ArticleNature communications2025
Disrupting bile acid metabolism by suppressing Fxr causes hepatocellular carcinoma induced by YAP activation.
Article in Nature communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed.
- The gut microbiome-bile acid-FXR interplay: a pivotal axis in metabolic and gastrointestinal diseases.Gut microbes · 2026Review
- Hippo Pathway-YAP/TAZ Signaling: Molecular Mechanisms, Biological Function, Diseases, and Therapeutic Targets.MedComm · 2026Review
- Gut‑liver‑kidney axis: A systems biology framework for understanding and treating chronic kidney disease (Review).International journal of molecular medicine · 2026Review
- The emerging role of the Hippo signaling pathway in interorgan crosstalk.The FEBS journal · 2026Review
- Epigenetic regulation and posttranslational modifications of FXR: underlying mechanisms and implications in digestive diseases.Acta pharmacologica Sinica · 2026Review
- FXR's double life in bile ducts.Nature metabolism · 2026Article
- FXR-YAP signalling maintains biliary epithelial cell identity and preserves liver homeostasis.Nature metabolism · 2026Article
- Article
- Constitutive AMPK activation prevents hepatocellular carcinoma development through inhibition of HNF4α activity.Science advances · 2026Article
- Gut microbiome and bile acid metabolism in liver disease: Mechanisms, clinical implications, and therapeutic opportunities.Pharmacological reviews · 2026Review
- GUDCA drives colorectal cancer progression via ALKBH5-mediated m6A modification of ENO1 and glycolytic reprogramming.Frontiers in pharmacology · 2026Article
- Single-cell RNA sequencing and spatial transcriptomic analysis reveal a distinct population of G6PDFrontiers in immunology · 2026Article
- Recent trends in lipid metabolism research in liver cancer: a bibliometric analysis.Frontiers in oncology · 2026Article
- The Dual Role of Gut Microbiota and Their Metabolites in Hepatocellular Carcinoma: A Context-Dependent Framework.Microorganisms · 2025Review
- 7-Ketolithocholic Acid Exerts Anti-Renal Fibrotic Effects Through FXR-Mediated Inhibition of TGF-β/Smad and Wnt/β-Catenin Pathways.Pharmaceuticals (Basel, Switzerland) · 2025Article
- Gut microbial metabolites in cancer immunomodulation.Molecular cancer · 2025Review
- FXR-mediated antigen-specific CD8Journal for immunotherapy of cancer · 2025Article
- Review
Corrections and comments
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Authors and funding
7 authors.
Funding
Abstract
Disruption of bile acid (BA) metabolism causes various liver diseases including hepatocellular carcinoma (HCC). However, the underlying molecular mechanism remains elusive. Here, we report that BA metabolism is directly controlled by a repressor function of YAP, which induces cholestasis by altering BA levels and composition via inhibiting the transcription activity of Fxr, a key physiological BA sensor. Elevated BA levels further activate hepatic YAP, resulting in a feedforward cycle leading to HCC. Mechanistically, Teads are found to bind Fxr in a DNA-binding-independent manner and recruit YAP to epigenetically suppress Fxr. Promoting BA excretion, or alleviating YAP repressor function by pharmacologically activating Fxr and inhibiting HDAC1, or overexpressing an Fxr target gene Bsep to promote BA exportation, alleviate cholestasis and HCC caused by YAP activation. Our results identify YAP's transcriptional repressor role in BA metabolism as a key driver of HCC and suggest its potential as a therapeutic target.
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