ArticleCell reports. Medicine2024
Tolerance to colibactin correlates with homologous recombination proficiency and resistance to irinotecan in colorectal cancer cells.
Article in Cell reports. Medicine, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
What it found
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Who cites it
9 citing papers in PubMed, 12 citations in OpenAlex.
- The Role of Selected Bacteria in Breast Cancer Initiation and Development.International journal of molecular sciences · 2026Review
- The Molecular and Functional Landscape of Resistance to FOLFIRI Chemotherapy in Metastatic Colorectal Cancer.Cancer discovery · 2026Article
- Gut microbiome-driven colorectal cancer via immune, metabolic, neural, and endocrine axes reprogramming.NPJ biofilms and microbiomes · 2026Review
- Gut microbiota drives cancer evolution and therapy resistance.Molecular cancer · 2026Review
- Gut microbiota-mediated chemotherapy resistance in colorectal cancer: mechanisms and precision interventions.Frontiers in oncology · 2026Review
- Selection, Comparative Genomics, and Potential Probiotic Features of Escherichia coli 5C, a pks-Negative Strain Isolated from Healthy Infant Donor Feces.Probiotics and antimicrobial proteins · 2026Article
- What is the relationship between microorganisms in the human body and upper tract urothelial carcinoma?Frontiers in immunology · 2025Review
- Review
- Early-onset cancers: Biological bases and clinical implications.Cell reports. Medicine · 2024Review
Corrections and comments
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Authors and funding
23 authors at 5 institutions in 1 country.
Funding
Abstract
The bacterial genotoxin colibactin promotes colorectal cancer (CRC) tumorigenesis, but systematic assessment of its impact on DNA repair is lacking, and its effect on response to DNA-damaging chemotherapeutics is unknown. We find that CRC cell lines display differential response to colibactin on the basis of homologous recombination (HR) proficiency. Sensitivity to colibactin is induced by inhibition of ATM, which regulates DNA double-strand break repair, and blunted by HR reconstitution. Conversely, CRC cells chronically infected with colibactin develop a tolerant phenotype characterized by restored HR activity. Notably, sensitivity to colibactin correlates with response to irinotecan active metabolite SN38, in both cell lines and patient-derived organoids. Moreover, CRC cells that acquire colibactin tolerance develop cross-resistance to SN38, and a trend toward poorer response to irinotecan is observed in a retrospective cohort of CRCs harboring colibactin genomic island. Our results shed insight into colibactin activity and provide translational evidence on its chemoresistance-promoting role in CRC.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.