ArticleScientific reports2018
Reversible senescence of human colon cancer cells after blockage of mitosis/cytokinesis caused by the CNF1 cyclomodulin from Escherichia coli.
Article in Scientific reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers, 1 of them a synthesis that pooled it.
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Who cites it
25 citing papers in PubMed, 1 synthesis or guideline pooled it, 44 citations in OpenAlex.
- Effects of theInternational journal of molecular sciences · 2021Pooled it
- Effects of mitotically active polyploid giant cancer cells on chemoresistance through interaction with cancer-associated fibroblasts.British journal of cancer · 2026Article
- Phenotypic characterization and complete genome of a tumorigenic pathobiont Escherichia coli LI60C3.Gut pathogens · 2025Article
- Gut microbes and their metabolites in relation to the classic tumor suppressor gene P53: a novel narrative.NPJ biofilms and microbiomes · 2025Review
- Metastasis and the Microbiome: The Impact of Bacteria in Disseminated Colorectal Cancer.Frontiers in bioscience (Landmark edition) · 2024Review
- Review
- Effect of gut microbiota on colorectal cancer progression and treatment.Saudi medical journal · 2022Article
- Review
- Host Genetics and Microbiota Interactions in Colorectal Cancer: Shared or Independent Risk?Microorganisms · 2022Review
- The Role of Cyclomodulins and Some Microbial Metabolites in Bacterial Microecology and Macroorganism Carcinogenesis.International journal of molecular sciences · 2022Review
- Emerging role of human microbiome in cancer development and response to therapy: special focus on intestinal microflora.Journal of translational medicine · 2022Review
- The Cytotoxic Necrotizing Factors (CNFs)-A Family of Rho GTPase-Activating Bacterial Exotoxins.Toxins · 2021Review
- Cyclomodulins and Hemolysis inLife (Basel, Switzerland) · 2021Article
- Exploring the Inflammatory Pathogenesis of Colorectal Cancer.Diseases (Basel, Switzerland) · 2021Review
- Translocation of intracellular CD24 constitutes a triggering event for drug resistance in breast cancer.Scientific reports · 2021Article
- Article
- Review
- Crystal structure of bacterial cytotoxic necrotizing factor CNFThe EMBO journal · 2021Article
- The Role of Gut Microbiota in Lung Cancer: From Carcinogenesis to Immunotherapy.Frontiers in oncology · 2021Review
- Gut Microbiota and Colon Cancer: A Role for Bacterial Protein Toxins?International journal of molecular sciences · 2020Review
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cytotoxic necrotizing factor 1 (CNF1), a protein toxin produced by extraintestinal pathogenic Escherichia coli, activates the Rho-family small GTPases in eukaryotic cell, thereby perturbing multiple cellular functions. Increasing epidemiological evidence suggests a link between CNF1 and human inflammatory bowel disease and colorectal cancer. At the cellular level, CNF1 has been hypothesized to reprogram cell fate towards survival due to the role in perturbing cell cycle and apoptosis. However, it remains undetermined how cells survive from CNF1 intoxication. In this work, we show that CNF1 treatment blocks mitosis/cytokinesis, elicits endoreplication and polyploidisation in cultured human colon cancer cells, and drives them into reversible senescence, which provides a survival route for cells via depolyploidisation. Senescence in CNF1-treated cells is demonstrated with upregulation of several senescence markers including senescence-associated β-galactosidase activity, p53, p21 and p16, and concomitant inhibition of the retinoblastoma protein phosphorylation. Importantly, progeny derived from CNF1 treatment exhibit genomic instability exemplified by increased aneuploidy and become more resistant to CNF1, but not to 5-fluorouracil and oxaliplatin, the two agents commonly used in chemotherapeutic treatment for colorectal cancer. These observations display survival features of the cell after CNF1 treatment that may have implications for the potential role of CNF1 in carcinogenesis.
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