| Literature DB >> 28093453 |
Johan Gagnière1,2,3, Virginie Bonnin1,2, Anne-Sophie Jarrousse4, Emilie Cardamone1,2, Allison Agus1,2,5, Nancy Uhrhammer5, Pierre Sauvanet1,2,3, Pierre Déchelotte4, Nicolas Barnich1,2, Richard Bonnet1,2,6, Denis Pezet1,2,3, Mathilde Bonnet7,2.
Abstract
Recent studies suggest that colonization of colonic mucosa by pathogenic Escherichia coli could be involved in the development of colorectal cancer (CRC), especially through the production of genotoxins such as colibactin and/or by interfering with the DNA mismatch repair (MMR) pathway that leads to microsatellite instability (MSI). The present study, performed on 88 CRC patients, revealed a significant increase in E. coli colonization in the MSI CRC phenotype. In the same way, E. coli persistence and internalization were increased in vitro in MMR-deficient cells. Moreover, we demonstrated that colibactin-producing E. coli induce inhibition of the mutL homologue 1 (MLH1) MMR proteins, which could lead to genomic instability. However, colibactin-producing E. coli were more frequently identified in microsatellite stable (MSS) CRC. The present study suggests differences in the involvement of colibactin-producing E. coli in colorectal carcinogenesis according to the CRC phenotype. Further host-pathogen interactions studies should take into account CRC phenotypes.Entities:
Keywords: Escherichia coli; colibactin; colorectal cancer; microsatellite instability; mutL homologue 1 (MLH1); oxidative stress
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Year: 2017 PMID： 28093453 DOI： 10.1042/CS20160876
Source DB: PubMed Journal: Clin Sci (Lond) ISSN： 0143-5221 Impact factor: 6.124