TIEG1 induces apoptosis through mitochondrial apoptotic pathway and promotes apoptosis induced by homoharringtonine and velcade |
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Authors: | Jin Wei Di Genhong Li Junjie Chen Ying Li Wenfeng Wu Jiong Cheng Tiewei Yao Ming Shao Zhimin |
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Institution: | Breast Cancer Institute, Cancer Hospital/Cancer Institute, Department of Oncology, Institute of Biomedical Science, Fudan University, Shanghai 200032, China. |
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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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Keywords: | HHT homoharringtonine ΔΨm mitochondrial membrane potential TIEG1 TGFβ inducible early gene PMSF phenylmethylsulphonyl fluoride |
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