Expression of Concern: TIEG1 induces apoptosis through mitochondrial apoptotic pathway and promotes apoptosis induced by homoharringtonine and velcade

Wei Jin(Fudan University Shanghai Cancer Center), Gen‐Hong Di(Fudan University Shanghai Cancer Center), Junjie Li(Fudan University Shanghai Cancer Center), Ying Chen(Fudan University Shanghai Cancer Center), Wenfeng Li(Fudan University Shanghai Cancer Center), Jiong Wu(Fudan University Shanghai Cancer Center), Tiewei Cheng(Fudan University Shanghai Cancer Center), Ming Yao(Rutgers, The State University of New Jersey), Zhimin Shao(Fudan University Shanghai Cancer Center)
FEBS Letters
July 16, 2007
Cited by 41Open Access
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Abstract

Overexpression of TGFbeta inducible early gene (TIEG1) mimics TGFbeta action and induces apoptosis. In this study, we found that TIEG1 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 (DeltaPsim). We concluded that TIEG1 is a key regulator which induces and promotes apoptosis through the mitochondrial apoptotic pathway.


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