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Int. J. Mol. Sci. 2017, 18(6), 1310; doi:10.3390/ijms18061310

Microbiota, Inflammation and Colorectal Cancer

M2iSH, UMR 1071 Inserm, University of Clermont Auvergne, INRA USC 2018, Clermont-Ferrand 63001, France
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Received: 17 May 2017 / Revised: 14 June 2017 / Accepted: 15 June 2017 / Published: 20 June 2017
(This article belongs to the Special Issue Inflammation and Cancer)
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Abstract

Colorectal cancer, the fourth leading cause of cancer-related death worldwide, is a multifactorial disease involving genetic, environmental and lifestyle risk factors. In addition, increased evidence has established a role for the intestinal microbiota in the development of colorectal cancer. Indeed, changes in the intestinal microbiota composition in colorectal cancer patients compared to control subjects have been reported. Several bacterial species have been shown to exhibit the pro-inflammatory and pro-carcinogenic properties, which could consequently have an impact on colorectal carcinogenesis. This review will summarize the current knowledge about the potential links between the intestinal microbiota and colorectal cancer, with a focus on the pro-carcinogenic properties of bacterial microbiota such as induction of inflammation, the biosynthesis of genotoxins that interfere with cell cycle regulation and the production of toxic metabolites. Finally, we will describe the potential therapeutic strategies based on intestinal microbiota manipulation for colorectal cancer treatment. View Full-Text
Keywords: colorectal cancer; intestinal microbiota; inflammation; genotoxins; host-pathogen interaction colorectal cancer; intestinal microbiota; inflammation; genotoxins; host-pathogen interaction
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This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. (CC BY 4.0).

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Lucas, C.; Barnich, N.; Nguyen, H.T.T. Microbiota, Inflammation and Colorectal Cancer. Int. J. Mol. Sci. 2017, 18, 1310.

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