微生物基因毒素引起与线粒体功能障碍相关的宿主 DNA 突变，线粒体功能障碍是结直肠癌发生的重要因素。
Microbial genotoxin-elicited host DNA mutations related to mitochondrial dysfunction, a momentous contributor for colorectal carcinogenesis.
发表日期：2024 Aug 27
作者：
Xue Yang, Yumeng Gan, Yuting Zhang, Zhongjian Liu, Jiawei Geng, Wenxue Wang
来源：
mSystems
摘要：
肠道微生物失调会增加重复性炎症反应，导致结直肠癌发病率增加。最近的研究表明，特定的微生物种类直接引发宿主细胞核DNA突变，从而加速结直肠癌的进展。鉴于线粒体功能障碍在促进结直肠癌中的明确作用，可以合理地假设肠道微生物可能诱导线粒体基因突变，从而诱发线粒体功能障碍。在这篇综述中，我们重点关注肠道微生物基因毒素及其在线粒体基因中的已知和潜在靶标。因此，我们提出，有针对性地破坏基因毒素转运途径可以有效降低线粒体基因突变率，并对预防结直肠癌产生实质性益处。
Gut microbe dysbiosis increases repetitive inflammatory responses, leading to an increase in the incidence of colorectal cancer. Recent studies have revealed that specific microbial species directly instigate mutations in the host nucleus DNA, thereby accelerating the progression of colorectal cancer. Given the well-established role of mitochondrial dysfunction in promoting colorectal cancer, it is reasonable to postulate that gut microbes may induce mitochondrial gene mutations, thereby inducing mitochondrial dysfunction. In this review, we focus on gut microbial genotoxins and their known and potential targets in mitochondrial genes. Consequently, we propose that targeted disruption of genotoxin transport pathways may effectively reduce the rate of mitochondrial gene mutations and yield substantial benefits for the prevention of colorectal carcinogenesis.