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本文旨在研究组蛋白甲基化修饰调控对胃癌细胞mi R-200c的表达调节以及对癌细胞的侵袭和迁移的作用。组蛋白甲基转移酶抑制剂DZNep(2.5μmol/L)处理MGC-803胃癌细胞系,用实时定量PCR(q RT-PCR)检测细胞mi R-200c的表达变化,用Western blot检测上皮间质转化相关蛋白、EZH2、EED、SUZ12、H3K27me3及MMP9的蛋白表达变化,用细胞划痕实验和Transwell法检测细胞迁移和侵袭。结果显示,与对照(DMSO处理)组相比,DZNep(2.5μmol/L)处理的MGC-803肿瘤细胞mi R-200c基因的表达显著提高,ZEB1、ZEB2、N-cadherin的表达显著下调,E-cadherin的表达上调,EZH2、EED、SUZ12、H3K27me3及MMP9的表达均显著降低,细胞迁移、侵袭能力均减弱。以上结果提示,DZNep通过上调mi R-200c的表达延缓胃癌细胞侵袭、迁移过程,其机制涉及对上皮间质转化相关蛋白和PRC2(polycomb repressive complex 2)的表达调节。
This article aims to study the regulation of histone methylation modification on gastric cancer cells mi R-200c expression regulation and invasion and migration of cancer cells. MGC-803 gastric cancer cell line was treated with histone methyltransferase inhibitor DZNep (2.5μmol / L), the expression of mi R-200c was detected by real-time quantitative PCR (q RT-PCR) Transforming protein, EZH2, EED, SUZ12, H3K27me3 and MMP9 protein expression were detected by cell scratch assay and Transwell assay of cell migration and invasion. The results showed that the expression of mi R-200c gene in MGC-803 cells treated with DZNep (2.5 μmol / L) was significantly increased, while the expression of ZEB1, ZEB2 and N-cadherin was significantly down-regulated compared with the control The expression of -cadherin was up-regulated, the expression of EZH2, EED, SUZ12, H3K27me3 and MMP9 were significantly decreased, and the ability of cell migration and invasion were weakened. The above results suggest that DZNep can delay the invasion and migration of gastric cancer cells by up-regulating the expression of mi R-200c, and its mechanism involves the regulation of the expression of epithelial-mesenchymal transition associated gene 2 (polycomb repressive complex 2).