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 coexpression 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 VEGF165 can stimulate the MGC803 cell growth in both dose-dependent and time-dependent manners by3H-thymidine incorporation. Furthermore, anti-VEGF165 monoclonal antibody and anti-KDR monoclonal antibody could dose-dependently block the VEGF165-induced cell growth. These results provided new evidence that VEGF could cause autocrine stimulation to the proliferation of gastric adenocarcinoma cells.
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Tian, X., Meng, L., Shou, C. et al. Coexpression of vascular endothelial growth factor and its receptor KDR on gastric adenocarcinoma MGC803 cell line and stimulation of exogenous VEGF165 to MGC803 cells. Sci. China Ser. C.-Life Sci. 43, 88–95 (2000). https://doi.org/10.1007/BF02881722
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DOI: https://doi.org/10.1007/BF02881722