Bcl-2 constitutively suppresses p53-dependent apoptosis in colorectal cancer cells

被引：131

作者：

Jiang, M ^{[1
]}

Milner, J ^{[1
]}

机构：

[1] Univ York, Dept Biol, Yorkshire Canc Res Lab P53, York YO10 5DD, N Yorkshire, England

来源：

GENES & DEVELOPMENT | 2003年 / 17卷 / 07期

关键词：

p53; Bcl-2; Bcl-x(L); Bax; colorectal cancer; apoptosis;

D O I：

10.1101/gad.252603

中图分类号：

Q2 [细胞生物学];

学科分类号：

071009 ; 090102 ;

摘要：

To dissect apoptotic genes governing the survival of colorectal carcinoma cells, we employed RNAi to silence Bcl-2 and Bcl-X-L in isogenic clones of p53+/+ and p53-/-cells, and of Bax+/- and Bax-/- cells. We identify a novel proapoptotic function of p53 that does not require activation by genotoxic agents and that appears to be constitutively suppressed by Bcl-2. Silencing of Bcl-2 induced massive p53-dependent apoptosis. The "Bcl-2/p53 axis" requires Bax and caspase 2 as essential apoptotic mediators. This newly discovered Bcl-2/p53 functional interface represents a key regulator of apoptosis which can be activated by targeting Bcl-2 in colorectal carcinoma cells.

引用

页码：832 / 837

页数：6

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