The concomitant loss of APC and HNF4α in adult hepatocytes does not contribute to hepatocarcinogenesis driven by β-catenin activation.

ABSTRACT:

Background & aims

Loss of hepatocyte nuclear factor-4α (HNF4α), a critical factor driving liver development and differentiation, is frequently associated with hepatocellular carcinoma (HCC). Our recent data revealed that HNF4α level was decreased in mouse and human HCCs with activated β-catenin signalling. In addition, increasing HNF4α level by miR-34a inhibition slowed tumour progression of β-catenin-activated HCC in mice.

Methods

We generated a Hnf4a^flox/flox/ Apc^flox/flox /TTR-Cre^{ERT 2} (Hnf4a/Apc^∆Hep ) mouse line and evaluated the impact of Hnf4a disruption on HCC development and liver homoeostasis.

Results

There was no significant impact of Hnf4a disruption on tumour onset and progression in Apc^∆Hep

SUBMITTER: Sartor C 

PROVIDER: S-EPMC7387933 | biostudies-literature | 2019 Apr

REPOSITORIES: biostudies-literature