Abstract: Objective The purpose of this study was to investigate the potential mechanism of hepatitis B virus (HBV) or hepatitis C virus (HCV) infection promoting the proliferation of hepatocellular carcinoma cells. Methods The proliferation of HepG2 and Huh7 cells after HBV or HCV infection was detected by MTT. The key genes that affected the proliferation of hepatoma cells after HBV or HCV infection were assayed by high-throughput transcriptome sequencing and small interfering ribonucleic acid genetic screening. After overexpression or knockdown of these genes, their functions were analyzed by high-throughput sequencing and pathway enrichment. Results After HBV transinfection, the proliferation of HepG2 and Huh7 cells were (1.01±0.09)and(0.97±0.09), significantly higher than [(0.61±0.12)and(0.60±0.12), respectively, P<0.05] before transinfection; the proliferation activities of HepG2 and Huh7 cells after HCV transinfection were (1.10±0.09)and(1.03±0.08), significantly higher than [(0.65±0.13)and(0.52±0.11), respectively, P<0.05] before transinfection; when the LSM11 was knocked down, the proliferation of HepG2 and Huh7 cells were (0.39±0.06)and(0.34±0.04), significantly lower than [(0.49±0.02)and (0.50±0.06), respectively, P<0.05] without knock-down; the proliferation of HepG2 and Huh7 cells when overexpression of LSM11 were (1.04±0.07)and(1.02±0.08), significantly higher than [(0.54±0.11)and(0.50±0.12), P<0.05] without overexpression; the high-throughput sequencing and pathway enrichment analysis of the regulated genes after LSM11 knockdown or overexpression showed that LSM11 could significantly affect the product expression of Wnt/β-catenin pathway; after LSM11 knockeddown, the β-catenin activity in HepG2 and Huh7 cells were(1235±69)and(884±95), significantly lower than [(23645±256)and(19482±119), P<0.05] without knocked-down; the activity of β-catenin after LSM11 overexpression in HepG2 and Huh7 cells were (43999±2345)and(39572±3912), significantly higher than [(25281±281)and(2004±145), P<0.05] without overexpression; in addition, the interaction between LSM11 and β-catenin was observed by immunoprecipitation. Conclusion After HBV or HCV transinfection, the expression of LSM11 in hepatocellular carcinoma cells is increased, and LSM11 could bind to β-catenin, a key transcription factor in Wnt/β-catenin signaling pathway, and enhance the functional activity of β-catenin.

Key words: HepG2, Huh7, LSM11, Wnt, β- catenin, HBV, HCV, In vitro