【摘 要】
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Objective: Toinvestigate the role of kallistatin on lymphatic metastasis of gastric cancer and its underlying molecular mechanism in vivo and ex vivo.Methods:(1)Inject gastric cancer cells into the fo
【机 构】
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Department of Biochemistry,Zhongshan Medical School,Sun Yat-sen University,Guangzhou 510080,China
【出 处】
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中国生物化学与分子生物学会2016年全国学术会议
论文部分内容阅读
Objective: Toinvestigate the role of kallistatin on lymphatic metastasis of gastric cancer and its underlying molecular mechanism in vivo and ex vivo.Methods:(1)Inject gastric cancer cells into the footpad of nude mice to build the lymphatic metastasis model of gastric cancer,take primary tumors and popliteal lymph nodes to test LVD and metastatic gastric cancer cells by IHC and IF after 30 days continuous dosing.(2)Incubate human gastric cancer cell lines SGC7901 and HCG27 with recombinant kallistatin and adenovirus kallistatin,and then examine the expression and secretion of VEGF-C from gastric cancer cells by Western Blotting and ELISA,while detecting the activation of NF-κ B signaling pathway by Western Blotting and IF.(3)test the proliferation,migration and tube formation capacity changes of lymphatic endothelial cells after kallistatin incubation.Results:Our results revealed that kallistatin not only significantly down-regulated the expression and secretion of VEGF-C in gastric cancer cells,but also inhibited the lymphangiogenesis in the gastric cancer by inhibiting the proliferation,migration and tube formation of hLECs.In the meantime,we find that kallistatin down-regulated the expression of VEGF-C through the NF-κB signaling pathway in gastric cancer cells.Thus,our findings revealed the function and mechanism of kallistatin in inhibiting the lymphatic metastasis of gastric cancer.
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