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目的:探讨RSK2在肝细胞癌(HCC)中的表达与化疗药物耐药的关系。方法:将HepG2细胞分为RSK2干扰组(PGCsi3.0-RSK2 siRNA转染细胞),5-FU处理组(10μg/mL 5-FU处理细胞24 h),5-FU处理+RSK2干扰组及空白对照组,采用MTT方法检测各组细胞增殖情况;用Western blot方法检测5-FU处理组和5-FU处理+RSK2干扰组细胞RSK2,c-Jun,Bcl-2,LKB1蛋白表达。结果:与空白对照组比较,沉默RSK2蛋白与5-FU干预均可明显抑制HepG2细胞增殖(均P<0.05),且其联合作用大于两者单独的作用(均P<0.05);与RSK2干扰组比较,5-FU处理+RSK2干扰组细胞RSK2,c-Jun,Bcl-2表达上调,LKB1表达下调(均P<0.05)。结论:抑制RSK2表达可以增强肝癌细胞对化疗药物5-FU的敏感性,机制作用可能与其调节c-Jun,Bcl-2,LKB1蛋白的表达有关。
Objective: To investigate the relationship between the expression of RSK2 in hepatocellular carcinoma (HCC) and chemotherapy drug resistance. Methods: HepG2 cells were divided into RSK2 interference group (PGCsi3.0-RSK2 siRNA transfected cells), 5-FU treatment group (10 μg / mL 5-FU treatment of cells for 24 h), 5-FU treatment + RSK2 interference group and blank The proliferation of cells in each group was detected by MTT assay. The expressions of RSK2, c-Jun, Bcl-2 and LKB1 in 5-FU treated group and RSK2-treated group were detected by Western blot. Results: Compared with the blank control group, the silencing of RSK2 protein and 5-FU significantly inhibited the proliferation of HepG2 cells (all P <0.05), and their combined effect was greater than that of both alone (all P <0.05) Compared with the control group, RSK2, c-Jun and Bcl-2 expressions were up-regulated and LKB1 was down-regulated in 5-FU + RSK2-treated group (all P <0.05). Conclusion: Inhibition of RSK2 expression can enhance the sensitivity of hepatoma cells to chemotherapeutic drug 5-FU. The mechanism may be related to the regulation of c-Jun, Bcl-2 and LKB1 protein expression.