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Gan To Kagaku Ryoho. 2019 Feb;46(2):199-204.

[Carcinogenesis and Gut Microbiota].

[Article in Japanese]

Author information

1
Division of Gastroenterology, Dept. of Internal Medicine, Kawasaki Medical School.

Abstract

Recent developments in techniques of metabologenomics have given a better understanding the association of gut microbiota with various diseases. Gut microbiota has a strong impact on host immunostasis and homeostasis of gut function for maintaining the health condition. Dysbiosis leads to an increase in bacterial populations that stimulate tumorigenesis, and contributes to epithelial carcinogenesis and tumor progression by altering metabolic properties(such as bile acid and butyric acid)and inflammatory process. Inflammation aid the bacterial translocation into the neoplastic tissue, which in turn promotes production of inflammatory cytokines subsequently leading to tumor growth. The colonic microbiota such as enterotoxigenic Bacteroides fragilis(ETBF)may also promote colorectal cancer by stimulating exaggerated immune responses via Th17 cells. Dysbiosis caused by a deficiency of the NLRP6 inflammasome promotes cancer development via interleukin-6(IL- 6)-induced epithelial proliferation. Emerging data suggest that certain groups of bacteria might promote whereas others might protect against colon cancer. Indeed, Fusobacteriumnucleatum (F. nucleatum)seems to play a central role in the tumor microenvironment as its abundance correlates with cancer progression as well as the dysbiotic tumor microbiota composition including Bacteroides and Prevotella species. Moreover, gut microbiota not only plays a key role in carcinogenesis but also influences the efficacy and toxicity of cancer immunotherapy, especially immune checkpoint inhibitors by targeting the programmed death receptor 1(PD-1)and the cytotoxic T lymphocyte antigen 4(CTLA-4).

PMID:
30914517

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