Induction of apoptosis by TPA and VP-16 is through translocation of TR3

作     者：LiuS WuQ 等 

作者机构：KeyLaboratoryoftheMinistryofEducationforCellBiologyandTumorCellEngineeringSchoolofLifeSciencesXiamenUniversityXiamen361005FujianProvinceChina KeyLaboratoryoftheMinistryofEducationforCellBiologyan 

出 版 物：《World Journal of Gastroenterology》 (世界胃肠病学杂志（英文版）)

年 卷 期：2002年第8卷第3期

页      面：446-450页

核心收录：

学科分类：1002[医学-临床医学] 100214[医学-肿瘤学] 10[医学] 

基　　金：the National Outstanding Youth Science foundation of China (B type,39825502) the National Natural Science Foundation of China (39880015,30170477) the Natural Science Foundation of Fujian Province (C0110004) 

主　　题：Active Transport, Cell Nucleus Apoptosis DNA-Binding Proteins Etoposide Gene Expression RNA, Messenger RNA, Neoplasm Receptors, Cytoplasmic and Nuclear Receptors, Steroid Research Support, Non-U.S. Gov't Signal Transduction Stomach Neoplasms Tetradecanoylphorbol Acetate Transcription Factors Tumor Cells, Cultured 

摘      要：AIM: To investigate the role of TR3 in induction of apoptosis in gastric cancer cells. METHODS: Human gastric cancer cell line, MGC80-3, was used. Expression of TR3 mRNA and its protein was detected by Northern blot and Western blot. Localization of TR3 protein was showed by immunofluorescence analysis under laser-scanning confocal microscope. Apoptotic morphology was observed by DAPI fluorescence staining, and apoptotic index was counted among 1000 cells randomly. Stable transfection assay was carried out by Lipofectamine. RESULTS: Treatment of MGC80-3 cells with TPA and VP-16 resulted in apoptosis, accompanied by the repression of Bcl-2 protein in a time-dependent manner. At the same time, TPA and VP-16 also up-regulated expression level of TR3 mRNA in MGC80-3 cells that expressed TR3 mRNA. When antisense-TR3 expression vector was transfected into the cells, expression of TR3 protein was repressed. In this case, TPA and VP-16 did not induce apoptosis. In addition, TPA and VP-16-induced apoptosis involved in translocation of TR3. In MGC80-3 cells, TR3 localized concentrative in nucleus, after treatment of cells with TPA and VP-16, TR3 translocated from nucleus to cytosol obviously. However, when this nuclear translocation was blocked by LMB, apoptosis was not occurred in MGC80-3 cells even in the presence of TPA and VP-16. CONCLUSION: Induction of apoptosis by TPA and VP-16 is through induction of TR3 expression and translocation of TR3 from nucleus to cytosol, which may be a novel signal pathway for TR3, and represent the new biological function of TR3 to exert its effect on apoptosis in gastric cancer cells.