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Adipocyte-derived FABP4 promotes MASLD-induced hepatocellular carcinoma by driving ITGB1-mediated β-catenin activation [rhFABP4]

ABSTRACT: The mechanism underlying regulatory role of FABP4 in MASLD-HCC development was examined using bulk RNA sequencing.

ORGANISM(S): Homo sapiens

PROVIDER: GSE292914 | GEO | 2025/10/02

REPOSITORIES: GEO

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Adipocyte-derived FABP4 promotes MASLD-induced hepatocellular carcinoma by driving ITGB1-mediated β-catenin activation

Project description:The mechanism underlying regulatory role of FABP4 in MASLD-HCC development was examined using bulk RNA sequencing.

2025-10-02 | GSE286130 | GEO

Adipocyte-derived FABP4 promotes MASLD-induced hepatocellular carcinoma by driving ITGB1-mediated β-catenin activation

Project description:Adipocyte-derived FABP4 promotes MASLD-induced hepatocellular carcinoma by driving ITGB1-mediated β-catenin activation

| PRJNA1207982 | ENA

Adipocyte-derived FABP4 promotes MASLD-induced hepatocellular carcinoma by driving ITGB1-mediated β-catenin activation [rhFABP4]

Project description:Adipocyte-derived FABP4 promotes MASLD-induced hepatocellular carcinoma by driving ITGB1-mediated β-catenin activation [rhFABP4]

| PRJNA1241862 | ENA

FABP4 overexpressed in intratumoral hepatic stellate cells within hepatocellular carcinoma with metabolic risk factors (part 2)

Project description:BACKGROUND & AIMS: Metabolic syndrome is a newly identified risk factor for hepatocellular carcinoma (HCC), however the molecular mechanisms still remain unclear. To elucidate this issue, cross-species analysis was performed to compare gene expression patterns of HCC from human patients and melanocortin 4 receptor-knockout (MC4R-KO) mice, developing HCC with obesity, insulin resistance and dyslipidemia. METHODS: Unsupervised hierarchical clustering and principle component analysis of 746 differentially expressed orthologous genes classified HCC of 152 human patients and MC4R-KO mice into two distinct subgroups, one of which included all the mouse HCC was etiologically associated with metabolic risk factors, such as obesity and diabetes. A specific biomarker was identified by the integrative analysis, and validated with in vitro studies and other cohort patients. RESULTS: As commonly overexpressed in human and mouse metabolic disease-associated HCC, FABP4 was remarkably enriched in intratumoral activated hepatic stellate cells (HSCs). Then, we established subclones constitutively expressing FABP4 from a human HSC cell line, in which the expression levels of inflammatory chemokines including IL1A and IL6 was upregulated through NF-κB nuclear translocation. An immunohistochemical validation study of other 106 human HCC samples indicated that FABP4-positive HSCs were distributed in tumors of 38 cases, and that the FABP4-high group was composed of patients with non-viral and non-alcoholic HCC (P=0.027) and with multiple metabolic risk factors (P<0.001) compared with the FABP4-low. CONCLUSIONS: FABP4 overexpression in HSCs could contribute to hepatocellular carcinogenesis in patients with metabolic risk factors via modulation of inflammatory pathway, and is a promising novel biomarker as well as a potential therapeutic target for this subtype of HCC.

2018-01-28 | GSE102080 | GEO

FABP4 overexpressed in intratumoral hepatic stellate cells within hepatocellular carcinoma with metabolic risk factors (part 3)

2018-01-28 | GSE102081 | GEO

FABP4 overexpressed in intratumoral hepatic stellate cells within hepatocellular carcinoma with metabolic risk factors (part 1)

2018-01-28 | GSE102079 | GEO

Effect of exogenous FABP4 (A-FABP/aP2) and FABP5 (E-FABP/mal1) on gene expression in adipocyte-derived stem cells (ADSC) and 233A cells

Project description:Gene expression profile of treatment with FABP4 or FABP5 in ADSC and 233A cells was examined. ADSC or 233A cells were treated with and without 1 ÂµM recombinant FABP4 or FABP5.

2016-06-23 | E-GEOD-83587 | biostudies-arrayexpress

Gene expression profile at single cell level of hepatocytes and non parenchymal cells (NPCs) isolated from a murine model of MASLD

Project description:Metabolic dysfunction-associated steatotic liver disease (MASLD) embraces different conditions, including metabolic dysfunction-associated steatohepatitis (MASH), fibrosis, cirrhosis and hepatocellular carcinoma (HCC). The landscape of cellular abnormalities occurring in the different stages of MASLD as well as the processes which drive MASLD evolution are not completely clarified. We used single cell RNAsequencing (scRNAseq) to unravel cellular heterogeneity affecting livers during the switching from simple steatosis towads MASH and and MASH-fibrosis.

2025-02-28 | GSE284186 | GEO

Intestinal organoid expression data from patients with MASLD-cirrhosis versus non-fibrotic MASLD

Project description:This study aimed to establish and characterize an in vitro model of human intestinal organoids isolated from duodenal samples of patients with non-fibrotic MASLD and those with MASLD-cirrhosis. Whole transcriptome analysis and the energetic and redox status of the organoids were assessed to characterize intestinal functional impairment in the context of MASLD. We used microarrays to detail the whole transcriptome dysregulation underlying intestinal dysfunction in organoids isolated from chirrotic versus non-fibrotic MASLD patients.

2025-09-04 | GSE299719 | GEO

FABP4 deficiency ameliorates alcoholic steatohepatitis in mice

Project description:Fatty acid-binding protein 4 (FABP4) plays an essential role in metabolism and inflammatory. However, the role of FABP4 in alcoholic steatohepatitis (ASH) remains unclear. This study aimed to investigate the function of FABP4 and the underlying mechanisms in the progression of ASH.

2024-04-24 | GSE265758 | GEO

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