Inactivation of fatty acid synthase impairs hepatocarcinogenesis driven by AKT in mice and humans.

ABSTRACT:

Background & aims

Cumulating evidence underlines the crucial role of aberrant lipogenesis in human hepatocellular carcinoma (HCC). Here, we investigated the oncogenic potential of fatty acid synthase (FASN), the master regulator of de novo lipogenesis, in the mouse liver.

Methods

FASN was overexpressed in the mouse liver, either alone or in combination with activated N-Ras, c-Met, or SCD1, via hydrodynamic injection. Activated AKT was overexpressed via hydrodynamic injection in livers of conditional FASN or Rictor knockout mice. FASN was suppressed in human hepatoma cell lines via specific small interfering RNA.

Results

Overexpression of FASN, either alone or in combination with other genes associated with hepatocarcinogenesis, did not induce histological liver altera

SUBMITTER: Li L 

PROVIDER: S-EPMC4718802 | biostudies-literature | 2016 Feb

REPOSITORIES: biostudies-literature