Disruption of β-catenin pathway or genomic instability define two distinct categories of liver cancer in transgenic mice
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Background & aims Human liver cancer can be divided into 2 categories that are characterized by activation of beta-catenin and genomic instability. Here we investigate whether similar categories exist among 5 transgenic models of liver cancer, including c-myc, transforming growth factor-alpha, E2F-1, c-myc/transforming growth factor-alpha, and c-myc/E2F-1 mice. Methods The random amplified polymorphic DNA method was used to assess the overall genomic instability, and chromosomal loci affected by genomic alterations were determined by microsatellite analysis. beta-Catenin mutations and deletions were analyzed by polymerase chain reaction and sequencing screening. Cellular localization of beta-catenin and expression of alpha-fetoprotein, a prognostic marker of hepatocellular carcinoma, were investigated by immunohistochemistry. Results Liver tumors from the transgenic mice could be divided into 2 broad categories characterized by extensive genomic instability (exemplified by the c-myc/transforming growth factor-alpha mouse) and activation of beta-catenin (exemplified by the c-myc/E2F-1 mouse). The c-myc/transforming growth factor-alpha tumors displayed extensive genomic instability with recurrent loss of heterozygosity at chromosomes 1, 2, 4, 6, 7, 9, 12, 14, and X and a low rate of beta-catenin activation. The genomic instability was evident from the early dysplastic stage and occurred concomitantly with increased expression of alpha-fetoprotein. The c-myc/E2F-1 tumors were characterized by a high frequency of beta-catenin activation in the presence of a relatively stable genome and low alpha-fetoprotein levels. Conclusions We have identified 2 prototype experimental models, i.e., c-myc/transforming growth factor-alpha and c-myc/E2F-1 mice, for the 2 categories of human hepatocellular carcinoma characterized by genomic instability and beta-catenin activation, respectively. These mouse models will assist in the elucidation of the molecular basis of human hepatocellular carcinoma.
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GOF CTNNB1 mutant human and mouse HCCs are known to be chromosomally stable.
“It is also worth noting that activation of YAP has been shown to induce chromosomal instability in HCC,[27] whereas GOF CTNNB1 mutant human and mouse HCCs are known to be chromosomally stable.[28]”
From TBX3 functions as a tumor suppressor downstream of activated CTNNB1 mutants during hepatocarcinogenesis (2021) · cites this paper as [28]
The ‘Frequency of β-Catenin Mutations’ section (page unavailable) reports that β-catenin mutations were found more often in human HCCs with stable genomes, and the Abstract describes the β-catenin-activated c-myc/E2F-1 mouse tumors as having relatively stable genomes. But the paper also finds β-catenin mutations in c-myc/TGF-α tumors, the model characterized by chromosomal instability. It supports an association, not the categorical claim that GOF CTNNB1-mutant human and mouse HCCs are chromosomally stable. (LLM, conf=0.88)
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Self-citation
- Authors
- Calvisi, D. F., Factor, V. M., Ladu, S., Conner, E. A., & Thorgeirsson, S. S.
- Affiliations
- National Institutes of Health (US)
- Corresponding author
- Thorgeirsson, Snorri S.
- Venue
- Gastroenterology
- Publisher
- Elsevier BV
- Published
- 2004-05
- Volume
- 126
- Issue
- 5
- Pages
- 1374-1386
- ISSN
- 0016-5085 (ISSN-L)
- OpenAlex
- W2135027457
- Cited by
- 100
- References
- 86
- Citations by year
- 2025: 1 · 2024: 2 · 2023: 3 · 2021: 3 · 2020: 1 · 2019: 4 · 2018: 3 · 2017: 2 · 2016: 1 · 2015: 8 · 2014: 1 · 2013: 5 · 2012: 5
- FWCI
- 3.32
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Gastroenterology (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Università degli Studi di Sassari
- Fondazione Italiana per la Ricerca sul Cancro
- 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
- hepatocellular carcinoma, genomic instability, transgenic mouse model, c-Myc, transforming growth factor-alpha, E2F1, alpha-fetoprotein, loss of heterozygosity, liver cancer classification
- MeSH terms
- alpha-Fetoproteins, Animals, Cytoskeletal Proteins, Disease Models, Animal, DNA-Binding Proteins, Gene Frequency, Liver Neoplasms, Mice, Transgenic, Mutation, Phenotype, Quinoxalines, Transcription Factors, Trans-Activators, Transforming Growth Factor alpha, Genes, myc, Gene Deletion, Cell Cycle Proteins, Loss of Heterozygosity, Genomic Instability, E2F Transcription Factors, E2F1 Transcription Factor, beta Catenin, Mice
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