ArticleThe Journal of experimental medicine2017
Liver carcinogenesis by FOS-dependent inflammation and cholesterol dysregulation.
Article in The Journal of experimental medicine, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 76 papers, 1 of them a synthesis that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
76 citing papers in PubMed, 1 synthesis or guideline pooled it, 132 citations in OpenAlex.
- A Meta-Analysis of Statin Use and Risk of Hepatocellular Carcinoma.Canadian journal of gastroenterology & hepatology · 2022Pooled it
- Article
- Regulation of immune tolerance in hepatocellular carcinoma by liver diseases: a review.Infectious agents and cancer · 2026Review
- Cell-free DNA fragmentomes for noninvasive detection of liver cirrhosis and other diseases.Science translational medicine · 2026Article
- The Contribution of Cholesterol and Squalene Synthase in Cancer: Molecular Mechanisms, Lipid Rafts and Therapeutic Approaches.Medicinal research reviews · 2026Review
- ScRNA-seq Identifies High CXCL8 Linked to Liver Fibrosis in HBeAg-negative Chronic Hepatitis B Patients With Low HBsAg.Gastro hep advances · 2026Article
- Nutritional c-Fos Induction Rewires Hepatic Metabolism and Can Promote Obesity-Associated Hepatocellular Carcinoma.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Cholesterol metabolism and cancer: Molecular mechanisms, immune regulation and an epidemiological perspective (Review).International journal of molecular medicine · 2025Review
- MEF2D-expressing cancer precursors reprogram tissue-resident macrophages to support liver tumorigenesis.Nature cancer · 2025Article
- Cholesterol metabolism in LUAD progression: GJB3 as a key target for cell‑based therapeutic interventions.Molecular medicine reports · 2025Article
- Transcription factor FOS promotes ferroptosis and inflammation in S. aureus- infected osteomyelitis via EIF5A.Journal of orthopaedic surgery and research · 2025Article
- NR4A1 suppresses breast cancer growth by repressing c-Fos-mediated lipid and redox dyshomeostasis.Experimental & molecular medicine · 2025Article
- A bioinformatics analysis to identify shared molecular pathways and hub genes between NAFLD and Gestational Diabetes Mellitus.Gastroenterology and hepatology from bed to bench · 2025Article
- A stage specific NETs-related signature in alcoholic steatohepatitis: from molecular subtyping to therapeutic vulnerabilities.Frontiers in immunology · 2025Article
- A new effLuc/Kate dual reporter allele for tumor imaging in mice.Disease models & mechanisms · 2025Article
- Mechanism and therapeutic potential of liver injury induced by cholesterol-associated proteins.Frontiers in pharmacology · 2025Review
- Hub Genes Involved in the Progression of Nonalcoholic Fatty Liver Disease to Hepatocellular Carcinoma.Current medicinal chemistry · 2025Article
- The mechanistic insights behind the anticancer effects of statins in liver cancer.Hepatology communications · 2024Article
- Lecithin-cholesterol acyltransferase is a potential tumor suppressor and predictive marker for hepatocellular carcinoma metastasis.World journal of gastrointestinal oncology · 2024Article
- Liver cancer development driven by the AP-1/c-Jun~Fra-2 dimer through c-Myc.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
16 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 3 institutions in 3 countries.
Funding
Abstract
Human hepatocellular carcinomas (HCCs), which arise on a background of chronic liver damage and inflammation, express c-Fos, a component of the AP-1 transcription factor. Using mouse models, we show that hepatocyte-specific deletion of c-Fos protects against diethylnitrosamine (DEN)-induced HCCs, whereas liver-specific c-Fos expression leads to reversible premalignant hepatocyte transformation and enhanced DEN-carcinogenesis. c-Fos-expressing livers display necrotic foci, immune cell infiltration, and altered hepatocyte morphology. Furthermore, increased proliferation, dedifferentiation, activation of the DNA damage response, and gene signatures of aggressive HCCs are observed. Mechanistically, c-Fos decreases expression and activity of the nuclear receptor LXRα, leading to increased hepatic cholesterol and accumulation of toxic oxysterols and bile acids. The phenotypic consequences of c-Fos expression are partially ameliorated by the anti-inflammatory drug sulindac and largely prevented by statin treatment. An inverse correlation between c-FOS and the LXRα pathway was also observed in human HCC cell lines and datasets. These findings provide a novel link between chronic inflammation and metabolic pathways important in liver cancer.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.