Failure of lamivudine to reverse hepatitis B virus-associated changes in ERK, Akt and cell cycle regulatory proteins

Abstract

Background: Chronic infection with hepatitis B virus (HBV) is a major factor associated with the development of hepatocellular carcinoma, but the mechanism by which this occurs is unknown. Treatment of chronic hepatitis B with lamivudine results in virological suppression and histological improvement; however, the role of lamivudine in preventing the development of hepatocellular carcinoma is less well defined. We recently reported that replication of HBV in a cell-culture system was associated with the upregulation of pERK, pAkt, pc-Myc, nuclear cyclin B1, p21cip1 and p53 together with G2 cell cycle arrest. Methods: In order to determine whether lamivudine is able to reverse the HBV-induced..