p53 suppresses stress-induced cellular senescence via regulation of autophagy under the deprivation of serum

Mol Med Rep. 2015 Feb;11(2):1214-20. doi: 10.3892/mmr.2014.2853. Epub 2014 Nov 4.

Abstract

The tumor suppressor p53 is widely known for its ability to induce cell cycle arrest or cell death, therefore preventing neoplastic progression. Previous studies have demonstrated novel roles for p53 in the regulation of autophagy and senescence. p53 can not only exert cell cycle‑arresting and senescence‑promoting or suppressing functions, but can also induce autophagic flux, particularly under conditions of nutrient deprivation. The present study demonstrated that p53 was capable of activating autophagy, which permits cell survival under conditions of serum starvation, and suppresses cellular senescence through inhibition of the mammalian target of rapamycin pathway. These results suggest that active autophagy may be a potential mechanism by which p53 suppresses cellular senescence, in response to serum starvation. The findings of the present study provide a potential mechanism for suppression of senescence by p53.

Publication types

  • Research Support, Non-U.S. Gov't
  • Retracted Publication

MeSH terms

  • Adenine / analogs & derivatives
  • Adenine / pharmacology
  • Autophagy / drug effects*
  • Cellular Senescence*
  • Culture Media, Serum-Free / pharmacology*
  • G1 Phase Cell Cycle Checkpoints / drug effects
  • HCT116 Cells
  • Humans
  • Phosphorylation / drug effects
  • Stress, Mechanical
  • TOR Serine-Threonine Kinases / metabolism
  • Tumor Suppressor Protein p53 / genetics
  • Tumor Suppressor Protein p53 / metabolism*

Substances

  • Culture Media, Serum-Free
  • Tumor Suppressor Protein p53
  • 3-methyladenine
  • TOR Serine-Threonine Kinases
  • Adenine