Bile Acids Activate YAP to Promote Liver Carcinogenesis
Open accessAbstract
Elevated bile acid levels increase hepatocellular carcinoma by unknown mechanisms. Here, we show that mice with a severe defect in bile acid homeostasis due to the loss of the nuclear receptors FXR and SHP have enlarged livers, progenitor cell proliferation, and Yes-associated protein (YAP) activation and develop spontaneous liver tumorigenesis. This phenotype mirrors mice with loss of hippo kinases or overexpression of their downstream target, YAP. Bile acids act as upstream regulators of YAP via a pathway dependent on the induction of the scaffold protein IQGAP1. Patients with diverse biliary dysfunctions exhibit enhanced IQGAP1 and nuclear YAP expression. Our findings reveal an unexpected mechanism for bile acid regulation of liver growth and tumorigenesis via the Hippo pathway.
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Liver cancers often have elevated bile acid levels, and animal models with intrahepatic bile acid retention through unchecked synthesis or export defects develop liver cancer spontaneously, suggesting direct bile acid involvement in liver cancer.
“Crucially, liver cancers often exhibit elevated levels of BAs, and animal models with intrahepatic retention of BAs through either unchecked BA synthesis or defects in BA export develop liver cancer spontaneously, suggesting the direct involvement of BAs in liver cancer (8-11).”
From Bile acid synthesis impedes tumor-specific T cell responses during liver cancer (2025) · cites this paper as [11]
Split into 2 atoms — 1 confirmed, 1 partially supported, 0 disputed, 0 misattributed, 0 unverifiable. Expand the claim to see per-atom verdicts.
Experimental — accuracy not yet measuredDeoxycholic acid is sufficient to stimulate YAP nuclear translocation, producing a 1.7-fold increase compared with DMSO control cells.
“DCA was sufficient to stimulate YAP nuclear translocation (1.7‐fold increase as compared to DMSO control cells, Fig 5B), consistent with earlier observations (Anakk et al, 2013).”
From Bile canaliculi remodeling activates YAP via the actin cytoskeleton during liver regeneration (2020) · cites this paper as Anakk et al, 2013
BA are also regulators of the Hippo pathway, acting via the induction of the scaffold protein IQGAP1.
“Besides signal messengers, BA are also regulators of the Hippo pathway, acting via the induction of the scaffold protein IQGAP1 (Anakk et al, 2013).”
From Bile canaliculi remodeling activates YAP via the actin cytoskeleton during liver regeneration (2020) · cites this paper as Anakk et al, 2013
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Self-citationBile canaliculi remodeling activates YAP via the actin cytoskeleton during liver regeneration
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- Authors
- Anakk, S., Bhosale, M., Schmidt, V. A., Johnson, R. L., Finegold, M. J., & Moore, D. D.
- Affiliations
- University of Illinois Urbana-Champaign (US)
- Stony Brook University (US)
- The University of Texas MD Anderson Cancer Center (US)
- Baylor College of Medicine (US)
- Corresponding author
- Anakk, Sayeepriyadarshini
- Moore, David D.
- Venue
- Cell Reports
- Publisher
- Elsevier BV
- Published
- 2013-11
- Volume
- 5
- Issue
- 4
- Pages
- 1060-1069
- ISSN
- 2211-1247 (ISSN-L)
- PMC
- PMC3961013
- OpenAlex
- W2008138667
- Cited by
- 196
- References
- 65
- Citations by year
- 2026: 11 · 2025: 15 · 2024: 19 · 2023: 14 · 2022: 14 · 2021: 24 · 2020: 13 · 2019: 21 · 2018: 14 · 2017: 8 · 2016: 15 · 2015: 15 · 2014: 12 · 2012: 1
- FWCI
- 8.12
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- Cell Reports (publishedVersion, cc-by-nc-nd)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- eScholarship (California Digital Library) (submittedVersion, cc-by-nc-nd)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion)
- Funders
- Cancer Prevention and Research Institute of Texas (DK56338, RP120138)
- University of Illinois at Urbana-Champaign (CPRIT RP120138)
- University of Texas MD Anderson Cancer Center (#CA16672)
- National Cancer Institute (CA-16672, P30CA016672)
- National Institute of Diabetes and Digestive and Kidney Diseases (DK56338, DK62434, R01DK068804, DK068804, U19DK062434, P30DK056338)
- Eunice Kennedy Shriver National Institute of Child Health and Human Development (R01HD060579)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Hippo pathway signaling and YAP/TAZ
- Health Sciences › Medicine › Hepatology › Liver physiology and pathology
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Cancer, Lipids, and Metabolism
- Keywords
- bile acids, YAP, Hippo signaling pathway, hepatocarcinogenesis, hepatocellular carcinoma, farnesoid X receptor, SHP, IQGAP1, liver progenitor cells, biliary dysfunction, bile acid homeostasis, liver growth, nuclear receptors
- MeSH terms
- Hippo Signaling Pathway, Serine-Threonine Kinase 3, YAP-Signaling Proteins, Receptor, Farnesoid X-Activated, Hippo Kinases, Adolescent, Animals, Bile Acids and Salts, Cells, Cultured, Child, Child, Preschool, Enzyme Activation, Carcinoma, Hepatocellular, Humans, Infant, Infant, Newborn, Liver Neoplasms, Male, Mice, Inbred C57BL, Phosphoproteins, Proto-Oncogene Proteins, Transcription Factors, Hepatocyte Growth Factor, Protein Serine-Threonine Kinases, Receptors, Cytoplasmic and Nuclear, Mice, Knockout, Cell Cycle Proteins, ras GTPase-Activating Proteins, Adaptor Proteins, Signal Transducing, Mice, Carcinogenesis
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