Mutant p53 facilitates pro-angiogenic, hyperproliferative phenotype in response to chronic relative hypoxia

Chandrashekhar D. Kamat, Dixy E. Green, Linda Warnke, Jessica E. Thorpe, Antonio Ceriello, Michael A. Ihnat

Research output: Contribution to journalArticlepeer-review

Abstract

There is much controversy in the literature regarding the role of p53 status response on hypoxia inducible factor (HIF) signaling in response to chronic relative hypoxia (CRH). The goal of this paper was to methodically examine this response in isogenically matched tumor cells. We report that p53-mutant (MUT) cells, versus p53-wild-type (WT) cells, showed decreased apoptosis, increased cell proliferation with higher basal HIF-1α levels in response to CRH. In addition, we found increased HIF-mediated transactivation and increased VEGF release with decreased HIF-1α/p53 and HIF-1α/MDM-2 partnering in p53-MUT versus p53-WT cells in response to CRH.

Original languageEnglish
Pages (from-to)209-219
Number of pages11
JournalCancer Letters
Volume249
Issue number2
DOIs
Publication statusPublished - May 8 2007

Keywords

  • Angiogenesis
  • Apoptosis
  • Chronic hypoxia
  • HIF-1α
  • p53
  • p53-mutant
  • Vascular endothelial growth factor

ASJC Scopus subject areas

  • Cancer Research
  • Molecular Biology
  • Oncology

Fingerprint Dive into the research topics of 'Mutant p53 facilitates pro-angiogenic, hyperproliferative phenotype in response to chronic relative hypoxia'. Together they form a unique fingerprint.

Cite this