PT  - JOURNAL ARTICLE
AU  - Mukhopadhyay, Debabrata
AU  - Tsiokas, Leonidas
AU  - Sukhatme, Vikas P.
TI  - Wild-Type p53 and v-Src Exert Opposing Influences on Human Vascular Endothelial Growth Factor Gene Expression
DP  - 1995 Dec 15
TA  - Cancer Research
PG  - 6161--6165
VI  - 55
IP  - 24
4099  - http://cancerres.aacrjournals.org/content/55/24/6161.short
4100  - http://cancerres.aacrjournals.org/content/55/24/6161.full
SO  - Cancer Res1995 Dec 15; 55
AB  - 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. ©1995 American Association for Cancer Research.