Genotoxic and non-genotoxic pathways of p53 induction

Cancer Lett. 2001 Dec 10;174(1):1-15. doi: 10.1016/s0304-3835(01)00698-x.


Since the initial concept of p53 as a sensor of DNA-damage, the picture of the role of p53 has widened to include the sensing of much more diverse forms of stress, including hypoxia and constitutive activation of growth-promoting cascades. The pathways by which these processes regulate p53 are partially overlapping, but imply different patterns of post-translational modifications. In this review, we summarize current knowledge on post-translational modifications of p53, and we discuss how hypoxia and oncogene activation stresses may induce p53 independently of DNA damage.

Publication types

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

MeSH terms

  • Apoptosis
  • Cell Cycle
  • Cell Hypoxia
  • DNA Damage
  • Gene Expression Regulation, Neoplastic
  • Humans
  • JNK Mitogen-Activated Protein Kinases
  • Mitogen-Activated Protein Kinases / metabolism
  • Mutagens / metabolism*
  • Nuclear Proteins*
  • Oncogenes / genetics
  • Protein Processing, Post-Translational
  • Proto-Oncogene Proteins / metabolism
  • Proto-Oncogene Proteins c-mdm2
  • Signal Transduction*
  • Tumor Suppressor Protein p53 / chemistry
  • Tumor Suppressor Protein p53 / genetics
  • Tumor Suppressor Protein p53 / metabolism*


  • Mutagens
  • Nuclear Proteins
  • Proto-Oncogene Proteins
  • Tumor Suppressor Protein p53
  • MDM2 protein, human
  • Proto-Oncogene Proteins c-mdm2
  • JNK Mitogen-Activated Protein Kinases
  • Mitogen-Activated Protein Kinases