Abstract
Colorectal cancer (CRC) is the third most common cancer worldwide and the leading cause of cancer-related deaths. Recently, several studies have demonstrated that gut microbiota can alter CRC susceptibility and progression by modulating mechanisms such as inflammation and DNA damage, and by producing metabolites involved in tumor progression or suppression. Dysbiosis of gut microbiota has been observed in patients with CRC, with a decrease in commensal bacterial species (butyrate-producing bacteria) and an enrichment of detrimental bacterial populations (pro-inflammatory opportunistic pathogens). CRC is characterized by altered production of bacterial metabolites directly involved in cancer metabolism including short-chain fatty acids and polyamines. Emerging evidence suggests that diet has an important impact on the risk of CRC development. The intake of high-fiber diets and the supplementation of diet with polyunsaturated fatty acids, polyphenols and probiotics, which are known to regulate gut microbiota, could be not only a potential mechanism for the reduction of CRC risk in a primary prevention setting, but may also be important to enhance the response to cancer therapy when used as adjuvant to conventional treatment for CRC. Therefore, a personalized modulation of the pattern of gut microbiome by diet may be a promising approach to prevent the development and progression of CRC and to improve the efficacy of antitumoral therapy.
Highlights
Microbiota is composed of different bacterial populations with a mutualistic relationship that reside in the epithelial barriers of different organs in the host
A dysbiosis in gut microbiota has been found in Colorectal cancer (CRC) patients compared with healthy controls, with enrichment in pro-inflammatory opportunistic pathogens and a decrease in butyrate-producing bacteria
The proposed mechanisms by which the gut microbiota dysbiosis could participate in colorectal carcinogenesis are the impairment of the intestinal epithelial barrier function, the triggering of proinflammatory responses, the biosynthesis of genotoxins that can interfere with cell cycle regulation, and the production of toxic metabolites by pathogenic bacteria
Summary
Microbiota is composed of different bacterial populations with a mutualistic relationship that reside in the epithelial barriers of different organs in the host. Alterations in the intestinal bacteria balance could lead to changes in the levels of gut microbial metabolites such as short-chain fatty acids (SCFAs), polyphenols, vitamins, tryptophan catabolites and polyamines [8], which could be related to the pathogenesis of the human diseases described above. Abnormal levels of SCFAs and molecules related to the metabolism of amino acid like polyamines have been involved in cancer progression and metastasis in different types of tumor [9]. In this review we discuss the potential role of gut microbiota in the carcinogenesis of colorectal cancer (CRC), the possible role of bacterial metabolites in CRC development and progression, and the influence that certain dietary mediators exert over the intestinal microbiota and CRC risk
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