APC and Oncogenic KRAS Are Synergistic in Enhancing Wnt Signaling in Intestinal Tumor Formation and Progression
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Background & aims Synchronous activation of the Wnt signaling pathway, mostly because of loss of function of the APC tumor suppressor, and of the oncogenic KRAS-signaling pathway is very frequent in colorectal cancer and is associated with poor prognosis.Methods We have generated a compound transgenic mouse model, KRAS(V12G)/Apc(+/1638N), to recapitulate the human disease and compared it with single transgenic littermates.Results Compound mutant mice are characterized by a 10-fold increase in tumor multiplicity and by accelerated tumor progression, resulting in strongly enhanced morbidity and mortality. Tumors from compound mutant mice proliferate faster and show decreased levels of apoptosis. Several lines of evidence indicate that the observed increase in tumor multiplicity and malignant transformation is caused by the synergistic activation of Wnt signaling in cells with oncogenic KRAS and loss-of-function Apc mutations. Activated KRAS is known to induce tyrosine phosphorylation of beta-catenin, leading to its release from E-cadherin at the adherens junction. This results in an increased beta-catenin pool in the cytoplasma, its subsequent translocation to the nucleus, and the transcriptional activation of Wnt downstream target genes. Accordingly, intestinal tumors from KRAS(V12G)/Apc(+/1638N) mice show a significant increase in cells with nuclear accumulation of beta-catenin when compared with Apc(+/1638N) animals. Moreover, Apc/KRAS-mutant embryonic stem cells show a significantly enhanced beta-catenin/T-cell factor-mediated transcriptional activation, accompanied by increased beta-catenin nuclear localization.Conclusions This KRAS-induced increase in Wnt/beta-catenin signaling may enhance the plasticity and self-renewal capacity of the tumor, thus resulting in the drastically augmented tumor multiplicity and malignant behavior in compound mutant animals.
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Several KRAS alleles had reduced comutation with NRAS and BRAF, and increased comutation with APC and PIK3CA.
“Several KRAS alleles had reduced comutation with NRAS and BRAF, and increased comutation with APC and PIK3CA”
From The origins and genetic interactions of KRAS mutations are allele- and tissue-specific (2021) · cites this paper as [34]
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- Authors
- Janssen, K., Alberici, P., Fsihi, H., Gaspar, C., Breukel, C., Franken, P., Rosty, C., Abal, M., El Marjou, F., Smits, R., Louvard, D., Fodde, R., & Robine, S.
- Affiliations
- TUM Klinikum (DE)
- Erasmus MC (NL)
- Biologie cellulaire et Cancer (FR)
- Leiden University Medical Center (NL)
- Institut Curie (FR)
- Corresponding author
- Fodde, Riccardo
- Robine, Sylvie
- ORCID
- Venue
- Gastroenterology
- Publisher
- Elsevier BV
- Published
- 2006-10
- Volume
- 131
- Issue
- 4
- Pages
- 1096-1109
- ISSN
- 0016-5085 (ISSN-L)
- OpenAlex
- W1992372073
- Cited by
- 298
- References
- 63
- Citations by year
- 2026: 8 · 2025: 8 · 2024: 8 · 2023: 7 · 2022: 14 · 2021: 21 · 2020: 21 · 2019: 9 · 2018: 12 · 2017: 15 · 2016: 30 · 2015: 19 · 2014: 23 · 2013: 15 · 2012: 18
- FWCI
- 4.62
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Gastroenterology (publishedVersion)
- PubMed (publishedVersion)
- EUR Research Repository (Erasmus University Rotterdam) (publishedVersion)
- EUR Research Repository (Erasmus University Rotterdam) (submittedVersion)
- mediaTUM – the media and publications repository of the Technical University Munich (Technical University Munich) (submittedVersion)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Wnt/β-catenin signaling in development and cancer
- Health Sciences › Medicine › Oncology › Colorectal Cancer Treatments and Studies
- Health Sciences › Medicine › Pathology and Forensic Medicine › Genetic factors in colorectal cancer
- Keywords
- APC, KRAS, Wnt signaling, β-catenin, colorectal cancer, tumor multiplicity, malignant transformation, E-cadherin, adherens junctions, apoptosis, tumor self-renewal
- MeSH terms
- Animals, Cell Division, Mice, Inbred C57BL, Mice, Inbred DBA, Mice, Transgenic, Colorectal Neoplasms, Signal Transduction, Oncogene Protein p21(ras), Gene Expression Regulation, Neoplastic, Apoptosis, Loss of Heterozygosity, Adenomatous Polyposis Coli Protein, Cell Line, Tumor, Wnt Proteins, beta Catenin, Mice
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