Induction of p53 and Bax during TGF-β1 initiated apoptosis in rat liver epithelial cells

被引：60

作者：

Teramoto, T ^{[1
]}

Kiss, A ^{[1
]}

Thorgeirsson, SS ^{[1
]}

机构：

[1] NCI, Expt Carcinogenesis Lab, Div Basic Sci, NIH, Bethesda, MD 20892 USA

来源：

BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS | 1998年 / 251卷 / 01期

关键词：

D O I：

10.1006/bbrc.1998.9411

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：

The relationship between transforming growth factor-beta 1 (TGF-beta 1) induced growth arrest and apoptosis in rat liver derived epithelial (RLE) cells was analyzed. TGF-beta 1 treatment of RLE cells induced both cell cycle arrest and apoptosis. However, pretreatment of the cells with either dexamethasone or cyclohexamide suppressed TGF-beta 1 induced apoptosis, without preventing the cell cycle arrest. Both p53 and Bax were subsequently shown to be overexpressed during the TGF-beta 1 induced apoptosis. Furthermore, it was revealed that cycloheximide suppressed expression of both p53 and Bax. In contrast, dexamethasone treatment prevented Bax expression alone. Treatment of RLE cells with several growth factors either alone or in combination was ineffective in counteracting TGF-beta 1 induced apoptosis. In additon, we show that TGF-alpha also induced both p53 and Bax expressions and augmented TGF-beta-induced apoptosis. Thus, p53 and Bax are likely to be key factors in TGF-beta 1 induced apoptosis in RLE cells. (C) 1998 Academic Press.

引用

页码：56 / 60

页数：5

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