Journal
CANCER CELL
Volume 3, Issue 2, Pages 117-130Publisher
CELL PRESS
DOI: 10.1016/S1535-6108(03)00021-7
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Funding
- NCI NIH HHS [CA 75180, CA 86306, CA 98013] Funding Source: Medline
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We show in this study that PTEN regulates p53 protein levels and transcriptional activity through both phosphatase-dependent and -independent mechanisms. The onset of tumor development in p53(+/-);Pten(+/-) mice is similar to p53(-/-) animals, and p53 protein levels are dramatically reduced in Pten(-/-) cells and tissues. Reintroducing wild-type or phosphatase-dead PTEN mutants leads to a significant increase in p53 stability. PTEN also physically associates with endogenous p53. Finally, PTEN regulates the transcriptional activity of p53 by modulating its DNA binding activity. This study provides a novel mechanism by which the loss of PTEN can functionally control two hits in the course of tumor development by concurrently modulating p53 activity.
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