Gene-specific mechanisms of p53 transcriptional control and prospects for cancer therapy

J Cell Biochem. 2006 Oct 15;99(3):679-89. doi: 10.1002/jcb.20925.


The regulation of gene-specific activation is critical to the tumor suppressor function by p53. p53 is a well-characterized transcription factor that responds to DNA damage and other genotoxic stresses by the activation of downstream targets that are involved with repair, differentiation, senescence, growth arrest, and apoptosis. Sequence-specific binding to DNA, conformation, post-translational modifications, cofactor binding, stability, and subcellular localization all influence the performance of p53. The purpose of this review is to define features that play a key role in gene-specific activation and to show that these are often incapacitated in cancer cells. Using such knowledge to design selective strategies for the restoration of p53 wild-type function in cancer cells represents a promising cancer therapy.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, U.S. Gov't, Non-P.H.S.
  • Review

MeSH terms

  • Animals
  • Gene Expression Regulation*
  • Humans
  • Neoplasms / genetics
  • Neoplasms / therapy*
  • Transcription, Genetic*
  • Tumor Suppressor Protein p53 / genetics
  • Tumor Suppressor Protein p53 / metabolism*


  • Tumor Suppressor Protein p53