Coexpression of vascular endothelial growth factor and its receptor KDR on gastric adenocarcinoma MGC803 cell line and stimulation of exogenous VEGF₁₆₅ to MGC803 cells

【摘要】 <正> Vascular endothelial growth factor (VEGF), also known as vascular permeability factor (VPF), is an angiogenic factor playing an important role in tumor growth. VEGF/VPF interacts with endothelial cells by way of two high-affinity receptor tyrosine kinases: flt-1 and KDR. The vast majority of published studies have described expression of the VPF/VEGF receptors specifically in endothelial cells. To elucidate the further function of VEGF in solid tumor development, the coex-pression of VEGF and KDR in gastric adenocarcinoma MGC803 cell lines was shown by reverse transcription polymerase chain reaction (RT-PCR). The MGC803 tumor cells could also be strongly immunostained for KDR by immunocytochemistry. It was further demonstrated that exogenous VEGF-165 can stimulate the MGC803 cell growth in both dose-dependent and time-dependent manners by 3H-thymidine incorporation. Furthermore, anti-VEGF165 monoclonal antibody and anti-KDR monoclonal antibody could dose-dependently block the VEGF166-induced cell growth更多还原

【Abstract】 Vascular endothelial growth factor (VEGF), also known as vascular permeability factor (VPF), is an angiogenic factor playing an important role in tumor growth. VEGF/VPF interacts with endothelial cells by way of two high-affinity receptor tyrosine kinases: flt-1 and KDR. The vast majority of published studies have described expression of the VPF/VEGF receptors specifically in endothelial cells. To elucidate the further function of VEGF in solid tumor development, the coex-pression of VEGF and KDR in gastric adenocarcinoma MGC803 cell lines was shown by reverse transcription polymerase chain reaction (RT-PCR). The MGC803 tumor cells could also be strongly immunostained for KDR by immunocytochemistry. It was further demonstrated that exogenous VEGF-165 can stimulate the MGC803 cell growth in both dose-dependent and time-dependent manners by 3H-thymidine incorporation. Furthermore, anti-VEGF165 monoclonal antibody and anti-KDR monoclonal antibody could dose-dependently block the VEGF166-induced cell growth. These results provided new evidence that VEGF could cause autocrine stimulation to the proliferation of gastric adenocarcinoma cells.更多还原