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Review
. 2020 May 29;12(6):1406.
doi: 10.3390/cancers12061406.

The Role of the Gut Microbiome in Colorectal Cancer Development and Therapy Response

Lidia Sánchez-Alcoholado  1 , Bruno Ramos-Molina  2 , Ana Otero  3 , Aurora Laborda-Illanes  1 , Rafael Ordóñez  3 , José Antonio Medina  3 , Jaime Gómez-Millán  3 , María Isabel Queipo-Ortuño  1
Affiliations
Review

The Role of the Gut Microbiome in Colorectal Cancer Development and Therapy Response

Lidia Sánchez-Alcoholado et al. Cancers (Basel). .

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.

Keywords: colorectal cancer; dietary fiber; dysbiosis; gut microbiota; inflammation; polyamines; polyphenols; polyunsaturated fatty acids; probiotics; short-chain fatty acids.

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Conflict of interest statement

The authors declare no conflict of interest.

Figures

Figure 1
Figure 1
Mechanisms of action of polyamines and SCFAs (microbiota-derived metabolites) in the inflammation and cellular proliferation of colon cancer cells. SCFAs: short-chain fatty acids; ODC: ornitina descarboxilasa; DFMO: alpha-difluoromethylornithine; AMXT 1501: polyamine transport inhibitor; GPR109a: G-protein–coupled receptors; IL: interleukin.
Figure 2
Figure 2
Beneficial effects of dietary supplementation with PUFAs, polyphenols and probiotics on the intestinal microbiota and colon cells for the reduction of CRC risk or to enhance the response to cancer therapy when are used as adjuvant to conventional treatment. PUFAs: omega-3 polyunsaturated fatty acids; 5-FU: 5-fluorouracil; SCFAs: short-chain fatty acids.
See this image and copyright information in PMC

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