ArticleMolecular biology of the cell2007
Cytotoxic necrotizing factor 1 prevents apoptosis via the Akt/IkappaB kinase pathway: role of nuclear factor-kappaB and Bcl-2.
Article in Molecular biology of the cell, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers, 1 of them a synthesis that pooled it.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
32 citing papers in PubMed, 1 synthesis or guideline pooled it, 50 citations in OpenAlex.
- Effects of theInternational journal of molecular sciences · 2021Pooled it
- E. Coli cytotoxic necrotizing factor-1 promotes colorectal carcinogenesis by causing oxidative stress, DNA damage and intestinal permeability alteration.Journal of experimental & clinical cancer research : CR · 2025Article
- Effects of the Rho GTPase-activating toxin CNF1 on fibroblasts derived from Rett syndrome patients: A pilot study.Journal of cellular and molecular medicine · 2023Article
- The Diversity ofMicroorganisms · 2023Review
- Relationships between gut microbiota, red meat consumption and colorectal cancer.Journal of carcinogenesis & mutagenesis · 2022Article
- Immunomodulatory properties of CNF1 toxin fromAmerican journal of cancer research · 2022Review
- The Cytotoxic Necrotizing Factors (CNFs)-A Family of Rho GTPase-Activating Bacterial Exotoxins.Toxins · 2021Review
- The Bacterial Toxin CNF1 Protects Human Neuroblastoma SH-SY5Y Cells against 6-Hydroxydopamine-Induced Cell Damage: The Hypothesis of CNF1-Promoted Autophagy as an Antioxidant Strategy.International journal of molecular sciences · 2020Article
- Reversible senescence of human colon cancer cells after blockage of mitosis/cytokinesis caused by the CNF1 cyclomodulin from Escherichia coli.Scientific reports · 2018Article
- Bacterial Toxins and Targeted Brain Therapy: New Insights from Cytotoxic Necrotizing Factor 1 (CNF1).International journal of molecular sciences · 2018Review
- Oral Bacterial and Fungal Microbiome Impacts Colorectal Carcinogenesis.Frontiers in microbiology · 2018Review
- Human LACC1 increases innate receptor-induced responses and a LACC1 disease-risk variant modulates these outcomes.Nature communications · 2017Article
- Electrophysiology of glioma: a Rho GTPase-activating protein reduces tumor growth and spares neuron structure and function.Neuro-oncology · 2016Article
- Article
- Urinary tract infections: epidemiology, mechanisms of infection and treatment options.Nature reviews. Microbiology · 2015Review
- Review
- Article
- The cytotoxic necrotizing factor 1 from E. coli: a janus toxin playing with cancer regulators.Toxins · 2013Review
- Bacterial oncogenesis in the colon.Future microbiology · 2013Review
- Article
Corrections and comments
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cytotoxic necrotizing factor 1 (CNF1) is a protein toxin produced by some pathogenic strains of Escherichia coli that specifically activates Rho, Rac, and Cdc42 GTPases. We previously reported that this toxin prevents the ultraviolet-B-induced apoptosis in epithelial cells, with a mechanism that remained to be defined. In this work, we show that the proteasomal degradation of the Rho GTPase is necessary to achieve cell death protection, because inhibition of Rho degradation abolishes the prosurvival activity of CNF1. We hypothesize that Rho inactivation allows the activity of Rac to become dominant. This in turn leads to stimulation of the phosphoinositide 3-kinase/Akt/IkappaB kinase/nuclear factor-kappaB prosurvival pathway and to a remarkable modification in the architecture of the mitochondrial network, mainly consisting in the appearance of elongated and interconnected mitochondria. Importantly, we found that Bcl-2 silencing reduces the ability of CNF1 to protect cells against apoptosis and that it also prevents the CNF1-induced mitochondrial changes. It is worth noting that the ability of a bacterial toxin to induce such a remodeling of the mitochondrial network is herein reported for the first time. The possible pathophysiological relevance of this finding is discussed.
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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.