p63, cellular senescence and tumor development

Cell Cycle. 2007 Feb 1;6(3):305-11. doi: 10.4161/cc.6.3.3794. Epub 2007 Feb 3.

Abstract

Deficiency of p63, a p53-related protein, causes severe defects in epithelial morphogenesis. Studies of p63-compromised mouse models reveal that p63 deficiency induces cellular senescence both in cultured cells and in vivo, through regulation p19(Arf)/p53 and p16(Ink4a)/Rb pathways. An extensive tumor study of p63-compromised mice demonstrated that p63 deficiency does not predispose to, but rather protects from, tumor development. These findings further implicate p63 as a negative regulator of the tumor suppressive mechanism of cellular senescence.

Publication types

  • Review

MeSH terms

  • Animals
  • Cellular Senescence / genetics
  • Cellular Senescence / physiology*
  • DNA-Binding Proteins / genetics
  • DNA-Binding Proteins / metabolism
  • DNA-Binding Proteins / physiology*
  • Humans
  • Models, Biological
  • Neoplasms / genetics
  • Neoplasms / pathology
  • Neoplasms / physiopathology*
  • Trans-Activators / genetics
  • Trans-Activators / metabolism
  • Trans-Activators / physiology*
  • Transcription Factors
  • Tumor Suppressor Proteins / genetics
  • Tumor Suppressor Proteins / metabolism
  • Tumor Suppressor Proteins / physiology*

Substances

  • DNA-Binding Proteins
  • TP63 protein, human
  • Trans-Activators
  • Transcription Factors
  • Tumor Suppressor Proteins