TIEG1 induces apoptosis through mitochondrial apoptotic pathway and promotes apoptosis induced by homoharringtonine and velcade

被引:40
作者
Jin, Wei
Di, Genhong
Li, Junjie
Chen, Ying
Li, Wenfeng
Wu, Jiong
Cheng, Tiewei
Yao, Ming
Shao, Zhimin [1 ]
机构
[1] Fudan Univ, Inst Biomed Sci, Dept Oncol, Canc Hosp Canc Inst,Breast Canc Inst, Shanghai 200032, Peoples R China
[2] Univ Med & Dent New Jersey, Robert Wood Johnson Med Sch, Canc Inst New Jersey, New Brunswick, NJ 08901 USA
关键词
TIEG1; apoptosis; homoharringtonine; velcade; mitochondrial pathway;
D O I
10.1016/j.febslet.2007.07.008
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Overexpression of TGF beta inducible early gene (TIEG1) mimics TGF beta action and induces apoptosis. In this study, we found that TIEG I was significantly up-regulated during apoptosis induced by homoharringtonine or velcade. Overexpression of TIEG1 could induce apoptosis in K562 cells and promote apoptosis induced by HHT or velcade. TIEG1-induced apoptosis was shown to involve Bax and Bim up-regulation, Bcl-2 and Bcl-XL down-regulation, release of cytochrome c from mitochondria into the cytosol, activation of caspase 3 and disruption of the mitochondrial membrane potential (Delta psi m). We concluded that TIEG1 is a key regulator which induces and promotes apoptosis through the mitochondrial apoptotic pathway. (c) 2007 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved.
引用
收藏
页码:3826 / 3832
页数:7
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