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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。
AIM: To investigate the effect of melatonin on epithelial-mesenchymal transition (EMT) induced by hypoxia in human gastric cancer SGC-7901 cells and to reveal its molecular mechanism. Methods: Based on the establishment of hypoxia-induced EMT in SGC-7901 human gastric cancer cells, the protein expression levels were detected by immunoblotting and the distribution and expression of protein in cells were detected by immunofluorescence. The effects of melatonin on EMT effect. RESULTS: Hypoxia caused EMT in SGC-7901 human gastric cancer cells, which showed morphological changes, decreased expression of epithelial markers and increased expression of mesenchymal markers. Melatonin could inhibit reactive oxygen species (ROS) Production and hypoxia inducible factor 1α (HIF-1α) expression and EMT. CONCLUSION: EMT can occur in SGC-7901 human gastric cancer cells under hypoxia, and melatonin can inhibit this process. These results reveal the inhibitory effect of melatonin in EMT induced by hypoxia and provide an important theoretical basis for the clinical application of melatonin.