lactone family, and it has exhibited antitumour activity in multiple cancer cell lines; however, the antitumour activities of muricatacin stereoisomers and their derivatives in colorectal cancer cells have not yet been systematically explored.
   Methods: The colorectal carcinoma cell line HCT116 was investigated in this study. Cell proliferation was assessed by MTT assay or crystal violet staining. Cell cycle arrest and cell apoptosis were evaluated by flow cytometry assay. The expression levels of p53, p21, cyclin E, cyclin D1, caspase-3, cleaved caspase-3, caspase-9, cleaved caspase-9 and LC3B were measured using western blot analysis. Autophagy induced by M2 was monitored by immunofluorescence assay with an antibody against LC3B.
   Results: Cell proliferation assays showed that both naturally occurring muricatacin (M4) and its synthetic stereoisomer (M2) are potent cell growth inhibitors in HCT116 cells, with IC50 values of 79.43 and 83.17 mu M, respectively; these values are much lower than those of the other two isomers, M1 and M3, and those of the six-membered lactone analogues. The flow cytometry analysis revealed that M2 and M4 induced significant cell cycle arrest during G(0)/G(1) phase and caused relatively low apoptosis rates in HCT1 16 cells. Further analysis indicated that M2 caused p53-independent p21 induction and cyclin E/cyclin D1 downregulation. In addition, M2 also markedly induced autophagy in the early stage of administration.
   Conclusion: Our results suggested that muricatacins possess potent antitumour activity against the colorectal carcinoma cell tine HCT116 through inducing G(0)/G(1) phase cell cycle arrest and autophagy in the early stage of administration.
C1 [Wang, Wencong; Zhang, Rui; Wang, Jinxing; Tang, Jun; Kuang, Yu] China Agr Univ, Coll Vet Med, Dept Basic Vet Med, Beijing 100193, Peoples R China.
   [Wang, Mingan] China Agr Univ, Coll Sci, Dept Appl Chem, Beijing 100193, Peoples R China.
RP Kuang, Y (corresponding author), Fac China Agr Univ, Dept Basic Vet Med, POB 100193, Beijing, Peoples R China.
EM kuangyu@cau.edu.cn
OI Zhang, Rui/0000-0001-9015-0819
FU National Natural Science Foundation of ChinaNational Natural Science
   Foundation of China (NSFC) [21172254, 31500703]
FX The research was supported by the National Natural Science Foundation of
   China (No. 21172254 and 31500703).
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NR 28
TC 0
Z9 0
U1 3
U2 14
PU BENTHAM SCIENCE PUBL LTD
PI SHARJAH
PA EXECUTIVE STE Y-2, PO BOX 7917, SAIF ZONE, 1200 BR SHARJAH, U ARAB
   EMIRATES
SN 1871-5206
EI 1875-5992
J9 ANTI-CANCER AGENT ME
JI Anti-Cancer Agents Med. Chem.
PY 2020
VL 20
IS 2
BP 254
EP 263
DI 10.2174/1871520619666191115111032
PG 10
WC Oncology; Chemistry, Medicinal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Pharmacology & Pharmacy
GA LI9NX
UT WOS:000529804200004
PM 31729294
DA 2022-04-25
ER

PT J
AU Zhang, L
   Rong, Y
   Zheng, J
   Yang, CL
   Chen, YZ
   Wang, J
   Wei, G
AF Zhang, Lei
   Rong, Ying
   Zheng, Jie
   Yang, Chengli
   Chen, Yongzheng
   Wang, Jing
   Wei, Gang
TI Design, synthesis and biological evaluation of novel nitric
   oxide-donating podophyllotoxin derivatives as potential
   antiproliferative agents against multi-drug resistant leukemia cells
SO RSC ADVANCES
LA English
DT Article
ID ANTI-MDR AGENTS; COLON-CANCER CELLS; ANTITUMOR AGENTS; SIGNALING
   PATHWAYS; IN-VITRO; AUTOPHAGY; CHEMOTHERAPY; DOXORUBICIN; APOPTOSIS;
   CYTOTOXICITY
AB Multidrug resistance remains a major obstacle for the effective treatment of carcinoma. To find new drugs for the chemotherapy of drug-resistant leukemia, in this study, two novel nitric oxide-donating podophyllotoxin derivatives were synthesized and preliminarily evaluated in vitro. Biological evaluation indicated that the more active molecule, S1, enhanced the intracellular NO level and significantly inhibited the proliferation of drug-resistant K562/VCR and K562/ADR cells with IC50 values of 0.008 +/- 0.001 and 0.007 +/- 0.001 mu M, respectively, which were similar to that of sensitive K562 cells. Furthermore, it was observed that S1 blocked the G2 phase of the K562/ADR cell cycle by disruption of the microtubule organization and inhibition of CDK1 and CDK2 expression. Meanwhile, S1 induced apoptosis of K562/ADR cells via mitochondrial depolarization and activation of caspase-3. In addition, S1 suppressed the P-gp expression, induced autophagy by regulation of Beclin1 and LC3-II, and inhibited the mTOR and STAT3 signaling in K562/ADR cells. Overall, S1 may be a promising candidate against drug-resistant leukemia.
C1 [Zhang, Lei; Yang, Chengli; Chen, Yongzheng; Wang, Jing] Zunyi Med Univ, Green Pharmaceut Engn Res Ctr Guizhou Prov, Gener Drug Res Ctr Guizhou Prov, Sch Pharm, Zunyi 563003, Peoples R China.
   [Rong, Ying] Zunyi Med Univ, Affiliated Hosp, Dept Pediat 2, Zunyi 563003, Peoples R China.
   [Zheng, Jie] Zunyi Med Univ, Affiliated Hosp, Dept Nephrol & Rheumatol, Zunyi 563003, Peoples R China.
   [Wei, Gang] CSIRO Mfg, POB 218, Lindfield, NSW 2070, Australia.
RP Zhang, L; Wang, J (corresponding author), Zunyi Med Univ, Green Pharmaceut Engn Res Ctr Guizhou Prov, Gener Drug Res Ctr Guizhou Prov, Sch Pharm, Zunyi 563003, Peoples R China.; Wei, G (corresponding author), CSIRO Mfg, POB 218, Lindfield, NSW 2070, Australia.
EM lzhang@zmc.edu.cn; wangjing@zmc.edu.cn; gang.wei@csiro.au
FU Ministry of Education "Chunhui Project" Foundation of China [Z2015008];
   National Natural Science Foundation of ChinaNational Natural Science
   Foundation of China (NSFC) [81860622]; Department of Science and
   Technology of Guizhou ProvinceDepartment of Science & Technology (DOST),
   PhilippinesDepartment of Science & Technology (India) [[2017]1219];
   Joint Fund of the Department of Science and Technology of Zunyi City and
   Zunyi Medical University [[2018]27]; National First-Rate Construction
   Discipline of Guizhou Province (Pharmacy) [YLXKJS-YX-04]
FX This work was supported by Ministry of Education "Chunhui Project"
   Foundation of China (No. Z2015008), National Natural Science Foundation
   of China (No. 81860622), Department of Science and Technology of Guizhou
   Province (No. [2017]1219), Joint Fund of the Department of Science and
   Technology of Zunyi City and Zunyi Medical University ([2018]27) and
   National First-Rate Construction Discipline of Guizhou Province
   (Pharmacy) (YLXKJS-YX-04).
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NR 50
TC 1
Z9 1
U1 0
U2 2
PU ROYAL SOC CHEMISTRY
PI CAMBRIDGE
PA THOMAS GRAHAM HOUSE, SCIENCE PARK, MILTON RD, CAMBRIDGE CB4 0WF, CAMBS,
   ENGLAND
SN 2046-2069
J9 RSC ADV
JI RSC Adv.
PY 2018
VL 8
IS 60
BP 34266
EP 34274
DI 10.1039/c8ra06360e
PG 9
WC Chemistry, Multidisciplinary
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Chemistry
GA GY3CK
UT WOS:000448423500010
OA gold, Green Submitted
DA 2022-04-25
ER

PT J
AU El-kott, AF
   Al-kahtani, MA
   Shati, AA
AF El-kott, Attalla Farag
   Al-kahtani, Mohammed Ali
   Shati, Ali A.
TI Calycosin induces apoptosis in adenocarcinoma HT29 cells by inducing
   cytotoxic autophagy mediated by SIRT1/AMPK-induced inhibition of
   Akt/mTOR
SO CLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY
LA English
DT Article
DE AMPK; autophagy; Calycosin; colorectal cancer; mTOR; SIRT1
ID COLORECTAL-CANCER CELLS; ADJUVANT TREATMENT; SIRT1; FAMILY; EXPRESSION;
   RESISTANCE; MIGRATION; HYPOXIA; STRESS; DEATH
AB Autophagy promotes cell survival or induces apoptosis in cancer cells. While SIRT1 and AMPK induce autophagy in both normal and cancer cells, Akt and mTOR can inhibit it. Calycosin, a methoxyisoflavone, protects against several types of solid tumours including colorectal cancer. However, the mechanisms behind the antitumour effect of Calycosin remain largely unknown. This study investigates if autophagy mediates the anti-tumourigenesis effect afforded by Calycosin and examines if this effect involves activation of SIRT1 and/or AMPK. Human colorectal (HT29) carcinoma cells were cultured under normal conditions with Calycosin (50 mu mol/L) in the presence or absence of chloroquine (10 mu mol/L), EX-527 (100 nmol/L, SIRT1 inhibitor), or IGF-1 (100 ng/mL, Akt/mTOR activator) for 48 hours. Calycosin inhibited cell growth, proliferation and invasion and increased protein levels of Beclin-1 and LC3II, markers of autophagy. It significantly increased protein levels of cleaved caspase-3, Bax, and SIRT1, and activity of AMPK and reduced those of Bcl-2. These effects were parallel with concomitant reduction in protein levels p-src, integrin-beta 1 and Cyclin-D1 and activities of Akt and mTOR. Inhibition of autophagy by CQ reversed all these effects except cell invasion. Interestingly, co-incubating the cells with either EX-527 or IGF-1 completely prevented Calycosin-induced autophagy and all other associated effects and increased cell invasion. Also, blockade of SIRT-1 prevented the activation of AMPK, Akt, and mTOR, suggesting it to be an upstream regulator of these markers. In conclusion, Calycosin stimulates CRC cell apoptosis and inhibits their invasion by acting as SIRT1 activator which induces activation of AMPK-induced inhibition of Akt/mTOR axis.
C1 [El-kott, Attalla Farag; Al-kahtani, Mohammed Ali; Shati, Ali A.] King Khalid Univ, Coll Sci, Biol Dept, Abha, Saudi Arabia.
   [El-kott, Attalla Farag] Damanhour Univ, Coll Sci, Zool Dept, Damanhour, Egypt.
RP El-kott, AF (corresponding author), King Khalid Univ, Coll Sci, POB 9004, Abha 61413, Saudi Arabia.
EM elkottaf@yahoo.com
RI El-kott, Attalla F/D-1971-2017; El-kott, Attalla/AAW-5325-2021
OI El-kott, Attalla/0000-0001-5060-0790; Shati, Ali/0000-0003-1800-7238
FU King Khalid University [R.G.P.1/46/39]
FX King Khalid University, Grant/Award Number: R.G.P.1/46/39
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NR 51
TC 18
Z9 21
U1 1
U2 24
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0305-1870
EI 1440-1681
J9 CLIN EXP PHARMACOL P
JI Clin. Exp. Pharmacol. Physiol.
PD OCT
PY 2019
VL 46
IS 10
BP 944
EP 954
DI 10.1111/1440-1681.13133
PG 11
WC Pharmacology & Pharmacy; Physiology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy; Physiology
GA IY2GM
UT WOS:000486208400009
PM 31276230
DA 2022-04-25
ER

PT J
AU Yao, JL
   Xie, JS
   Xie, BB
   Li, YR
   Jiang, WL
   Sui, XB
   Zhou, XY
   Pan, HM
   Han, WD
AF Yao, Junlin
   Xie, Jiansheng
   Xie, Binbin
   Li, Yiran
   Jiang, Wiling
   Sui, Xinbing
   Zhou, Xiaoyun
   Pan, Hongming
   Han, Weidong
TI Therapeutic effect of hydroxychloroquine on colorectal carcinogenesis in
   experimental murine colitis
SO BIOCHEMICAL PHARMACOLOGY
LA English
DT Article
DE Hydroxychloroquine; Colitis-associated colorectal cancer; Macrophages;
   Toll-like receptor 4; Reactive oxygen species
ID INFLAMMATORY-BOWEL-DISEASE; TOLL-LIKE RECEPTOR-3; CANCER CELLS; REACTIVE
   OXYGEN; AUTOPHAGY INHIBITION; OXIDATIVE STRESS; TNF-ALPHA; CHLOROQUINE;
   MODEL; MICE
AB Chronic inflammation in the intestine is a strong risk factor for colitis-associated colorectal cancer (CAC). Hydroxychloroquine (HCQ) is widely used as an anti-inflammatory drug in the treatment of immune mediated inflammatory disorders and various tumors. However, little is known regarding the effects of HCQ on colitis-associated tumorigenesis. In this study, mice treated with HCQ showed a significant reduction in early-stage colitis following azoxymethane (AOM)/dextran sodium sulfate (DSS) administration, as well as a remarkable inhibition of colonic tumorigenesis and tumor growth at late stages of CAC. Mechanistically, the therapeutic effects of HCQ were attributed to inhibition of inflammatory responses and production of mutagenic reactive oxygen species (ROS) in immune cells and subsequent promotion of apoptosis and cell cycle arrest in tumor cells. Furthermore, we found that HCQ inhibited the production of inflammatory cytokines and ROS in response to toll-like receptor 4 (TLR4) activation in macrophages. Our data presented herein may help guide the clinical use of HCQ as a prevention and treatment strategy for CAC. (C) 2016 Elsevier Inc. All rights reserved.
C1 [Yao, Junlin; Xie, Binbin; Li, Yiran; Jiang, Wiling; Sui, Xinbing; Pan, Hongming; Han, Weidong] Zhejiang Univ, Inst Clin Sci, Sir Run Run Shaw Hosp, Dept Med Oncol,Coll Med, Hangzhou, Zhejiang, Peoples R China.
   [Xie, Jiansheng; Pan, Hongming; Han, Weidong] Zhejiang Univ, Inst Clin Sci, Sir Run Run Shaw Hosp, Lab Canc Biol,Coll Med, Hangzhou, Zhejiang, Peoples R China.
   [Zhou, Xiaoyun] Hangzhou Xiasha Hosp, Dept Med Oncol, Hangzhou, Zhejiang, Peoples R China.
RP Pan, HM; Han, WD (corresponding author), Zhejiang Univ, Sch Med, Sir Run Run Shaw Hosp, 3 East Qinchun Rd, Hangzhou 310016, Zhejiang, Peoples R China.
EM hongmingpan@gmail.com; hanwd@zju.edu.cn
FU National Natural Science Foundation of ChinaNational Natural Science
   Foundation of China (NSFC) [81272593, 81572592, 81372621]; Key Projects
   of Natural Foundation of Zhejiang Province [LZ15H160001]; National
   Health and Family Planning Commission Fund [2015112271]; Zhejiang
   Province Preeminence Youth Fund [LR16H160001]
FX This work was supported by the National Natural Science Foundation of
   China (81272593, 81572592), the Key Projects of Natural Foundation of
   Zhejiang Province (LZ15H160001), and the National Health and Family
   Planning Commission Fund (2015112271) to H. Pan; and the National
   Natural Science Foundation of China (81372621) and Zhejiang Province
   Preeminence Youth Fund (LR16H160001) to W. Han.
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NR 64
TC 10
Z9 12
U1 1
U2 19
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0006-2952
EI 1873-2968
J9 BIOCHEM PHARMACOL
JI Biochem. Pharmacol.
PD SEP 1
PY 2016
VL 115
BP 51
EP 63
DI 10.1016/j.bcp.2016.06.004
PG 13
WC Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA DT5TO
UT WOS:000381545700006
PM 27288548
DA 2022-04-25
ER

PT S
AU Pawelek, JM
   Chakraborty, AK
AF Pawelek, John M.
   Chakraborty, Ashok K.
BE VandeWoude, GF
   Klein, G
TI The Cancer Cell-Leukocyte Fusion Theory of Metastasis
SO ADVANCES IN CANCER RESEARCH, VOL 101
SE Advances in Cancer Research
LA English
DT Review; Book Chapter
ID N-ACETYLGLUCOSAMINYLTRANSFERASE-V; HEPATOCYTE GROWTH-FACTOR;
   EPITHELIAL-MESENCHYMAL TRANSITIONS; MELANOCYTE-STIMULATING HORMONE;
   FOCAL-ADHESION KINASE; MARROW-DERIVED CELLS; NORMAL MOUSE CELLS;
   FACTOR-KAPPA-B; BETA-1-6 BRANCHED OLIGOSACCHARIDES; CUTANEOUS
   MALIGNANT-MELANOMA
AB The cause of metastasis remains elusive despite vast information oil cancer cells. We posit that cancer cell fusion with microphages or other migratory bone marrow-derived cells (BMDCs) provides an explanation. BMDCs fused with tumor cells were present in animal tumor xenografts where they were associated with metastases. In myeloma patients, transcriptionally active myeloma nuclei were incorporated into osteoclasts through fusion. In patients with renal cell carcinoma arising poststem cell transplant, donor genes were incorporated in recipient cancer cell nuclei, most likely through fusion, and showed Minor distribution patterns characteristic of cancer stern cells. Melanoma-macrophage hybrids generated ill vitro contained chromosomes front both parental partners, showed increased ploidy, and transcribed and translated genes front both parents. They exhibited chemotactic migration in vitro toward fibronectin and exhibited high frequencies of metastasis when implanted in mice. They produced macromolecules that are characteristic of macrophages and known indicators of metastasis (c-Met, SPARC, MCR1, GnT-V, and the integrin subunits alpha(3), alpha(5), alpha(6), alpha(v), beta(1), beta(3)). They also produced high levels of beta 1,6-branched oligosaccharides-predictors of poor survival in patients with melanoma or carcinomas of the breast, lung, and colon. WC thus hypothesize such gene expression patterns in cancer are generated through fusion. Tumor hybrids also showed active autophagy, a characteristic of both metastatic Cancers and macrophages. BMDC-tumor cell fusion explains epidermal-mesenchymal transition in cancer since BMDCs express mesodermal traits and epithelial-mesenchymal transition regulators (Twist, SPARC, and others). If BMDC-tumor cell fusion underlies invasion and metastasis in human Cancer, new approaches for therapeutic intervention would lie mandated. (c) 2008 Elsevier Inc.
C1 [Pawelek, John M.; Chakraborty, Ashok K.] Yale Univ, Sch Med, Dept Dermatol, New Haven, CT 06510 USA.
   [Pawelek, John M.; Chakraborty, Ashok K.] Yale Univ, Sch Med, Yale Canc Ctr, New Haven, CT USA.
RP Pawelek, JM (corresponding author), Yale Univ, Sch Med, Dept Dermatol, New Haven, CT 06510 USA.
RI Chakraborty, A/AAI-2479-2020
OI Chakraborty, A/0000-0001-8054-4574
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NR 268
TC 117
Z9 123
U1 4
U2 25
PU ELSEVIER ACADEMIC PRESS INC
PI SAN DIEGO
PA 525 B STREET, SUITE 1900, SAN DIEGO, CA 92101-4495 USA
SN 0065-230X
BN 978-0-12-374359-6
J9 ADV CANCER RES
JI Adv.Cancer Res.
PY 2008
VL 101
BP 397
EP +
DI 10.1016/S0065-230X(08)00410-7
PG 51
WC Oncology
WE Book Citation Index – Science (BKCI-S); Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA BIO91
UT WOS:000261403100010
PM 19055949
DA 2022-04-25
ER

PT J
AU Wang, YF
   Zhang, SY
   Dang, SW
   Fang, X
   Liu, M
AF Wang, Yunfeng
   Zhang, Songyan
   Dang, Shuwei
   Fang, Xuan
   Liu, Ming
TI Overexpression of microRNA-216a inhibits autophagy by targeting
   regulated MAP1S in colorectal cancer
SO ONCOTARGETS AND THERAPY
LA English
DT Article
DE miR-216a; MAP1S; autophagy; TGF-beta; colorectal cancer
ID CELL-PROLIFERATION; SUPPRESSES PROLIFERATION; PROMOTES AUTOPHAGY; TUMOR
   INVASION; APOPTOSIS; MIGRATION; EXPRESSION
AB Background: Autophagy executes the rapid degradation of unneeded proteins and organelles through the lysosomal pathway, and is a crucial catabolic process widely conserved among eukaryotes. miRNAs can modulate autophagy by targeting genes encoding proteins involved in the process. A great deal of researchhas indicated that miR-216a was a functional miRNA related to tumorigenesis. However, the contribution of miR-216a to autophagy in colorectal cancer (CRC) remains unclear. The purpose of this study was to investigate the role of miR-216a in autophagy in CRC cells.
   Methods: The expression levels of miR-216a in 67 paired CRC patients were evaluated by qRT-PCR. Direct gene targeting predicted by TargetScan and miRanda was confirmed by luciferase activity. Western blot and flow cytometry were used to identify the regulatory mechanism of miR-216a on autophagy in CRC cells.
   Results: We determined that miR-216a is downregulated in CRC by screening its expression in 67 CRC tissue samples. Dual luciferase reporter assays showed that miR-216a binds the 3'-UTR of MAP1S, suggesting that MAP1S is a direct target of miR-216a. miR-216a could inhibit autophagy in HCT-116 and HT-29 CRC cells through downregulating MAP1S expression. Flow cytometry and Western blot analysis demonstrated that overexpression of miR-216a reduced MAP1S mRNA and protein levels. Moreover, we determined that miR-216a-regulated inhibition of autophagy via MAP1S regulation involves the TGF-beta pathway.
   Conclusion: Taken together, our findings indicate that miR-216a was a tumor-suppressor miRNA in human CRC, which can inhibit autophagy via the TGF-beta/MAP1S pathway.
C1 [Wang, Yunfeng; Zhang, Songyan; Dang, Shuwei; Fang, Xuan; Liu, Ming] Harbin Med Univ, Affiliated Hosp 4, Dept Gen Surg, 37 Yiyuan Rd, Harbin 150001, Heilongjiang, Peoples R China.
RP Liu, M (corresponding author), Harbin Med Univ, Affiliated Hosp 4, Dept Gen Surg, 37 Yiyuan Rd, Harbin 150001, Heilongjiang, Peoples R China.
EM mingliu35@hrbmu.edu.cn
FU National Natural Science Foundation of ChinaNational Natural Science
   Foundation of China (NSFC) [81372612, 81302059]
FX This work was supported by funds from the National Natural Science
   Foundation of China (Grant No. 81372612 and 81302059).
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NR 27
TC 7
Z9 8
U1 1
U2 1
PU DOVE MEDICAL PRESS LTD
PI ALBANY
PA PO BOX 300-008, ALBANY, AUCKLAND 0752, NEW ZEALAND
SN 1178-6930
J9 ONCOTARGETS THER
JI OncoTargets Ther.
PY 2019
VL 12
BP 4621
EP 4629
DI 10.2147/OTT.S196992
PG 9
WC Biotechnology & Applied Microbiology; Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biotechnology & Applied Microbiology; Oncology
GA ID4FO
UT WOS:000471632500001
PM 31354295
OA Green Published, gold, Green Submitted
DA 2022-04-25
ER

PT J
AU Zhang, XQ
   Hu, XB
   Mu, SJ
   Zhan, YH
   An, QX
   Liu, ZX
   Huang, XF
AF Zhang, Xianqing
   Hu, Xingbin
   Mu, Shijie
   Zhan, Yonghua
   An, Qunxing
   Liu, Zhixin
   Huang, Xiaofeng
TI RETRACTED: Apogossypolone inhibits the proliferation of LNCaP cells in
   vitro and in vivo (Retracted article. See vol. 17, pg. 6927, 2018)
SO MOLECULAR MEDICINE REPORTS
LA English
DT Article; Retracted Publication
DE apogossypolone; autophagy; apoptosis; LNCaP cell; nude mouse
ID SUPPRESSES TUMOR-GROWTH; BCL-2 FAMILY PROTEINS; HUMAN-PROSTATE-CANCER;
   HEPATOCELLULAR-CARCINOMA; COLON-CARCINOMA; APOPTOSIS; AUTOPHAGY;
   (-)-GOSSYPOL; GOSSYPOL; RADIATION
AB The aim of the present study was to investigate the anti-tumor effect of apogossypolone (ApoG2) on human LNCaP cells in vitro and in vivo. Cell viability was evaluated using an MTT assay. Cell autophagy and apoptosis-were detected by flow cytometry and using a terminal deoxynucleotidyl transferase dUTP nick end labeling assay, respectively. Morphological autophagy alterations were observed by transmission electron microscopy. The formation of acidic vesicular organelles was assessed by acridine orange staining and fluorescence microscopy. Quantitative polymerase chain reaction (qPCR) was conducted to detect the expression levels of apoptosis-associated protein B-cell lymphoma 2 (Bcl-2) and Bak. The models of transplantation tumors in nude mice were established via subcutaneous injection of LNCaP cells. Growth of LNCaP cells was inhibited by ApoG2 treatment. Flow cytometry demonstrated that ApoG2 induced apoptosis in LNCaP cells. The Bcl-2 expression was decreased while Bak expression was increased. In addition, activation of cysteine aspartate protease (caspase)-3 and -8 was observed and 3-methyladenine (3-MA) enhanced apoptosis of LNCaP cells. Furthermore, nude mice treated with ApoG2 demonstrated a significant decrease in tumor volume and a significant increase in cell viability. Immunohistochemical analysis of tumor tissues demonstrated that ApoG2 enhanced caspase-3, -8, LC-3B and beclin-1 expression and reduced the expression of Bcl-2. ApoG2 was able to effectively suppress the growth of LNCaP cells through the induction of autophagy and apoptosis.
C1 [Zhang, Xianqing; Hu, Xingbin; Mu, Shijie; An, Qunxing; Liu, Zhixin] Fourth Mil Med Univ, Xijing Hosp, Dept Blood Transfus, Xian 710032, Shaanxi, Peoples R China.
   [Zhan, Yonghua] Xidian Univ, Sch Life Sci & Technol, Engn Res Ctr Mol & Neuroimaging, Xian 710071, Shaanxi, Peoples R China.
   [Huang, Xiaofeng] Fourth Mil Med Univ, Sch Basic Med, Cent Lab, Xian 710032, Shaanxi, Peoples R China.
RP Huang, XF (corresponding author), Fourth Mil Med Univ, Sch Basic Med, Cent Lab, 17 West Changle Rd, Xian 710032, Shaanxi, Peoples R China.
EM xiaofenghuang2012@126.com
FU National Nature Science Foundation of ChinaNational Natural Science
   Foundation of China (NSFC) [81101100]; Natural Science Basic Research
   Plan in Shanxi Province of China [2012JQ4015]; Fundamental Research
   Funds for the Central UniversitiesFundamental Research Funds for the
   Central Universities [K50510100002, K50510100004]
FX This study was supported by the National Nature Science Foundation of
   China (no. 81101100), the Natural Science Basic Research Plan in Shanxi
   Province of China under Grant (no. 2012JQ4015) and the Fundamental
   Research Funds for the Central Universities (nos. K50510100002 and
   K50510100004).
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NR 28
TC 3
Z9 3
U1 0
U2 23
PU SPANDIDOS PUBL LTD
PI ATHENS
PA POB 18179, ATHENS, 116 10, GREECE
SN 1791-2997
EI 1791-3004
J9 MOL MED REP
JI Mol. Med. Rep.
PD SEP
PY 2014
VL 10
IS 3
BP 1184
EP 1194
DI 10.3892/mmr.2014.2379
PG 11
WC Oncology; Medicine, Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Research & Experimental Medicine
GA AN8LA
UT WOS:000340854500002
PM 25060748
OA Green Published, hybrid, Green Submitted
DA 2022-04-25
ER

PT J
AU Yan, SC
   Tang, D
   Hong, ZY
   Wang, J
   Yao, H
   Lu, L
   Yi, HM
   Fu, SJ
   Zheng, CJ
   He, GC
   Zou, H
   Hou, XY
   He, Q
   Xiong, L
   Li, QL
   Deng, XY
AF Yan, Shichao
   Tang, Da
   Hong, Zhangyong
   Wang, Jing
   Yao, Hui
   Lu, Lu
   Yi, Huimei
   Fu, Shujun
   Zheng, Chanjuan
   He, Guangchun
   Zou, Heng
   Hou, Xuyang
   He, Qing
   Xiong, Li
   Li, Qinglong
   Deng, Xiyun
TI CD133 peptide-conjugated pyropheophorbide-a as a novel photosensitizer
   for targeted photodynamic therapy in colorectal cancer stem cells
SO BIOMATERIALS SCIENCE
LA English
DT Article
ID IN-VIVO; PROGNOSTIC MARKER; TUMOR; PHTHALOCYANINES; IDENTIFICATION;
   NANOPARTICLES; CHALLENGES; PRINCIPLES; RESISTANCE; SURVIVAL
AB Colorectal cancer (CRC) is the third most common cancer around the world. Recent findings suggest that cancer stem cells (CSCs) play a pivotal role in the resistance to current therapeutic modalities, including surgery and chemotherapy. Photodynamic therapy (PDT) is a promising non-invasive therapeutic strategy for advanced metastatic CRC. Traditional photosensitizers such as pyropheophorbide-a (Pyro) lack tumor selectivity, causing unwanted treatment-related toxicity to the surrounding normal tissue. In order to enhance the targeting properties of Pyro, we synthesize a novel photosensitizer, CD133-Pyro, via the conjugation of Pyro to a peptide domain targeting CD133, which is highly expressed on CRC CSCs and correlated with poor prognosis of CRC patients. We demonstrate that CD133 Pyro possesses the targeted delivery capacity both in CRC CSCs derived from HT29 and SW620 cell lines and in a xenograft mouse model of tumor growth. CD133 Pyro PDT can promote the production of reactive oxygen species (ROS), suppress the sternness properties, and induce autophagic cell death in CRC CSCs. Furthermore, CD133-Pyro PDT has a potent inhibitory effect on CRC CSC-derived xenograft tumors in nude mice. These findings may offer a useful and important strategy for the treatment of CRC through targeting CSCs.
C1 [Yan, Shichao; Zou, Heng; Hou, Xuyang; He, Qing; Xiong, Li; Li, Qinglong] Cent South Univ, Xiangya Hosp 2, Dept Gen Surg, Changsha 410011, Hunan, Peoples R China.
   [Yan, Shichao; Yao, Hui; Lu, Lu; Yi, Huimei; Fu, Shujun; Zheng, Chanjuan; He, Guangchun; Deng, Xiyun] Hunan Normal Univ, Key Lab Translat Canc Stem Cell Res, Changsha 410013, Hunan, Peoples R China.
   [Yan, Shichao; Yao, Hui; Lu, Lu; Yi, Huimei; Fu, Shujun; Zheng, Chanjuan; He, Guangchun; Deng, Xiyun] Hunan Normal Univ, Dept Pathol, Sch Med, Changsha 410013, Hunan, Peoples R China.
   [Yan, Shichao; Yao, Hui; Lu, Lu; Yi, Huimei; Fu, Shujun; Zheng, Chanjuan; He, Guangchun; Deng, Xiyun] Hunan Normal Univ, Dept Pathophysiol, Sch Med, Changsha 410013, Hunan, Peoples R China.
   [Tang, Da] Cent South Univ, Xiangya Hosp 3, Dept Gen Surg, Changsha 410013, Hunan, Peoples R China.
   [Hong, Zhangyong; Wang, Jing] Nankai Univ, Coll Life Sci, State Key Lab Med Chem Biol, Tianjin Key Lab Prot Sci, Tianjin 300071, Peoples R China.
   [Xiong, Li] Cent South Univ, Mol Imaging Res Ctr, Changsha 410013, Hunan, Peoples R China.
RP Xiong, L; Li, QL (corresponding author), Cent South Univ, Xiangya Hosp 2, Dept Gen Surg, Changsha 410011, Hunan, Peoples R China.; Deng, XY (corresponding author), Hunan Normal Univ, Key Lab Translat Canc Stem Cell Res, Changsha 410013, Hunan, Peoples R China.; Deng, XY (corresponding author), Hunan Normal Univ, Dept Pathol, Sch Med, Changsha 410013, Hunan, Peoples R China.; Deng, XY (corresponding author), Hunan Normal Univ, Dept Pathophysiol, Sch Med, Changsha 410013, Hunan, Peoples R China.; Xiong, L (corresponding author), Cent South Univ, Mol Imaging Res Ctr, Changsha 410013, Hunan, Peoples R China.
EM lixionghn@csu.edu.cn; liqinglonga@sina.com; dengxiyunmed@hunnu.edu.cn
OI Deng, Xiyun/0000-0003-2203-970X
FU Natural Science Foundation of ChinaNational Natural Science Foundation
   of China (NSFC) [81773293, 81872167, 81472496, 31660266, 81873640,
   81970569]; Key Project of Science and Technology Program of Hunan
   Provincial Science and Technology Department [2015GK3117, 2017WK2063];
   Natural Science Foundation of Hunan ProvinceNatural Science Foundation
   of Hunan Province [2019JJ50874, 2020JJ4790]; Science and Technology
   Program of Changsha [kq1907079]
FX Xiangya Biomedical Electron Microscopy Core Facility of Central South
   University provided professional service with transmission electron
   microscopy. We thank H. Nikki March, PhD, from Edanz Group for editing a
   draft of this manuscript. This work was supported by the Natural Science
   Foundation of China (81773293, 81872167, 81472496, 31660266, 81873640,
   81970569), the Key Project of Science and Technology Program of Hunan
   Provincial Science and Technology Department (2015GK3117, 2017WK2063),
   the Natural Science Foundation of Hunan Province (2019JJ50874,
   2020JJ4790), and the Science and Technology Program of Changsha
   (kq1907079).
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NR 51
TC 2
Z9 2
U1 9
U2 16
PU ROYAL SOC CHEMISTRY
PI CAMBRIDGE
PA THOMAS GRAHAM HOUSE, SCIENCE PARK, MILTON RD, CAMBRIDGE CB4 0WF, CAMBS,
   ENGLAND
SN 2047-4830
EI 2047-4849
J9 BIOMATER SCI-UK
JI Biomater. Sci.
PD MAR 21
PY 2021
VL 9
IS 6
BP 2020
EP 2031
DI 10.1039/d0bm01874k
PG 12
WC Materials Science, Biomaterials
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Materials Science
GA RB5FB
UT WOS:000632135400033
PM 33439161
DA 2022-04-25
ER

EF