The Role Of Liver Fatty Acid Binding Protein In HBV-associated Hepatocellular Carcinoma

Background and purpose:Chronic hepatitis B virus (HBV) infection has been identified as a causative factor in the development of HCC, which HBV X protein (HBx) plays crucial roles. Previous studies already confirmed HBx may induces hepatic steatosis, a risk factor for the development of HCC. However, liver fatty acid binding proteins (L-FABP), an important transduction protein in lipid signal transport and lipid metabolism in hepatic cells. The correlation between HBx and FABP and the role of FABP in HBV-related HCC is seldom reported. In this study, we investigated the correlation between HBx and FABP in the pathogenesis of HBV-induced HCC.Methods:The expression of L-FABP and HBx was detected by western blot into human HCC cell line HepG2. Oil red O staining was used to measure the degree of cellular fatty degeneration in L-FABP siRNA silence cells and none-silence cells. Also, the proliferation ability was investigated by MTT assay and DAPI fluorescence stain, also, cell cycle and apoptosis were examined by flow-cytometric analysis in L-FABP siRNA silence cells and none-silence cells.Results:Western blot showed that the expression of L-FABP in FIBx transfected cells was much higher than untransfected cells. Oil red O staining revealed that the transfected L-FABP siRNA cells produced less lipid droplets than untransfected cells. Compared to the controls, MTT assay and DAPI fluorescence stain reported cell proliferation was restrained in cells transfected with L-FABP siRNA, Flow-cytometric analysis show that cell cycle was shortened in cells transfected with L-FABP siRNA, and the apoptosis rate was increased in cells transfected with L-FABP.Conclusion:Our results suggested HBx may induces the expression of L-FABP. L-FABP may promotes hepatic lipogenesis, meanwhile, L-FABP was involved in the HCC pathogenesis through incresaesing cell proliferation and inhibitting cell apoptosis.