Journal
NATURE STRUCTURAL & MOLECULAR BIOLOGY
Volume 14, Issue 3, Pages 215-223Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/nsmb1208
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Funding
- NCI NIH HHS [CA90663] Funding Source: Medline
- NIGMS NIH HHS [GM075299] Funding Source: Medline
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Many features of the cancer cell phenotype emerge as a result of cooperation between multiple oncogenic mutations. Here we show that activated Ras(V12) and loss of p53 function can cooperate to promote cell motility, a feature closely associated with cancer progression to malignancy. Our analysis indicates that Ras(V12) and loss of p53 synergistically induce RhoA activity, revealing a previously unknown role for p53 in tumor suppression. p53 prevents activation of RhoA and thus induction of cell motility by Ras(V12) through a simple signaling circuit, which integrates multiple inputs that converge on RhoA. Our data suggest that p53 suppresses cancer progression to malignancy by modulating the quality of Ras signaling.
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