TP53 and MTOR crosstalk to regulate cellular senescence

Lorenzo Galluzzi^1,^2,³, Oliver Kepp^1,^2,³, Guido Kroemer^1,^4,^5,^6,⁷

¹INSERM, U848, F-94805 Villejuif, France
²Institut Gustave Roussy, F-94805 Villejuif, France
³Université Paris-Sud, Paris 11, F-94805 Villejuif, France
⁴Metabolomics Platform, Institut Gustave Roussy, F-94805 Villejuif, France
⁵Centre de Recherche des Cordoliers, F-75005 Paris, France
⁶Pôle de Biologie, Hôpital Européen Georges Pompidou, AP-HP, F-75908 Paris, France
⁷Université Paris Descartes, Paris 5, F-75270 Paris, France

Received: September 16, 2010Accepted: September 18, 2010Published: September 18, 2010

https://doi.org/http://dx.doi.org/10.18632/aging.100202

Copyright: © 2010 Galluzzi et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Abstract

The full spectrum of activities of the tumor suppressor p53 (TP53) has not been completely elucidated yet. Recently, it was demonstrated that TP53 communicates with the metabolic regulator mechanistic target of rapamycin (MTOR) to determine whether stressed cells undergo cell death, reversible quiescence or irreversible senescence, thereby adding yet another level of complexity to the signaling network that emanate from TP53.