摘要
目的探讨类泛素蛋白FAT10在肝癌细胞中的异常表达和功能活化及其分子机制。方法将38例肝癌大鼠随机分为空白组、pc DNA3.1-FAT10组、FAT10 si RNA组。采用RT-PCR法检测肝癌及癌旁组织中FAT10 m RNA的表达水平,电穿孔法分别将FAT10 si RNA和重组表达载体pc DNA3.1-FAT10转染人肝癌SMMC-7721后,流式细胞术检测细胞周期和细胞凋亡的变化,RT-PCR检测PI3K/Akt通路的变化。结果 FAT10 m RNA在大鼠肝癌组织中的相对表达水平明显高于癌旁组织(P<0.05),沉默FAT10后,对细胞周期无明显影响,细胞凋亡率上升,PI3K/Akt信号通路表达下调;促进FAT10表达后,对细胞周期无明显影响,细胞凋亡率显著下降,PI3K/Akt通路表达上调。结论 FAT10可通过上调PI3K/Akt通路表达,减少细胞凋亡,增强肝癌细胞的侵袭能力,FAT10可能成为预防和治疗肝癌的靶点。
Objective To investigate the ubiquitin protein FAT10 abnormal expression in hepatoma cells and activation of function and its molecular mechanism.Methods 38 cases of liver cancer rats were randomly divided into blank group,pc DNA3.1-FAT10 group,FAT10 si RNA group.The expression level of FAT10 m RNA was detected by RT-PCR method.After respectively FAT10 si RNA and pc DNA3.1-FAT10 recombinant expression vector transfected into human hepatoma SMMC-7721 cells by electroporation,and flow cytometry to detect cell cycle and apoptosis,RT-PCR detection of PI3K/Akt pathway.Results FAT10 m RNA in rats hepatocellular carcinoma relative expression levels were significantly higher than adjacent tissues（P〈0.05）,after gene silencing in cancer cells FAT10 expression of cell cycle distribution had no significant impact on the rate of increase in apoptosis,PI3K/Akt path expression signals down;after FAT10 promote gene expression in cells,no significant effect on the cell cycle,apoptosis was significantly decreased,PI3K/Akt pathway upregulation.Conclusion FAT10 can increase the expression of PI3K/Akt pathway signal,reduce apoptosis,enhanced invasive ability of liver cancer cells,FAT10 may become targets for prevention and treatment.
出处
《中国当代医药》
2016年第25期16-18,共3页
China Modern Medicine
