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引用次数: 0
摘要
肠道微生物菌群失调会增加重复性炎症反应,导致结直肠癌发病率上升。最近的研究发现,特定的微生物种类会直接导致宿主细胞核 DNA 发生突变,从而加速结直肠癌的发展。鉴于线粒体功能障碍在促进结直肠癌方面的作用已得到证实,我们有理由推测,肠道微生物可能会诱发线粒体基因突变,从而诱发线粒体功能障碍。在这篇综述中,我们将重点关注肠道微生物基因毒素及其线粒体基因的已知和潜在靶点。因此,我们建议,有针对性地破坏基因毒素转运途径可有效降低线粒体基因突变率,并为预防结直肠癌的发生带来巨大益处。
Microbial genotoxin-elicited host DNA mutations related to mitochondrial dysfunction, a momentous contributor for colorectal carcinogenesis.
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.
mSystemsBiochemistry, Genetics and Molecular Biology-Biochemistry
CiteScore
10.50
自引率
3.10%
发文量
308
审稿时长
13 weeks
期刊介绍:
mSystems™ will publish preeminent work that stems from applying technologies for high-throughput analyses to achieve insights into the metabolic and regulatory systems at the scale of both the single cell and microbial communities. The scope of mSystems™ encompasses all important biological and biochemical findings drawn from analyses of large data sets, as well as new computational approaches for deriving these insights. mSystems™ will welcome submissions from researchers who focus on the microbiome, genomics, metagenomics, transcriptomics, metabolomics, proteomics, glycomics, bioinformatics, and computational microbiology. mSystems™ will provide streamlined decisions, while carrying on ASM''s tradition of rigorous peer review.