褪黑素抑制缺氧引起的SGC-7901人胃癌细胞上皮-间充质转化

Melatonin inhibits hypoxia induced epithelial- mesenchymal transition of SGC-7901 gastric cancer cells

目的:研究褪黑素对缺氧引起的SGC-7901人胃癌细胞上皮-间充质转化(EMT)的作用,并初步揭示其分子机制。方法:在建立缺氧诱导SGC-7901人胃癌细胞发生EMT的基础上,通过免疫印迹方法检测蛋白表达水平、免疫荧光的方法检测蛋白在细胞中的分布和表达,研究褪黑素对EMT过程的作用。结果:缺氧使SGC-7901人胃癌细胞发生EMT,表现为形态发生改变,上皮标志物表达量减少、间充质标志物表达增加,褪黑素可抑制缺氧条件下活性氧簇(ROS)的产生和缺氧诱导因子1α(HIF-1α)的表达及EMT。结论:在缺氧条件下SGC-7901人胃癌细胞可发生EMT,褪黑素可抑制该过程。这些结果揭示了褪黑素在缺氧引起的肿瘤细胞EMT过程中发挥的抑制作用,为褪黑素的临床应用提供了重要的理论依据。

Objective：To elucidate the function of melatonin on hypoxia -induced epithelial- mesenchymal transition （EMT） of SGC-7901 gastric cancer cells and to reveal the mechanisms underlying. Methods：After hypoxia for 96h,expression of epithelial and mesenchymal makers of SGC-7901 gastric cancer cells was detected using Western blot and immunofluorescence was employed to investigate distribution of proteins to see if EMT acured. Then we treated SGC-7901 gastric cancer cells by 1 mmol/L concentration of melatonin under hypoxia environment to see if EMT was inhibited. Results：Hypoxia induced morphological change of SGC-7901 gastric cancer cells,as well as decreased E-cadherin and increased vimnetin and α-SMA. The reactive oxygen species （ ROS） and exprssion of hypoxia-inducible factor-1α（HIF-1α） both abolished by treatment of melatonin,so as EMT. Conclusion：We found that melatonin can abolish hypoxia-induced EMT of SGC-7901 gastric cancer cells,which can be used for clinical application.