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微生物群与癌症:肠道微生物代谢物激活宿主细胞的机制。

Microbiota and cancer: host cellular mechanisms activated by gut microbial metabolites.

机构信息

Microbiology Lab, ChemBio Cluster, ITMO University, 197101 St. Petersburg, Russian Federation.

出版信息

Int J Med Microbiol. 2020 May;310(4):151425. doi: 10.1016/j.ijmm.2020.151425. Epub 2020 Apr 24.

Abstract

In recent years, more and more data indicate the effect of human microbiota on carcinogenesis. Despite the numerous studies on the relationship between gut microbiota and carcinogenesis, the exact mechanisms of this interaction are not well studied. It becomes apparent that this relationship can be mediated by microbial metabolites. Mechanisms of some well-known bacterial genotoxins and oncogenes, such as colibactin, CagA, IpgD, VirA, P37, have been studied in detail. At the same time, a role in carcinogenesis of a large group of gut microbial metabolites, including short-chain fatty acids, polyamines, and products of polyphenol and tryptophan catabolism, is less well understood. However, more and more evidence data show the effect of bacterial metabolites on cancer development and progression. In this review, we summarize relevant data regarding the possible mechanisms that can account for the effects of gut microbial metabolites mentioned above in carcinogenesis.

摘要

近年来,越来越多的数据表明了人类微生物组对致癌作用的影响。尽管有大量关于肠道微生物群与致癌作用之间关系的研究,但这种相互作用的确切机制尚未得到很好的研究。显然,这种关系可以通过微生物代谢物来介导。一些众所周知的细菌遗传毒素和致癌基因,如 colibactin、CagA、IpgD、VirA、P37 的作用机制已经得到了详细研究。同时,肠道微生物代谢物中的一大类物质,包括短链脂肪酸、多胺以及多酚和色氨酸代谢产物的产物,在致癌作用中的作用还不太清楚。然而,越来越多的证据数据表明细菌代谢物对癌症发展和进展的影响。在这篇综述中,我们总结了相关数据,阐述了可能的机制,可以解释上述肠道微生物代谢物在致癌作用中的作用。

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