Bypass of abnormal MDM2 inhibition of p53-dependent growth suppression

Clin Cancer Res. 1998 Jan;4(1):251-9.

Abstract

Oncoprotein MDM2 inhibits p53-dependent cell cycle arrest and apoptosis. MDM2-overexpressing human cancer cell lines (n = 3) were found to be resistant to growth inhibition after infection by p53-expressing adenovirus (Ad-p53), as compared to low MDM2-expressing tumors (n = 3), in vitro. The growth of MDM2-overexpressing tumors, however, was inhibited by p21-expressing adenovirus (Ad-p21) infection, and the cyclin-dependent kinase-inhibitory region of p21 was sufficient to bypass the MDM2-p53 feedback loop. The phosphorylation state of Rb correlated with the response to either p53 or p21 gene therapy. MDM2-overexpressing cancer cells infected by Ad-p21 also developed a quiescent large-cell morphology. The results suggest that MDM2-mediated resistance to p53 may be bypassed by p21 and that the Rb phosphorylation state may predict the effects on growth after Ad-p53 or Ad-p21 infection.

Publication types

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

MeSH terms

  • Adenoviridae / genetics
  • Cell Division
  • Cell Survival
  • Genes, p53 / physiology*
  • Genetic Therapy*
  • Humans
  • Neoplasms / therapy*
  • Nuclear Proteins*
  • Phosphorylation
  • Proto-Oncogene Proteins / analysis
  • Proto-Oncogene Proteins / physiology*
  • Proto-Oncogene Proteins c-mdm2
  • Retinoblastoma Protein / metabolism
  • Tumor Cells, Cultured

Substances

  • Nuclear Proteins
  • Proto-Oncogene Proteins
  • Retinoblastoma Protein
  • MDM2 protein, human
  • Proto-Oncogene Proteins c-mdm2