Bcl-2 constitutively suppresses p53-dependent apoptosis in colorectal cancer cells
AUTOR(ES)
Jiang, Ming
FONTE
Cold Spring Harbor Laboratory Press
RESUMO
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.
ACESSO AO ARTIGO
http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=196025Documentos Relacionados
- Bcl-2 blocks p53-dependent apoptosis.
- Bcl-2 Blocks p53-Dependent Apoptosis
- p300 regulates p53-dependent apoptosis after DNA damage in colorectal cancer cells by modulation of PUMA/p21 levels
- Resistance to apoptosis in CTLL-2 cells constitutively expressing c-Myb is associated with induction of BCL-2 expression and Myb-dependent regulation of bcl-2 promoter activity
- Apoptosis and expression of Bax, Bcl-x, and Bcl-2 apoptotic regulatory proteins in colorectal carcinomas, and association with p53 genotype/phenotype.
