HBx enhances cell viability, migration and invasion of hepatocellular carcinoma via PD-L1

Programmed death 1 ligand (PD-L1) is expressed in many cancers. Many studies have confirmed that PD-L1 is involved in multiple behaviors of cancers, such as cell viability, proliferation, migration, invasion, apoptosis and immune escape. In hepatocellular carcinoma (HCC), some studies show that PD-L1 expression is related to HBx, which is encoded by the X gene in Hepatitis B virus (HBV). In our study, HBx gene was transfected into HepG2 cell (HBV negative cell line), expressing HBx protein. Moreover, the HBx gene was down-regulated through small interfering RNA (siRNA). Meanwhile, PD-L1 gene was also transfected into HepG2 cell alone. PD-L1-siRNA can decrease the expression of PD-L1. The results showed that the ability of cell viability, migration, and invasion was promoted when HBx and PD-L1 increased. However, the results were opposite when HBx and PD-L1 were inhibited. Confirmed results indicate that HBx enhances cell proliferation, migration and invasion of hepatocellular carcinoma via PD-L1. These studies suggest that knocking down HBx gene and blocking PD-1 (programmed death 1)/PD-L1 immune detection point may be expected as an immunotherapy for HBV positive HCC patients.