DLAT activates EMT to promote HCC metastasis by regulating GLUT1-mediated aerobic glycolysis.

ABSTRACT:

Background

Metabolic reprogramming is a hallmark of hepatocellular carcinoma (HCC) progression, driving aberrant cellular processes in response to pathological stimuli. While dihydrolipoyl transacetylase (DLAT) has been implicated in the development of various cancers, its specific role and underlying mechanisms in HCC remain unclear. This study aimed to investigate the expression, function, and mechanistic impact of DLAT in HCC.

Methods

A comprehensive analysis was conducted using RNA sequencing data, tissue microarrays, in vitro and in vivo functional assays, and mechanistic studies to evaluate DLAT expression, its functional role in tumor progression, and associated molecular pathways in HCC.

Results

Our study revealed a significant upregulation of DLAT expression

SUBMITTER: Yin Q 

PROVIDER: S-EPMC11844032 | biostudies-literature | 2025 Feb

REPOSITORIES: biostudies-literature