A p53-independent pathway for induction of p21waf1cip1 and concomitant G1 arrest in UV-irradiated human skin fibroblasts

Cancer Res. 1997 Aug 15;57(16):3390-4.

Abstract

Largely on the basis of studies using the potent clastogen ionizing radiation, it has been widely assumed that up-regulation of the cyclin-dependent kinase inhibitor p21(waf1cip1) in cultured cells exposed to DNA-damaging agents is contingent upon the presence of functional p53 tumor suppressor protein. Nevertheless, we demonstrate here that the model mutagen 254-nm UV light induces p21(waf1cip1) protein and concomitant G1 arrest in normal human skin fibroblasts, as well as in p53-deficient fibroblasts derived from cancer-prone Li-Fraumeni syndrome patients. However, as expected, following exposure to ionizing radiation, elevated p21(waf1cip1) protein levels and G1 arrest were observed only in normal fibroblasts. These data provide a prominent and clinically relevant example in which p21(waf1cip1)-mediated growth arrest occurs independently of p53 in human cells treated with a model DNA-damaging agent.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Aneuploidy
  • Cell Line
  • Cyclin-Dependent Kinase Inhibitor p21
  • Cyclins / biosynthesis*
  • DNA Damage
  • Fibroblasts / metabolism
  • Fibroblasts / radiation effects
  • G1 Phase / genetics
  • G1 Phase / radiation effects
  • Humans
  • Polyploidy
  • S Phase / genetics
  • S Phase / radiation effects
  • Skin / cytology
  • Tumor Suppressor Protein p53 / metabolism
  • Tumor Suppressor Protein p53 / radiation effects*

Substances

  • CDKN1A protein, human
  • Cyclin-Dependent Kinase Inhibitor p21
  • Cyclins
  • Tumor Suppressor Protein p53