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Institute of Cancer Research, London SW3 6JB, United Kingdom
SUMMARY
Altered regulation of cell cycle, DNA repair, and apoptosis may not be the only ways that loss of p53 contributes to tumorigenesis. Roux and colleagues describe how the tumor suppressor protein p53 can regulate Cdc42-dependent (but neither RhoA- nor Rac-dependent) effects on cell morphology. The activation of p53 tends to inhibit the formation of Cdc42-dependent filopodia, pointing to a new way in which p53 exerts its tumor-suppressing activity: the prevention of cell spreading and motility. Sahai reviews these observations and discusses how insights gained from these studies will most likely lead to the identification of new targets for cancer therapy.
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