Adipocyte-derived FABP4 promotes metabolism-associated steatotic liver-induced hepatocellular carcinoma by driving ITGB1-mediated β-catenin activation.

ABSTRACT: Metabolic dysfunction-associated steatotic liver disease-induced (MASLD-induced) hepatocellular carcinoma (HCC) is an emerging malignancy linked to excessive accumulation of adipose tissue and hepatic fat. Understanding the role of adipocytes in the development of MASLD-induced HCC is crucial. In an in vitro coculture system, differentiated adipocytes were found to enhance cancer stemness and drug resistance in HCC through paracrine signaling. Fatty acid-binding protein 4 (FABP4) was preferentially secreted by adipocytes, and recombinant FABP4 further augmented the cancer stem cell (CSC) properties of HCC cells. Notably, Fabp4-/- mice exhibited a marked delay in the progression of MASLD-HCC, which correlated with the increased HCC risk observed in MASLD patients with elevated FABP4 express

SUBMITTER: Leung CON 

PROVIDER: S-EPMC12700556 | biostudies-literature | 2025 Dec

REPOSITORIES: biostudies-literature