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TIEG1 induces apoptosis through mitochondrial apoptotic pathway and promotes apoptosis induced by homoharringtonine and velcade
Author(s) -
Jin Wei,
Di Genhong,
Li Junjie,
Chen Ying,
Li Wenfeng,
Wu Jiong,
Cheng Tiewei,
Yao Ming,
Shao Zhimin
Publication year - 2007
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/j.febslet.2007.07.008
Subject(s) - homoharringtonine , apoptosis , cytochrome c , mitochondrion , microbiology and biotechnology , chemistry , cytosol , regulator , intrinsic apoptosis , cancer research , caspase , programmed cell death , biology , biochemistry , gene , myeloid leukemia , enzyme
Overexpression of TGFβ inducible early gene (TIEG1) mimics TGFβ 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 (Δ Ψ m). We concluded that TIEG1 is a key regulator which induces and promotes apoptosis through the mitochondrial apoptotic pathway.