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P53 Differentially regulates hypoxia-inducible pro-angiogenic cytokines in malignant glioma


, : P53 Differentially regulates hypoxia-inducible pro-angiogenic cytokines in malignant glioma. FASEB Journal 17(4-5): Abstract No 406 8, March

In glioblastoma, both hypoxia and genetic alterations regulate angiogenesis. We investigated if the pro-angiogenic cytokines VEGF, IL-8, and bFGF were induced by hypoxia and if p53 altered their expression. 2024 cells were cloned from p53 null LNZ308 glioma cells after introducing wt TP53 under a tet-on promoter. 2024 cells grown +/-doxycycline for 24 hrs were placed in normoxia (20% O2), hypoxia (1% O2), or CoCl2. RNA, protein, and conditioned media were collected at 24 hrs. Gene and protein expression of p53, p21, VEGF, IL-8, bFGF, and HIF-1alpha were determined by Northern blot, Western blot, immunohistochemistry, and ELISA. Nuclear HIF-1alpha protein increased moderately in hypoxia and markedly in CoCl2. p53 expression caused a modest decrease in hypoxia-induced HIF-1alpha mRNA and protein. The HIF target VEGF showed corresponding increases in gene and protein expression in hypoxia and p53 repressed this induction. p53 also reduced both hypoxia-and CoCl2-induced bFGF mRNA expression. IL-8 mRNA and protein increased following CoCl2, but not 1% O2, and was not altered by p53. Thus, p53 repressed hypoxia-induced gene expression of VEGF and bFGF and attenuated hypoxia-induced secretion of VEGF. Decreased VEGF expression is likely due to reduced HIF mediated VEGF transcription, while bFGF gene transcription is believed to be directly repressed by p53. p53 loss favors angiogenesis in gliomas by augmenting pro-angiogenic cytokine expression.

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