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目的 探讨血清和糖皮质激素诱导的蛋白激酶(SGK2)在肝癌组织与正常肝脏组织中的表达差异以及介导肝细胞癌(HCC)细胞中糖原合成酶激酶-3β(GSK-3β)/β-连环蛋白(β-catenin)信号传导的相关机制. 方法 收集配对的HCC及正常组织20对,采用实时荧光定量PCR技术检测SGK2 mRNA表达情况.应用蛋白质印迹法检测人肝癌细胞系Huh-7、SMMC-7721以及正常人肝细胞系L02中SGK2蛋白水平.应用SGK2 siRNA转染人肝癌细胞系SMMC-7721、Huh-7,然后使用蛋白质印迹方法检测上述转染成功细胞系中GSK-3 β、β-catenin的蛋白质表达水平.计量资料以均值±标准差((x)±s)表示,统计学方法采用Student f检验. 结果 与配对正常肝组织中的表达水平相比,所有20个HCC样品中SGK2 mRNA表达上调.在两种人肝癌细胞系(Huh-7和SMMC-7721)中SGK2蛋白水平显著高于正常人肝细胞系(P＜0.01).在人HCC细胞系SMMC-7721和Huh-7中,SGK2表达下调抑制了未磷酸化GSK-3 β表达.另外,在HCC细胞系中SGK2表达下调通过阻止p-catenin蛋白酶体降解来降低β-catenin的去磷酸化.结论 SGK2在HCC中过表达并介导HCC细胞中GSK-3 β/β-catenin信号传导.“,”Objective To investigate the differential expression of serum-and-glucocorticoid-inducible-kinase-2 (SGK2) in hepatocellular carcinoma (HCC) and normal liver tissues and the related mechanism mediating signal transduction of GSK-3 β / β catenin in HCC cells.Methods Twenty pairs of matched HCC and normal tissues were collected and the situation of expression of SGK2 mRNA was detected by real-time fluorescence quantitative PCR.Western blot was used to detect the levels of SGK2 protein in human HCC cell lines (Huh-7,SMMC-7721) and normal human liver cell line (L02).SGK2 siRNA was used to transfect human HCC cell lines (SMMC-7721 and Huh-7),and then the protein expression levels of GSK-3 β/β-catenin was successfully detected with the above-mentioned transfected cell line by western blot.Measurement data were expressed as mean + standard deviation ((x) + s),and the Student t-test was used as the statistical method.Results SGK2 mRNA expression was up-regulated in all 20 HCC samples than that of the expression of matched normal liver tissues.SGK2 protein levels were significantly higher in Huh-7 and SMMC-7721 than normal human liver cell lines (P ＜ 0.01).The downregulation of SGK2 expression in human HCC cell lines (SMMC-7721 and Huh-7) had inhibited the expression of unphosphorylated GSK-3 β.In addition,the downregulation of SGK2 expression in HCC cell lines had decreased the dephosphorylation of β-catenin to prevent degradation of the β-catenin proteasome.Conclusion SGK2 is overexpressed in HCC and mediates GSK-3β/β-catenin signaling in HCC cells.