Coordinated Cross-Talk Between the Myc and Mlx Networks in Liver Regeneration and Neoplasia.

ABSTRACT:

Background & aims

The c-Myc (Myc) Basic helix-loop-helix leucine zipper (bHLH-ZIP) transcription factor is deregulated in most cancers. In association with Max, Myc controls target genes that supervise metabolism, ribosome biogenesis, translation, and proliferation. This Myc network crosstalks with the Mlx network, which consists of the Myc-like proteins MondoA and ChREBP, and Max-like Mlx. Together, this extended Myc network regulates both common and distinct gene targets. Here, we studied the consequence of Myc and/or Mlx ablation in the liver, particularly those pertaining to hepatocyte proliferation, metabolism, and spontaneous tumorigenesis.

Methods

We examined the ability of hepatocytes lacking Mlx (MlxKO) or Myc+Mlx (double KO [DKO]) to repopulate the liver over an ex

SUBMITTER: Wang H 

PROVIDER: S-EPMC9046243 | biostudies-literature | 2022

REPOSITORIES: biostudies-literature