Microarray of SIRT6 KO in hepatocellular carcinoma

We identified the specific role of Sirtuin 6 (SIRT6) in the progression of hepatocellular carcinoma (HCC) and evaluated its therapeutic and prognostic potential. SIRT6 knockdown by shRNA inhibited the proliferation of HCC cells; moreover, depletion of SIRT6 suppressed HCC tumor growth in vivo. SIRT6 silencing significantly down regulated the growth of HCC cell lines via induction of cellular senescence, which was attributed by DNA damage in p16/Rb and p53/p21-independent manners. We also showed that SIRT6 knockdown increased the number of G2/M phase arrested cells by increasing cyclin B1 and 14-3-3-∂. Moreover, SIRT6 levels were significantly higher in HCC cell lines than a normal hepatic cell line, and were higher in HCC than non-tumor tissues. Aberrant SIRT6 expression correlated with poor prognostic features of HCC. Taken together, our findings suggest SIRT6 may act as a tumor promoter by preventing cellular senescence attributed by DNA damage and suggests that targeting SIRT6 could be a promising therapeutic approach for cancer treatment. Two-condition experiment, Control vs. SIRT6 KO. Biological replicates: 2 control replicates, 2 KO replicates.