Wild-Type p53 and v-Src Exert Opposing Influences on Human Vascular Endothelial Growth Factor Gene Expression

Debabrata Mukhopadhyay, Leonidas Tsiokas, Vikas P. Sukhatme

Research output: Contribution to journalArticle

396 Scopus citations

Abstract

Angiogenesis, the development of new capillaries, is tightly controlled by the balance of positive and negative regulatory pathways. A newly described angiogenic factor, vascular endothelial growth factor/vascular permeability factor (VEGF/VPF), binds exclusively to endothelial cells and promotes their proliferation. Here we have studied the role of p53, a tumor suppressor, and v-Src, an oncogene on VEGF regulation. Wild-type p53 down-regulated endogenous VEGF mRNA level, as well as VEGF promoter activity, in a dose-dependent manner, whereas mutant forms of p53 had no effect. Overexpression of v-Src, known to up-regulate VEGF expression, activated a VEGF promoter-luciferase construct in a dose-dependent manner. Moreover, v-Src, in the presence of wt-p53, was unable to activate transcription of the VEGF promoter. Collectively, these data suggest that wild-type p53 may play a role in suppressing angiogenesis.

Original languageEnglish (US)
Pages (from-to)6161-6165
Number of pages5
JournalCancer research
Volume55
Issue number24
StatePublished - Dec 15 1995

ASJC Scopus subject areas

  • Oncology
  • Cancer Research

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