mTORC1 and p53: Clash of the gods?

Research output: Contribution to journalReview article

40 Scopus citations

Abstract

A balance must be struck between cell growth and stress responses to ensure that cells proliferate without accumulating damaged DNA. This balance means that optimal cell proliferation requires the integration of pro-growth and stress-response pathways. mTOR (mechanistic target of rapamycin) is a pleiotropic kinase found in complex 1 (mTORC1). The mTORC1 pathway governs a response to mitogenic signals with high energy levels to promote protein synthesis and cell growth. In contrast, the p53 DNA damage response pathway is the arbiter of cell proliferation, restraining mTORC1 under conditions of genotoxic stress. Recent studies suggest a complicated integration of these pathways to ensure successful cell growth and proliferation without compromising genome maintenance. Deciphering this integration could be key to understanding the potential clinical usefulness of mTORC1 inhibitors like rapamycin. Here we discuss how these p53-mTORC1 interactions might play a role in the suppression of cancer and perhaps the development of cellular senescence and organismal aging.

Original languageEnglish (US)
Pages (from-to)20-25
Number of pages6
JournalCell Cycle
Volume12
Issue number1
DOIs
StatePublished - Jan 1 2013

Keywords

  • Aging
  • Cancer
  • Cellular senescence
  • MTORC1
  • p53

ASJC Scopus subject areas

  • Molecular Biology
  • Developmental Biology
  • Cell Biology

Fingerprint Dive into the research topics of 'mTORC1 and p53: Clash of the gods?'. Together they form a unique fingerprint.

  • Cite this