PTEN deficiency potentiates HBV-associated liver cancer development through augmented GP73/GOLM1.

ABSTRACT:

Background

Although hepatitis B virus (HBV) infection is a major risk factor for hepatic cancer, the majority of HBV carriers do not develop this lethal disease. Additional molecular alterations are thus implicated in the process of liver tumorigenesis. Since phosphatase and tensin homolog (PTEN) is decreased in approximately half of liver cancers, we investigated the significance of PTEN deficiency in HBV-related hepatocarcinogenesis.

Methods

HBV-positive human liver cancer tissues were checked for PTEN expression. Transgenic HBV, Alb-Cre and Pten^fl/fl mice were inter-crossed to generate WT, HBV, Pten^-/- and HBV; Pten^-/- mice. Immunoblotting, histological analysis and qRT-PCR were used to study these livers. Gp73^-/- mice were then

SUBMITTER: Huang F 

PROVIDER: S-EPMC10924424 | biostudies-literature | 2024 Mar

REPOSITORIES: biostudies-literature