Nonangiogenic Function of VEGF and Enhanced Radiosensitivity of HeLa Cells by Inhibition of VEGF Expression

Vascular endothelial growth factor (VEGF) plays an important role in the initiation and regulation of angiogenesis in various tumor tissues. Recently, several therapeutic approaches based on the inhibition of VEGF function during angiogenesis. However, VEGF function in cervical cancer may not be limited to angiogenesis, and VEGF signaling may be important for the ability of these tumor cells to evade apoptosis and progress towards invasive and metastatic diseases. In our study, VEGF expression was knocked down using plasmid-based RNA interference (RNAi) and detected in cervical carcinoma cells using real-time RT-PCR to screen the best RNA interference plasmid and reveal the VEGF expression level by radiation. Cell apoptosis and tumor xenografts in nude mice were measured by flow cytometry and immunohistochemistry, respectively, to further verify the possibility of enhancing apoptosis and radiosensitivity of cervical carcinoma cells by inhibition of VEGF expression. VEGF expression was significantly inhibited and the apoptosis was efficiently increased by RNAi. Moreover, the expression of VEGF was increased in HeLa cells in vivo and in vitro only by radiation. Increased apoptotic cell death and knockdown of VEGF expression in HeLa cells indicated increased cellular sensitivity to radiation. The data suggested that inhibited VEGF expression enhances radiosensitivity in cervical cancer therapy.