下调CDH17基因对那可丁耐药性人胃癌细胞作用的分析

发布时间：2018-03-20 00:11

本文选题：肝肠钙黏连蛋白　切入点：那可丁　出处：《基因组学与应用生物学》2017年05期 　论文类型：期刊论文

【摘要】：探讨下调肝肠钙黏连蛋白(CDH17)基因对抑制那可丁耐药性人胃癌MGC-803细胞增殖的分子机制,为临床治疗胃癌提供新的治疗手段。本研究以人胃癌MGC-803细胞为研究材料,通过体外MTT实验检测细胞活力、流式细胞术观察细胞增殖与凋亡情况,蛋白免疫印迹检测凋亡通路相关蛋白的表达水平变化。那可丁药物处理实验和MTT实验表明,下调CDH17可以提高人胃癌MGC-803细胞对那可丁的敏感性;流式细胞术观察结果表明,下调CDH17基因促进引起细胞凋亡;蛋白免疫印迹实验表明线粒体途径参与那可丁诱导人胃癌MGC-803细胞凋亡的过程。综上所述,下调CDH17基因通过提高人胃癌MGC-803细胞对那可丁的敏感性,引起线粒体途径相关蛋白功能障碍促进细胞凋亡,从而抑制胃癌细胞的增殖。
[Abstract]:To explore the molecular mechanism of down-regulation of liver-intestinal calmodulin (CDH17) gene on inhibiting the proliferation of nakodin-resistant human gastric cancer MGC-803 cells, and to provide a new therapeutic method for clinical treatment of gastric cancer. In this study, human gastric cancer MGC-803 cells were used as the research materials. In vitro MTT assay was used to detect cell viability, flow cytometry was used to observe cell proliferation and apoptosis, and Western blot was used to detect the expression of apoptosis-related proteins. Down-regulation of CDH17 could increase the sensitivity of MGC-803 cells to nakodin, flow cytometry showed that down-regulation of CDH17 gene promoted apoptosis. Western blot analysis showed that mitochondrial pathway was involved in the apoptosis of human gastric cancer MGC-803 cells induced by nakodin. In summary, down-regulated CDH17 gene enhanced the sensitivity of human gastric cancer MGC-803 cells to nakodin. Mitochondrial pathway related protein dysfunction promotes cell apoptosis and inhibits the proliferation of gastric cancer cells.
【作者单位】：武汉市第三医院;
【基金】：武汉市卫计委(WX14C18) 湖北省自然科学基金(2013CFB358)共同资助
【分类号】：R735.2

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