RNF43/ZNRF3 loss predisposes to hepatocellular-carcinoma by impairing liver regeneration and altering the liver lipid metabolic ground-state
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RNF43/ZNRF3 negatively regulate WNT signalling. Both genes are mutated in several types of cancers, however, their contribution to liver disease is unknown. Here we describe that hepatocyte-specific loss of Rnf43 / Znrf3 results in steatohepatitis and in increase in unsaturated lipids, in the absence of dietary fat supplementation. Upon injury, Rnf43 / Znrf3 deletion results in defective hepatocyte regeneration and liver cancer, caused by an imbalance between differentiation/proliferation. Using hepatocyte-, hepatoblast- and ductal cell-derived organoids we demonstrate that the differentiation defects and lipid alterations are, in part, cell-autonomous. Interestingly, ZNRF3 mutant liver cancer patients present poorer prognosis, altered hepatic lipid metabolism and steatohepatitis/NASH signatures. Our results imply that RNF43/ZNRF3 predispose to liver cancer by controlling the proliferative/differentiation and lipid metabolic state of hepatocytes. Both mechanisms combined facilitate the progression towards malignancy. Our findings might aid on the management of those RNF43/ZNRF3 mutated individuals at risk of developing fatty liver and/or liver cancer.
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ZNRF3 and RNF43 cooperate to restrict WNT/β-catenin signalling during homeostasis to prevent uncontrolled proliferation and tumour formation, while enabling metabolic zonation.
“ZNRF3 and RNF43 cooperate to restrict WNT/β-catenin signalling during homeostasis to prevent uncontrolled proliferation and tumour formation, while enabling metabolic zonation.22,92”
From Distinct hepatocyte identities in liver homeostasis and regeneration (2023) · cites this paper as [92]
The Introduction identifies RNF43 and ZNRF3 as negative regulators of WNT signalling, and the Results and Discussion link their loss to increased hepatocyte proliferation and disrupted lipid zonation. The claim overstates the homeostasis finding: the Discussion reports progression to liver cancer following chronic injury, not tumour formation during homeostasis, and describes metabolic and regeneration defects alongside increased WNT sensitivity. Page numbers are not provided in our copy. (LLM, conf=0.86)
Experimental — accuracy not yet measuredRedundant regulatory mechanisms, such as ZNRF3 and RNF43, balance WNT/β-catenin activity and prevent tumour formation.
“Redundant regulatory mechanisms, such as the two ubiquitin ligases ZNRF3 and RNF43,22,92 therefore balance WNT/β-catenin activity and prevent tumour formation.”
From Distinct hepatocyte identities in liver homeostasis and regeneration (2023) · cites this paper as [92]
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- Authors
- Belenguer, G., Mastrogiovanni, G., Pacini, C., Hall, Z., Dowbaj, A. M., Arnes-Benito, R., Sljukic, A., Prior, N., Kakava, S., Bradshaw, C. R., Davies, S., Vacca, M., Saeb-Parsy, K., Koo, B.-K., & Huch, M.
- Affiliations
- Max Planck Institute of Molecular Cell Biology and Genetics (DE)
- Wellcome/MRC Cambridge Stem Cell Institute (GB)
- Wellcome Sanger Institute (GB)
- Imperial College London (GB)
- University of Cambridge (GB)
- Cambridge University Hospitals NHS Foundation Trust (GB)
- Institute of Molecular Biotechnology (AT)
- Corresponding author
- Huch, Meritxell
- ORCID
- Venue
- Nature Communications
- Published
- 2022-01-17
- Volume
- 13
- Issue
- 1
- Pages
- 334-334
- ISSN
- 2041-1723 (ISSN-L)
- PMC
- PMC8764073
- OpenAlex
- W4206270373
- Cited by
- 71
- References
- 71
- Citations by year
- 2026: 14 · 2025: 18 · 2024: 16 · 2023: 14 · 2022: 9
- FWCI
- 8.49
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Locations
- Nature Communications (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- ePrints Soton (University of Southampton) (acceptedVersion)
- CINECA IRIS Institutional Research Information System (University of Bari Aldo Moro) (submittedVersion, cc-by)
- RePEc: Research Papers in Economics (submittedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Spiral (Imperial College London) (submittedVersion, other-oa)
- Apollo (University of Cambridge) (submittedVersion, cc-by)
- Apollo
- Apollo (cc-by)
- Funders
- Max-Planck-Gesellschaft (Lise Meitner LMA MOZG0001)
- EC | Horizon 2020 Framework Programme (LSFM4LIFE)
- Wellcome Trust (104151/Z/14/Z)
- Topics
- Health Sciences › Medicine › Hepatology › Liver physiology and pathology
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Wnt/β-catenin signaling in development and cancer
- Health Sciences › Medicine › Epidemiology › Liver Disease Diagnosis and Treatment
- Keywords
- RNF43, ZNRF3, hepatocellular carcinoma, liver regeneration, Wnt signaling, steatohepatitis, nonalcoholic steatohepatitis, hepatic lipid metabolism, unsaturated lipids, hepatocyte differentiation, hepatocyte proliferation, hepatocyte organoids, hepatoblasts, ductal cells, cancer susceptibility, prognosis
- MeSH terms
- Lipidomics, Adult, Animals, Cell Differentiation, Fatty Liver, Gene Expression Regulation, Carcinoma, Hepatocellular, Hepatomegaly, Humans, Hyperplasia, Liver, Liver Neoplasms, Liver Regeneration, Prognosis, Gene Deletion, Hepatocytes, Ubiquitin-Protein Ligases, Cell Proliferation, Lipid Metabolism, Mice, Lipid Droplets
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