Transcriptomic analysis of HepG2 cells overexpressing DNMT3A

Chronic hepatitis B virus (HBV) infection is the main etiology of liver fibrosis (LF), leading to cirrhosis and liver tumors. DNA methylation caused by HBV protein changes the liver microenvironment and activates hepatic stellate cells, which is an important mechanism of liver fibrosis. However, the exact mechanism remains unclear. DNA methyltransferase 3A (DNMT3A) is a major enzyme that promotes DNA methylation. HBV infection promotes the expression of DNMT3A. To determine the specific roles of DNMT3A, we used lentivirus to overexpress DNMT3A in hepatocellular carcinoma cell line (HepG2). And the changes of transcriptome were analysed by RNA-seq. Overall design: To explore the changes of transcriptome by DNMT3A, HepG2 cells were divided into two groups: cells infected with control lentivirus and cells infected with DNMT3A-overexpressing lentivirus. RNA-seq profiling the control and DNMT3A overexpression HepG2 cells.