Effect of Sirt2 deletion in mouse hepatocytes on gene experession in mouse livers overexpressed with GFP or MET/CAT
There is a gap in our understanding of mechanisms promoting hepatocellular carcinoma (HCC), and this limits our ability to provide targeted therapy interventions for HCC. In HCC samples, NAD-dependent deacetylase sirtuin 2 (SIRT2) levels are increased and associated with a significantly worse prognosis, but the role of SIRT2 in hepatocarcinInogenesis remains controversial. In this study, we investigated the role of SIRT2 in HCC development and examined the effect of Sirt2 deletion in hepatocytes on gene expression in mouse livers overexpressed with GFP control or MET/CAT. Overall design: To assess the role of SIRT2 in hepatocarcinogenesis, we used a hepatocyte-specific knockout of SIRT2 and two plasmid overexpression  MET/CAT HCC model. RNA-sequencing of mouse liver tissue was performed,