β‐catenin deficiency in hepatocytes aggravates hepatocarcinogenesis driven by oncogenic β‐catenin and MET
Open accessAbstract
Both activating and inactivating mutations in catenin β1 (ctnnb1), which encodes β‐catenin, have been implicated in liver tumorigenesis in humans and mice, although the underlying mechanisms are not fully understood. Herein, we show that deletion of endogenous β‐catenin in hepatocytes aggravated hepatocellular carcinoma (HCC) development driven by an oncogenic version of β‐catenin (CAT) in combination with the hepatocyte growth factor receptor MET proto‐oncogene receptor tyrosine kinase (MET). Although the mitogenic signaling and cell cycle progression was modestly impaired after CAT/MET transfection, the β‐catenin‐deficient livers displayed changes in transcriptomes, increased DNA damage response, expanded Sox9+ cells, and up‐regulation of protumorigenic cytokines, including interleukin‐6 and transforming growth factor β1. These events eventually exacerbated CAT/MET‐driven hepatocarcinogenesis in β‐catenin‐deficient livers, featured by up‐regulation of extracellular signal‐regulated kinase (Erk), protein kinase B (Akt), and Wnt/β‐catenin signaling and cyclin D1 expression. The resultant mouse tumors showed similar transcriptomes to human HCC samples with concomitant CTNNB1 mutations and MET overexpression. Conclusion: These data argue that while dominantly activating mutants of β‐catenin are oncogenic, inhibiting the oncogenic signaling pathway generates a pro‐oncogenic microenvironment that may facilitate HCC recurrence following a targeted therapy of the primary tumor. An effective therapeutic strategy must require disruption of the oncogenic signaling in tumor cells and suppression of the secondary tumor‐promoting stromal effects in the liver microenvironment. (H epatology 2018;67:1807‐1822)
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Elevated conjugated bile acids were also observed in other mouse liver cancer models, including hydrodynamic tail vein injection of Δ90-β-catenin plus hMET and DEN plus high-fat diet.
“Similarly, elevated conjugated BAs were observed in other mouse models of liver cancer such as hydrodynamic tail vein injection of constitutively active β-catenin (Δ90-β-catenin) plus human hepatocyte growth factor receptor (hMET) (17) and diethylnitrosamine (DEN) plus high-fat diet (HFD) (fig. S2C) (18).”
From Bile acid synthesis impedes tumor-specific T cell responses during liver cancer (2025) · cites this paper as [17]
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- Authors
- Liang, Y., Feng, Y., Zong, M., Wei, X., Lee, J., Feng, Y., Li, H., Yang, G., Wu, Z., Fu, X., & Feng, G.
- Affiliations
- University of California San Diego (US)
- Second Military Medical University (CN)
- Department of Pathology and Division of Biological Sciences, Moores Cancer Center,University of California San Diego,La Jolla,CA
- Department of Hepatology, First Affiliated Hospital,Chong‐Qing Medical University,Chong‐Qing,China
- Corresponding author
- Feng, Gen‐Sheng
- Venue
- Hepatology
- Published
- 2018-04-06
- Volume
- 67
- Issue
- 5
- Pages
- 1807-1822
- ISSN
- 0270-9139 (ISSN-L)
- 1527-3350
- PMC
- PMC5906147
- OpenAlex
- W2769590730
- Cited by
- 36
- References
- 42
- Citations by year
- 2025: 3 · 2024: 4 · 2023: 1 · 2022: 7 · 2021: 5 · 2020: 8 · 2019: 3 · 2018: 5
- FWCI
- 1.79
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Hepatology (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- eScholarship (California Digital Library) (submittedVersion)
- Funders
- National Institutes of Health
- University of California, San Diego
- National Cancer Institute (R01CA176012, R01CA188506)
- National Institute of General Medical Sciences (R01GM052872)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Wnt/β-catenin signaling in development and cancer
- Health Sciences › Medicine › Hepatology › Hepatocellular Carcinoma Treatment and Prognosis
- Health Sciences › Medicine › Hepatology › Liver physiology and pathology
- Keywords
- β-catenin, hepatocellular carcinoma, hepatocarcinogenesis, MET, tumor microenvironment, DNA damage response, SOX9, interleukin-6, TGF-β1, ERK signaling, Akt signaling, Wnt/β-catenin signaling, cyclin D1, tumor recurrence, targeted therapy resistance, liver transcriptome
- MeSH terms
- Proto-Oncogene Mas, Animals, Carcinoma, Hepatocellular, Humans, Liver, Liver Neoplasms, Oncogenes, Signal Transduction, Gene Expression Regulation, Neoplastic, Proto-Oncogene Proteins c-met, Gene Expression Profiling, Hepatocytes, beta Catenin, Mice, Carcinogenesis
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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