[Serum-and-glucocorticoid-inducible-kinase-2 is overexpressed and mediates glycogen synthase kinase-3beta/ beta-catenin signal transduction in hepatocellular carcinoma].

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 beta / beta 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 beta/ beta - 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 beta. In addition, the downregulation of SGK2 expression in HCC cell lines had decreased the dephosphorylation of beta - catenin to prevent degradation of the beta - catenin proteasome. Conclusion: SGK2 is overexpressed in HCC and mediates GSK-3beta/beta- catenin signaling in HCC cells.