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肠道微生物衍生代谢物与结直肠癌:新的见解和更新。

Gut microbiota-derived metabolites and colorectal cancer: New insights and updates.

机构信息

Digestive Endoscopy Center, The Affiliated Hospital of North Sichuan Medical College, Nanchong, Sichuan 637000, China.

Digestive Endoscopy Center, The Affiliated Hospital of North Sichuan Medical College, Nanchong, Sichuan 637000, China.

出版信息

Microb Pathog. 2020 Dec;149:104569. doi: 10.1016/j.micpath.2020.104569. Epub 2020 Oct 16.

DOI:10.1016/j.micpath.2020.104569
PMID:33075518
Abstract

Abundant evidence from in-vitro as well as in-vivo studies supports the gut microbiota-derived metabolites as crucial executors of diet effect on the host physiology. As such, a number of microbiota-derived metabolites produced from diet have been connected to complex forms of human diseases such as colorectal cancer (CRC). Despite current unresolved questions concerning molecular mechanisms between metabolites, host signaling pathways, and CRC, some new progresses promise continued advancement of the field. Therefore, clarification of the molecular events underlying which metabolites may regulate proliferation of colonocytes will hopefully open up new avenues for seeking the possibilities affecting host health and exploitation of these capabilities for therapeutic purpose. In this Review, we will discuss recent insights into contributions of the gut microbiota-derived metabolites to CRC and argue that the cumulative effects of metabolites should be considered with the intention of better predict and prevent cancer progression. We will also discuss the signaling pathways induced by specific metabolites toward down-regulation and/or up-regulation of immune system that eventually trigger progression and/or inhibition of CRC.

摘要

大量来自体外和体内研究的证据支持肠道微生物衍生代谢物是饮食对宿主生理影响的关键执行者。因此,许多源自饮食的微生物衍生代谢物已与人类疾病的复杂形式相关联,例如结直肠癌(CRC)。尽管目前对于代谢物、宿主信号通路和 CRC 之间的分子机制存在一些未解决的问题,但一些新的进展有望推动该领域的持续发展。因此,阐明潜在的分子事件,即代谢物可能调节结肠细胞的增殖,有望为寻求影响宿主健康的可能性以及利用这些能力进行治疗目的开辟新途径。在这篇综述中,我们将讨论肠道微生物衍生代谢物对 CRC 的贡献的最新见解,并认为应该考虑代谢物的累积效应,以便更好地预测和预防癌症进展。我们还将讨论特定代谢物诱导的信号通路,这些信号通路下调和/或上调免疫系统,最终引发 CRC 的进展和/或抑制。

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