p53 Does Not Repress Hypoxia-induced Transcription of the Vascular Endothelial Growth Factor Gene

摘要: Hypoxia-induced neovascularization mediated by vascular endothelial growth factor (VEGF) contributes to tumor progression. Based on its effects when overexpressed in transient transfection assays, p53 has been proposed repress VEGF transcription. To investigate this hypothesis, we have analyzed endogenous mRNA levels Hep3B cells stably expressing an inducible p53-estrogen receptor fusion protein and irradiated RKO wild-type p53. In both cell lines, increased response hypoxia, either the presence or absence of functional Our data provide no evidence for a causal relationship between loss activity expression that is observed during Studies attribute repressor functions based analysis transiently overexpressing should be interpreted cautiously.