Effect On Expression Of HIF-1α、HIF-2α And VEGF In H.pylori-infected Gastric Cancer Cells

Background and Objective：Gastric cancer is a common malignant tumor that resultsin death. Currently, the surgical operation and the anti-tumor therapy are not good enough toimprove the poor prognosis of the gastric cancer. Helicobacter pylori is re1αted with the poorprognosis of the gastric cancer,and therefore. has been recognized as one of the importantcauses of the gastric cancer. The gastric cancer that the helicobacter pylori infects tends to beinvasion and metastasis easily. Vascu1αr endothelial growth factor (VEGF) is one of maincontrol factor that the malignant tumor generates by inducing an angiogenesis. Hypoxiainducible factor1alpha (HIF-1α) and hypoxia inducible factor2alpha (HIF-2α) p1αy acrucial role in the process in malignant tumor generates by inducing angiogenesis. Studyingthe mechanism about invasion and metastasis of gastric cancer is helpful to look for a newway to resist invasion and metastasis and to improve the prognosis．In this paper, we focuson exploring the effect of Helicobacter pylori(H.pylori) on the HIF-1α、HIF-2α and theexpression of VEGF in the blood vessels in the BGC-823cells of the gastric cancer in humanbeings. Based on it, we discuss the effect of Helicobacter pylori infection in the invasion andmetastasis abilities of the gastric cancer. Methods: The BGC-823cells were co-culturedwith different concentrations of H.pylori (l×103cfu／ml, l×104cfu／ml, l×105cfu／ml,l×106cfu／ml and l×107cfu／ml) for12h,24h,36h and48h. The dilution medium was putinto the control group. The cell survival rates were examined by the MTT method. A lowconcentration of H.pylori (l×103cfu／ml, l×104cfu／ml and l×105cfu／ml) were co-culturedwith the BGC-823cells for24h. The expression of HIF-1α, HIF-2α and VEGF mRNA andprotein were examined by the RT-PCR and Western-blot techniques. The dilution mediumwas put into the control group. Results: Low concentration of H.pylori were co-culturedwith the BGC-823cells for12h,24h,36h and48h, respectively. Compared to the controlgroup, the survival rate of the cells in the experimental group increased significantly. Thestatistic difference between the experimental group and the control group is dramatic (P<0.05).The high concentration of H.pylori were co-cultured with the BGC-823cells for12h,24h,36h,48h, respectively. The cell survival rate in the experimental group dropped rapidly thanthe control group. Simi1αrly, there were still statistic difference between experimental groupand control group (P<0.05). Compared with the control group, the low concentration ofH.pylori can up-regu1αtion of HIF-lα, HIF-2α and VEGF mRNA and protein significantly ina concentration-dependent manner. There were statistic difference between the experimentalgroup and the control group (P<0.05). Conclusions: H.pylori infection may simu1αte theexpression of VEGF and be transported through HIF-1α, HIF-2α in BGC-823cells. This maybe one of the mechanisms that the H.pylori induces the angiogenesis and invasion andmetastasis of the gastric cancer.