Microbial genotoxin-elicited host DNA mutations related to mitochondrial dysfunction, a momentous contributor for colorectal carcinogenesis
Xue Yang,
Yumeng Gan,
Yuting Zhang,
Zhongjian Liu,
Jiawei Geng,
Wenxue Wang
Affiliations
Xue Yang
Department of Infectious Disease and Hepatic Disease, The Affiliated Hospital of Kunming University of Science and Technology, The First People’s Hospital of Yunnan Province, Kunming, Yunnan, China
Yumeng Gan
Department of Infectious Disease and Hepatic Disease, The Affiliated Hospital of Kunming University of Science and Technology, The First People’s Hospital of Yunnan Province, Kunming, Yunnan, China
Yuting Zhang
Department of Infectious Disease and Hepatic Disease, The Affiliated Hospital of Kunming University of Science and Technology, The First People’s Hospital of Yunnan Province, Kunming, Yunnan, China
Zhongjian Liu
Institute of Basic and Clinical Medicine, First People’s Hospital of Yunnan Province, Affiliated Hospital of Kunming University of Science and Technology, Kunming, Yunnan, China
Jiawei Geng
Department of Infectious Disease and Hepatic Disease, The Affiliated Hospital of Kunming University of Science and Technology, The First People’s Hospital of Yunnan Province, Kunming, Yunnan, China
Wenxue Wang
Department of Infectious Disease and Hepatic Disease, The Affiliated Hospital of Kunming University of Science and Technology, The First People’s Hospital of Yunnan Province, Kunming, Yunnan, China
ABSTRACT 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.
