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Regulation of collagen-derived antiangiogenic factors by p53

Sarah Assadian1, Jose G Teodoro

  • 1McGill University, McGill Cancer Center, 3655 Promenade Sir William Osler, Montreal, QC, Canada.

Expert Opinion on Biological Therapy
|June 14, 2008
PubMed
Abstract

Insights

The p53 tumor suppressor protein limits tumor growth by boosting antiangiogenic factors. Restoring these factors therapeutically may help treat cancers with mutated p53.

Area of Science:

  • Oncology
  • Molecular Biology
  • Biochemistry

Background:

  • The p53 tumor suppressor protein plays a role in limiting tumor angiogenesis.
  • This function is partly mediated by p53's ability to enhance the production of endogenous angiogenesis inhibitors, including collagen-derived antiangiogenic factors (CDAFs) like endostatin and tumstatin.

Purpose of the Study:

  • To review the clinical and therapeutic implications of CDAFs.
  • To examine the regulation of CDAFs by the p53 protein.

Main Methods:

  • Highlighting the inhibitory role of CDAFs in angiogenesis.
  • Summarizing evidence for p53's regulation of CDAF expression, synthesis, assembly, and activation.

Main Results:

  • The p53 gene is mutated in approximately 50% of human tumors.
  • Tumors with p53 mutations are predicted to have reduced levels of CDAFs.

Conclusions:

  • Therapeutic administration of CDAFs could potentially compensate for lost p53 function in cancer.
  • CDAF-based therapies represent a promising new strategy for cancer treatment.

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