Disruption of Dicer1 induces dysregulated fetal gene expression and promotes hepatocarcinogenesis.

ABSTRACT:

Background & aims

Growing evidence suggests that microRNAs coordinate various biological processes in the liver. We describe experiments to address the physiologic roles of these new regulators of gene expression in the liver that are as of yet largely undefined.

Methods

We disrupted Dicer, an enzyme essential for the processing of microRNAs, in hepatocytes using a conditional knockout mouse model to elucidate the consequences of loss of microRNAs.

Results

The conditional knockout mouse livers showed the efficient disruption of Dicer1 at 3 weeks after birth. This resulted in prominent steatosis and the depletion of glycogen storage. Dicer1-deficient liver exhibited increased growth-promoting gene expression and the robust expression of fetal stage-specific genes. The

SUBMITTER: Sekine S 

PROVIDER: S-EPMC3167383 | biostudies-literature | 2009 Jun

REPOSITORIES: biostudies-literature