ARID1A deficiency promotes malignant proliferation of hepatocellular carcinoma by activating HDAC7/ENO1 signaling pathway.

ABSTRACT:

Background

Epigenetic dysregulation constitutes one of the mechanisms in the pathogenesis of HCC, thereby underscoring its critical scientific importance for early diagnosis and therapeutic interventions. The chromatin remodeling factor AT-rich interaction domain 1A (ARID1A) serves as an essential epigenetic regulator and is frequently subject to inactivating mutations across various cancer types. Nevertheless, the precise molecular pathways by which ARID1A deficiency facilitates the progression of HCC remain inadequately elucidated.

Methods

RNA sequencing (RNA-seq) was employed to identify genes that were significantly upregulated following the knockdown of ARID1A. Immunohistochemistry was used to assess the expression levels of ARID1A and histone deacetylase 7 (HDAC7) in H

SUBMITTER: Zhang S 

PROVIDER: S-EPMC12180837 | biostudies-literature | 2025 Jul

REPOSITORIES: biostudies-literature