The quiescent cellular state is Arf/p53-dependent and associated with H2AX downregulation and genome stability

Int J Mol Sci. 2012;13(5):6492-6506. doi: 10.3390/ijms13056492. Epub 2012 May 24.

Abstract

Cancer is a disease associated with genomic instability and mutations. Excluding some tumors with specific chromosomal translocations, most cancers that develop at an advanced age are characterized by either chromosomal or microsatellite instability. However, it is still unclear how genomic instability and mutations are generated during the process of cellular transformation and how the development of genomic instability contributes to cellular transformation. Recent studies of cellular regulation and tetraploidy development have provided insights into the factors triggering cellular transformation and the regulatory mechanisms that protect chromosomes from genomic instability.

Keywords: Arf/p53; H2AX; cancer; genome stability; immortality; senescence; tetraploidy.

Publication types

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

MeSH terms

  • Animals
  • Cell Transformation, Neoplastic / genetics*
  • Cyclin-Dependent Kinase Inhibitor p16 / genetics*
  • Down-Regulation
  • Gene Expression Regulation, Neoplastic
  • Histones / metabolism*
  • Humans
  • Mutation
  • Neoplasms / genetics*
  • Neoplasms / metabolism
  • Neoplasms / pathology
  • Tetraploidy
  • Tumor Suppressor Protein p14ARF / genetics*
  • Tumor Suppressor Protein p53 / genetics*

Substances

  • Cyclin-Dependent Kinase Inhibitor p16
  • H2AX protein, human
  • Histones
  • TP53 protein, human
  • Tumor Suppressor Protein p14ARF
  • Tumor Suppressor Protein p53