Loss of KDM6B epigenetically confers resistance to lipotoxicity in nonalcoholic fatty liver disease-related HCC.

Megumi HatanoYoshimitsu Akiyama Shu ShimadaKohei YagiKeiichi AkahoshiMichiko ItohMinoru TanabeYoshihiro OgawaShinji Tanaka

Published in: Hepatology communications (2023)

KDM6B-disrupted HCC acquires resistance to lipotoxicity via ATGL/PNPLA2 activation caused by epigenetic downregulation of G0S2 expression. Reduced KDM6B and G0S2 expression levels are common in NAFLD-related HCC. Targeting the KDM6B-G0S2-ATGL/PNPLA2 pathway may be a useful therapeutic strategy for NAFLD-related HCC.

Keyphrases

poor prognosis
dna methylation
gene expression
cell proliferation
signaling pathway
binding protein
drug induced