ArticleScientific reports2019
Upregulation of cancer-associated gene expression in activated fibroblasts in a mouse model of non-alcoholic steatohepatitis.
Article in Scientific reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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14 citing papers in PubMed, 22 citations in OpenAlex.
- Targeting circulating mechanoresponsive monocytes and macrophages to reduce fibrosis.Nature biomedical engineering · 2026Article
- Autocrine GDF10 Inhibits Hepatic Stellate Cell Activation via BMPR2/ALK3 Receptor to Prevent Liver Fibrosis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Global, regional, and national burden of liver cancer in adolescents and young adults from 1990 to 2021: an analysis of the global burden of disease study 2021 and forecast to 2040.Frontiers in public health · 2025Article
- Orphan receptor GPR176 in hepatic stellate cells exerts a profibrotic role in chronic liver disease.JHEP reports : innovation in hepatology · 2024Article
- Loss of SFXN1 mitigates lipotoxicity and predicts poor outcome in non-viral hepatocellular carcinoma.Scientific reports · 2023Article
- Cancer-Associated Fibroblasts in Hepatocellular Carcinoma and Cholangiocarcinoma.Cellular and molecular gastroenterology and hepatology · 2023Review
- Implications of genetic heterogeneity in hepatocellular cancer.Advances in cancer research · 2022Review
- Steatosis is involved in the progression of kidney disease in a high-fat-diet-induced non-alcoholic steatohepatitis mouse model.PloS one · 2022Article
- Initiation of hepatic stellate cell activation extends into chronic liver disease.Cell death & disease · 2021Article
- Biofabricated 3D in vitro model of fibrosis-induced abnormal hepatoblast/biliary progenitors' expansion of the developing liver.Bioengineering & translational medicine · 2021Article
- HOTAIRM1 Promotes Malignant Progression of Transformed Fibroblasts in Glioma Stem-Like Cells Remodeled MicroenvironmentFrontiers in oncology · 2021Article
- Current mechanisms in obesity and tumor progression.Current opinion in clinical nutrition and metabolic care · 2020Review
- Chronic inflammation as a molecular basis of nonalcoholic steatohepatitis: role of macrophages and fibroblasts in the liver.Nagoya journal of medical science · 2020Review
- Expression of hepatic stellate cell activation-related genes in HBV-, HCV-, and nonalcoholic fatty liver disease-associated fibrosis.PloS one · 2020Article
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Authors and funding
17 authors at 6 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Non-alcoholic steatohepatitis (NASH), characterized by chronic inflammation and fibrosis, is predicted to be the leading cause of cirrhosis and hepatocellular carcinoma (HCC) in the next decade. Although recent evidence suggests the importance of fibrosis as the strongest determinant of HCC development, the molecular mechanisms underlying NASH-induced carcinogenesis still remain unclear. Here we performed RNA sequencing analysis to compare gene expression profiles of activated fibroblasts prepared from two distinct liver fibrosis models: carbon tetrachloride-induced fibrosis as a model without obesity and HCC and genetically obese melanocortin 4 receptor-deficient (MC4R-KO) mice fed Western diet, which develop steatosis, NASH, and eventually HCC. Our data showed that activated fibroblasts exhibited distinct gene expression patterns in each etiology, and that the 'pathways in cancer' were selectively upregulated in the activated fibroblasts from MC4R-KO mice. The most upregulated gene in these pathways was fibroblast growth factor 9 (FGF9), which was induced by metabolic stress such as palmitate. FGF9 exerted anti-apoptotic and pro-migratory effects in fibroblasts and hepatoma cells in vitro and accelerated tumor growth in a subcutaneous xenograft model. This study reveals upregulation of cancer-associated gene expression in activated fibroblasts in NASH, which would contribute to the progression from NASH to HCC.
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