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Published online July 2, 2007
doi:10.1083/jcb.200701120
The Journal of Cell Biology, Vol. 178, No. 1, 23-30
The Rockefeller University Press, 0021-9525 $30.00
© 2007 Gadea et al.
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Loss of p53 promotes RhoA–ROCK-dependent cell migration and invasion in 3D matrices



Gilles Gadea, Marion de Toledo, Christelle Anguille, and Pierre Roux

Centre de Recherche en Biochimie Macromoléculaire, Centre National de la Recherche Scientifique, Universite Mixte de Recherche 5237, Institut Federatif de Recherche 122, F-34293 Montpellier, Cedex 5, France

Correspondence to Pierre Roux: pierre.roux{at}crbm.cnrs.fr

In addition to its role in controlling cell cycle progression, the tumor suppressor protein p53 can also affect other cellular functions such as cell migration. In this study, we show that p53 deficiency in mouse embryonic fibroblasts cultured in three-dimensional matrices induces a switch from an elongated spindle morphology to a markedly spherical and flexible one associated with highly dynamic membrane blebs. These rounded, motile cells exhibit amoeboid-like movement and have considerably increased invasive properties. The morphological transition requires the RhoA–ROCK (Rho-associated coil-containing protein kinase) pathway and is prevented by RhoE. A similar p53-mediated transition is observed in melanoma A375P cancer cells. Our data suggest that genetic alterations of p53 in tumors are sufficient to promote motility and invasion, thereby contributing to metastasis.

G. Gadea's present address is Institute of Cancer Research, London SW3 6JB, UK.

Abbreviations used in this study: DIC, differential interference contrast; F-actin, filamentous actin; MEF, mouse embryonic fibroblast; ROCK, Rho-associated coil-containing protein kinase; wt, wild type.


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