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miR-1在多种肝癌细胞中被甲基化沉默,导致其下游多个癌基因MET,FoxP1,HDAC4等大量表达,促进了肝癌的增殖.本研究利用非复制型腺病毒Ad-easy携带miR-1(Ad-miR-1)在肝癌细胞PLC/PRF/5和HepG2中过表达miR-1,探讨miR-1抑制肝癌细胞的作用机制.结果表明,肝癌细胞PLC/PRF/5和HepG2中miR-1表达水平极低,感染Ad-miR-1后miR-1表达水平显著上升.肝癌细胞PLC/PRF/5和HepG2感染Ad-miR-1后,MET和FoxP1的mRNA水平和蛋白表达水平被显著下调,细胞凋亡水平显著增加,肝癌细胞的增殖被抑制.可见,miR-1在肝癌细胞中可能是一个重要的抑癌因子.同时,利用腺病毒载体携带抗癌的microRNA(如miR-1),也为今后的基因治疗研究提供了一种新方法.
miR-1 is methylated and silenced in a variety of hepatocellular carcinoma cells, resulting in the massive expression of several downstream oncogenes MET, FoxP1, HDAC4 and so on, promoting the proliferation of hepatocellular carcinoma.In this study, Ad-easy adenovirus carrying miR 1 (Ad-miR-1) overexpression of miR-1 in hepatoma cells PLC / PRF / 5 and HepG2 to explore the mechanism of miR-1 inhibition of hepatocellular carcinoma cells.The results showed that in PLC / PRF / 5 and HepG2 cells The expression level of miR-1 was extremely low, and the expression of miR-1 was significantly increased after Ad-miR-1 infection.After Ad-miR-1 was transfected into PLC / PRF / 5 and HepG2 cells, the mRNA and protein expression levels of MET and FoxP1 Was significantly downregulated, the level of apoptosis increased significantly, and the proliferation of hepatoma cells was inhibited.It can be seen that miR-1 may be an important tumor suppressor in hepatoma cells.At the same time, adenovirus vector carrying anti-cancer microRNAs -1), but also for the future of gene therapy research provides a new method.