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

By Ming Jiang and Jo Milner

Abstract

To dissect apoptotic genes governing the survival of colorectal carcinoma cells, we employed RNAi to silence Bcl-2 and Bcl-xL 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

Topics: Research Communication
Publisher: Cold Spring Harbor Laboratory Press
Year: 2003
DOI identifier: 10.1101/gad.252603
OAI identifier: oai:pubmedcentral.nih.gov:196025
Provided by: PubMed Central
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