Effect of lncRNA pvt1 on HBV replication in HepG2.2.15 cells, and its possible mechanism of action

Abstract

Purpose: To investigate the influence of lncRNA pvt1 on hepatitis B virus replication in HepG2.2.15 cells and the underlying mechanism of action. Methods: Concentrations of lncRNA pvt1 in HBV-positive liver cancer cell lines (HepAD38+, HepG2.2.15+, HepG2+, and HepaRG+), and 3 HBV-negative liver cancer cell lines were determined and compared. Differences in HBV DNA content, levels of HBsAg and HBeAg, and STAT3 axis signal pathway among groups were evaluated. Results: LncRNA pvt1 levels in HBV-positive hepatoma cells were significantly higher than the corresponding expression levels in HBV-negative hepatoma cells. after si-pvt1 treatment in HepG2.2.15 cells, the 3.2K HBV DNA content increased significantly (p < 0.05), and the expression levels of HBsAg and HBeAg in HepG2.2.15 cells also significantly increased. In all groups, STAT3 protein level was comparable, but p-STAT3 protein expression in si-pvt1 group was significantly reduced, relative to those in Si NC and control groups (p < 0.05). Conclusion: Levels of lncRNA pvt1 expression in HBV-positive and HBV-negative hepatoma cells differ significantly. Treatment with si-pvt1 decrease HBV DNA content in HepG2.2.15 cells through a mechanism that relates to the STAT3 axis signal pathway. This finding may be beneficial for follow-up treatment of HBV.