抑癌基因Tg737下调对肝癌细胞增殖的影响及其机制

Inhibition of Tg737 expression promotes hepatocellular carcinoma cell proliferation through upregulation of cyclinD1 induced G1/S transition in the cell cycle

目的 探讨下调Tg737表达对肝癌细胞增殖能力的影响及其下游机制.方法 SMMC7721和MHCC97-H细胞分别转染空白对照病毒和干扰Tg737表达的慢病毒后,用CCK-8法绘制肝癌细胞生长曲线检测其增殖能力变化.通过流式细胞仪检测肝癌细胞周期变化,并进一步检测细胞周期调控蛋白的表达变化,推断可能的分子机制.结果 与转染空白对照病毒的细胞相比,稳定下调Tg737的SMMC7721和MHCC97-H细胞增殖能力增强,G1期细胞比例减少,S期细胞比例增高,调控细胞周期完成G1/S转化的cyclinD1的表达水平增高.结论 在肝癌细胞SMMC7721和MHCC97-H下调Tg737表达可能通过上调cylinD1的表达促进肝癌细胞周期由G1期向S期转化,进而促进肝癌细胞的增殖.

Objective To study the influence of Tg737 inhibition on proliferation of hepatocellular carcinoma （HCC） cells and to explore the underlying mechanism.Methods A lentivirus with meaningless nucleotide sequence and anti Tg737 shRNA nucleotide sequence was transfected into the SMMC7721 and MHCC97-H HCC cells respectively.We then compared the proliferation ability of the SMMC7721 and MHCC97-H cells with or without Tg737 inhibition,and detected the change of cell cycle constitution using flow cytometry.Finally,the Tg737 related signaling pathways were studied to determine the underlying molecular mechanism.Results When compared with the cells which were transfected with blank control virus,the proliferative capacities of the SMMC7721 and MHCC97-H cells were enhanced through down-regulation of the gene Tg737.The cell percentage decreased in the G1 stage,but it was enhanced in the S stage.Furthermore,with Tg737 inhibition,the expression level of cyclinD1,which drives the G1/S transition in the cell cycle,was upregulated.Conclusion Inhibition of Tg737 expression promoted SMMC7721 and MHCC97-H proliferation through upregulating cyclinD1 to induce G1/S transition in the cell cycle.