Hepatitis B virus (HBV)-encoded X antigen (HBx) contributes to the development of hepatocellular carcinoma (HCC). Although HBx has been implicated in the progression of HCC, its precise function in HBV-associated HCC remains unclear. In the present study, HBx affected 3-phosphoinositide-dependent protein kinase-1 (PDK1) and with-no-lysine (K) kinase (WNK1) signaling, which was identified to be involved in the viability and metastasis of hepatic cells. The phosphorylation of WNK1 was decreased when the hepatic cells were treated with a PDK1 inhibitor. The inhibition of PDK1 activity inhibited the viability and migration of hepatic cells. To the best of our knowledge, the present study is the first to identify the activation of PDK1 in HCC tissues, confirmed using western blot analysis. PDK1-WNK1 signaling may be a potential therapeutic target in HBV-associated liver cancer.
Keywords: 3-phosphoinositide-dependent protein kinase-1; hepatitis B virus-encoded X antigen; hepatocellular carcinoma.