Colibactin-driven colon cancer requires adhesin-mediated epithelial binding
Open accessAbstract
Various bacteria are suggested to contribute to colorectal cancer (CRC) development 1-5, including pks+ Escherichia coli, which produces the genotoxin colibactin that induces characteristic mutational signatures in host epithelial cells 6. However, it remains unclear how the highly unstable colibactin molecule is able to access host epithelial cells to cause harm. Here, using the microbiota-dependent ZEB2-transgenic mouse model of invasive CRC 7, we demonstrate that the oncogenic potential of pks+ E. coli critically depends on bacterial adhesion to host epithelial cells, mediated by the type 1 pilus adhesin FimH and the F9 pilus adhesin FmlH. Blocking bacterial adhesion using a pharmacological FimH inhibitor attenuates colibactin-mediated genotoxicity and CRC exacerbation. We also show that allelic switching of FimH strongly influences the genotoxic potential of pks+ E. coli and can induce a genotoxic gain-of-function in the probiotic strain Nissle 1917. Adhesin-mediated epithelial binding subsequently allows the production of the genotoxin colibactin in close proximity to host epithelial cells, which promotes DNA damage and drives CRC development. These findings present promising therapeutic routes for the development of anti-adhesive therapies aimed at mitigating colibactin-induced DNA damage and inhibiting the initiation and progression of CRC, particularly in individuals at risk for developing CRC.
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Very recent studies indicate that E. coli Nissle 1917 is less oncogenic than extremely pathogenic strains like E. coli 11G5 but may not be considered harmless.
“Very recent studies indicate that, in contrast to extremely pathogenic strains like E. coli 11G5, E. coli Nissle 1917 is less oncogenic but may not be considered harmless [155].”
From Selection, Comparative Genomics, and Potential Probiotic Features of Escherichia coli 5C, a pks-Negative Strain Isolated from Healthy Infant Donor Feces (2026) · cites this paper as [155]
The difference in oncogenicity between Nissle 1917 and more oncogenic strains can be explained by the lower adhesion capabilities to the intestinal epithelium shown by Nissle 1917.
“This difference in oncogenicity can be explained by observing the actual lower adhesion capabilities to the intestinal epithelium shown by the E. coli Nissle 1917 strain when compared to that of the more oncogenic strains [155].”
From Selection, Comparative Genomics, and Potential Probiotic Features of Escherichia coli 5C, a pks-Negative Strain Isolated from Healthy Infant Donor Feces (2026) · cites this paper as [155]
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Self-citation
- Authors
- Jans, M., Kolata, M., Blancke, G., D’Hondt, A., Gräf, C., Ciers, M., Sze, M., Thiran, A., Petta, I., Andries, V., Verbandt, S., Shokry, E., Sumpton, D., Vande Voorde, J., Berx, G., Tejpar, S., van Loo, G., Iliev, I. D., Remaut, H., & Vereecke, L.
- Affiliations
- Ghent University (BE)
- Vrije Universiteit Brussel (BE)
- KU Leuven (BE)
- Cancer Research UK Scotland Institute (GB)
- Cornell University (US)
- Corresponding author
- Vereecke, Lars
- ORCID
- Venue
- Nature
- Published
- 2024-11-06
- Volume
- 635
- Issue
- 8038
- Pages
- 472-480
- ISSN
- 0028-0836 (ISSN-L)
- 1476-4687
- OpenAlex
- W4404105354
- Cited by
- 84
- References
- 67
- Citations by year
- 2026: 43 · 2025: 38 · 2024: 3
- FWCI
- 25.04
- Type
- journal article
- Language
- en
- Update notices
- correction (2026-02-05)
- Open access
- green
- biblio.ugent.be
- Licence
- Locations
- Nature (publishedVersion)
- PubMed (publishedVersion)
- Ghent University Academic Bibliography (Ghent University) (submittedVersion, other-oa)
- VUBIR (Vrije Universiteit Brussel) (submittedVersion, other-oa)
- RePEc: Research Papers in Economics (submittedVersion)
- Lirias (KU Leuven) (submittedVersion)
- Funders
- Cancer Research Institute
- University of Bern
- Cancer Research UK (100001, RCCCDF-Nov23/100001)
- Fonds Wetenschappelijk Onderzoek (G026520N, EOS‐G0H2522N‐40007505, G090322N, G012618N)
- Universiteit Gent (BOF23/GOA/001, F/2020/1421, BOF/24J/2021/052)
- Fondation Charcot
- Fondation contre le Cancer
- Foundation for Research in Rheumatology
- National Cancer Institute (R01CA286920)
- National Institute of Diabetes and Digestive and Kidney Diseases (R01DK121977, R01DK113136)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Endocrinology › Escherichia coli research studies
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Bacterial Genetics and Biotechnology
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Biotechnology › Cancer Research and Treatments
- Keywords
- colibactin, colorectal cancer, bacterial adhesion, fimH, type 1 pilus, genotoxicity, DNA damage, Nissle 1917, probiotics, gut microbiota, mutational signatures
- MeSH terms
- Animals, Bacterial Adhesion, Colonic Neoplasms, Disease Models, Animal, DNA Damage, Epithelial Cells, Escherichia coli, Female, Humans, Male, Mice, Transgenic, Mutagens, Peptides, Colorectal Neoplasms, Adhesins, Escherichia coli, Probiotics, Fimbriae Proteins, Cell Line, Tumor, Mice, Polyketides
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