fig3

Figure 3. Possible role of SND1 in lipid metabolism. Exposure of human HCC cells to cholesterol-lowering drug or a lipoprotein-deficient medium triggers SREBP2 activation and increases SND1 promoter activity. Studies in rat hepatoma cells show that SND1 overexpression accumulates de novo synthesized cholesteryl esters. SND1 is induced by TNFα and subsequent profiling in human hepatoma cells revealed that SND1 binds to the promoter regions of a group of glycerolipid metabolic genes including CHPT1, LPGAT1, PTDSS1 and LPIN1 involved in the biosynthesis of phophatidylcholine, phosphatidylglycerol, phosphatidylserine and triacylglycerol, respectively. As yet functional consequence of SND1 binding to the promoter of these genes has not been studied. In human HCC cells SND1 interacts with MGLL and results in ubiquitination and proteosomal degradation of MGLL. The increase in monoglyceride (MG) levels is predicted from the known role of MGLL. Studies in mouse adipocytes have shown that SND1 is a co-activator of PPARγ in adipogenesis. SND1: staphylococcal nuclease and tudor domain containing 1; HCC: hepatocellular carcinoma