NDLI: Cellular inhibitor of apoptosis protein 1 (cIAP1) stability contributes to YM155 resistance in human gastric cancer cells.

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Cellular inhibitor of apoptosis protein 1 (cIAP1) stability contributes to YM155 resistance in human gastric cancer cells.

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Cellular inhibitor of apoptosis protein 1 (cIAP1) stability contributes to YM155 resistance in human gastric cancer cells.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Kim, Kyu-pyo Choi, Eun Kyung Hong, Seung-woo Kim, Jeong Hee Shin, Jae-sik Lee, Dae-hee Jung, Soo-a Lee, Ha-reum Hong, Yong Sang Kim, Jeong Eun Ha, Seung-hee Kim, Seung-mi Moon, Jai-hee Kim, Taewon Jin, Dong-hoon Park, Yong-man Lee, Jung Shin
Description	Author Affiliation: Jung SA ( From the Innovative Cancer Research, Asan Institute for Life Science, Departments of Oncology.); Park YM ( From the Innovative Cancer Research, Asan Institute for Life Science, Departments of Oncology.); Hong SW ( From the Innovative Cancer Research, Asan Institute for Life Science, Departments of Oncology.); Moon JH ( From the Innovative Cancer Research, Asan Institute for Life Science, Departments of Oncology.); Shin JS ( From the Innovative Cancer Research, Asan Institute for Life Science, Departments of Oncology.); Lee HR ( From the Innovative Cancer Research, Asan Institute for Life Science, Departments of Oncology, the Department of Life Sciences, Sookmyung Women's University, Seoul, Republic of Korea.); Ha SH ( From the Innovative Cancer Research, Asan Institute for Life Science, Departments of Oncology.); Lee DH ( From the Innovative Cancer Research, Asan Institute for Life Science, Departments of Oncology.); Kim JH ( From the Innovative Cancer Research, Asan Institute for Life Science, Departments of Oncology.); Kim SM ( From the Innovative Cancer Research, Asan Institute for Life Science, Departments of Oncology.); Kim JE ( From the Innovative Cancer Research, Asan Institute for Life Science, Departments of Oncology.); Kim KP ( From the Innovative Cancer Research, Asan Institute for Life Science, Departments of Oncology.); Hong YS ( From the Innovative Cancer Research, Asan Institute for Life Science, Departments of Oncology.); Choi EK ( From the Innovative Cancer Research, Asan Institute for Life Science, Radiation Oncology, and.); Lee JS ( From the Innovative Cancer Research, Asan Institute for Life Science, Departments of Oncology.); Jin DH ( From the Innovative Cancer Research, Asan Institute for Life Science, Departments of Oncology, Convergence Medicine, University of Ulsan College of Medicine, Asan Medical Center, 88 Olympicro-43gil, Songpa-gu, Seoul and inno183@amc.seoul.kr.); Kim T ( From the Innovative Cancer Research, Asan Institute for Life Science, Departments of Oncology, twkimmd@amc.seoul.kr.)
Abstract	YM155, which blocks the expression of survivin, a member of the inhibitor of apoptosis (IAP) family, induces cell death in a variety of cancer types, including prostate, bladder, breast, leukemia, and non-small lung cancer. However, the mechanism underlying gastric cancer susceptibility and resistance to YM155 is yet to be specified. Here, we demonstrate that cIAP1 stability dictates resistance to YM155 in human gastric cancer cells. Treatment of human gastric cancer cells with YM155 differentially induced cell death dependent on the stability of cIAP1 as well as survivin. Transfection with cIAP1 expression plasmids decreased cell sensitivity to YM155, whereas knockdown of endogenous cIAP1 using RNA interference enhanced sensitivity to YM155. In addition, double knockdown of survivin and cIAP1 significantly induced cell death in the YM155-resistant cell line, MKN45. We also showed that YM155 induced autoubiquitination and proteasome-dependent degradation of cIAP1. Surprisingly, survivin affected the stability of cIAP1 through binding, contributing to cell sensitivity to YM155. Thus, our findings reveal that YM155 sensitizes human gastric cancer cells to apoptotic cell death by degrading cIAP1, and furthermore, cIAP1 in gastric cancer cells may act as a PD marker for YM155 treatment.
ISSN	00219258
e-ISSN	1083351X
Journal	Journal of Biological Chemistry
Issue Number	16
Volume Number	290
Language	English
Publisher	American Society for Biochemistry and Molecular Biology (United States)
Publisher Date	2015-04-17
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Antineoplastic Agents Pharmacology Gastric Mucosa Drug Effects Gene Expression Regulation, Neoplastic Imidazoles Inhibitor Of Apoptosis Proteins Genetics Naphthoquinones Cell Death Cell Line, Tumor Drug Resistance, Neoplasm Metabolism Pathology Antagonists & Inhibitors Protein Binding Protein Stability Proteolysis RNA, Small Interfering Signal Transduction Ubiquitination Research Support, Non-U.S. Gov't Biochemistry Molecular Biology
Content Type	Text
Resource Type	Article
Subject	Cell Biology Biochemistry Molecular Biology

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