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Molecular Biology and Genetics

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

Debabrata Mukhopadhyay, Leonidas Tsiokas and Vikas P. Sukhatme
Debabrata Mukhopadhyay
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Leonidas Tsiokas
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Vikas P. Sukhatme
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DOI:  Published December 1995
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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, and 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.

Footnotes

  • ↵1 This work was supported in part by NIH Grant DK44921 (to V. P. S.).

  • ↵2 To whom requests for reprints should be addressed, at Beth Israel Hospital, 330 Brookline Avenue, Boston, MA 02215. Phone: (617) 667-2105; Fax: (617) 667-7843.

  • Received July 11, 1995.
  • Accepted October 11, 1995.
  • ©1995 American Association for Cancer Research.
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December 1995
Volume 55, Issue 24
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Wild-Type p53 and v-Src Exert Opposing Influences on Human Vascular Endothelial Growth Factor Gene Expression
Debabrata Mukhopadhyay, Leonidas Tsiokas and Vikas P. Sukhatme
Cancer Res December 15 1995 (55) (24) 6161-6165;

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Wild-Type p53 and v-Src Exert Opposing Influences on Human Vascular Endothelial Growth Factor Gene Expression
Debabrata Mukhopadhyay, Leonidas Tsiokas and Vikas P. Sukhatme
Cancer Res December 15 1995 (55) (24) 6161-6165;
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