Abstract
Colorectal cancer is a multifactorial disease involving genetic, environmental, and lifestyle risk factors. Intestinal microbiota plays an important role in the occurrence and development of colorectal cancer. Studies have shown that the behavior of intestinal microbiota can lead to pathological changes in the host intestine, which can be divided into epigenetic changes and carcinogenic changes at the gene level, and ultimately promote the formation and development of colorectal cancer. Intestinal microbiota is mainly distributed in the intestinal epithelium, which is composed of a large number of microorganisms interacting with the host intestinal cells. It can affect the immune-inflammation and metabolism of the gastrointestinal tract, and may be used as a biomarker for disease diagnosis. Regulation of gut microbiota is a promising strategy for the prevention and treatment of colorectal cancer. This article reviews the role of intestinal microbiota in the development of colorectal cancer, including the related mechanisms of intestinal microbiota promoting colorectal cancer, the use of intestinal microbiota in the diagnosis of colorectal cancer, and the regulation of intestinal microbiota in the prevention or treatment of colorectal cancer.
Highlights
Colorectal cancer (CRC) accounts for about 10% of the new cancer cases worldwide
The results showed that compared with the control group, the number of colon tumors in the GOSLu group was significantly reduced
Intestinal microbiota plays an important role in the development of CRC by destroying the homeostasis of the microenvironment, changing immune response, producing toxic metabolites, and directly or indirectly affecting epigenetic modification
Summary
Colorectal cancer (CRC) accounts for about 10% of the new cancer cases worldwide. Its incidence rate is third among all cancers worldwide, and its mortality rate ranks second among all cancers (Bray et al, 2018). ETBF can upregulate the expression of spermine oxidase (SMO) in colonic epithelial cells, increasing the SMO-dependent reactive oxygen species (ROS), promoting the release of inflammatory cytokines and causing DNA damage, and promoting the development of CRC. C. jejuni has a mutated CDTb subunit, which makes the bacteria unable to produce CDT, inhibiting its carcinogenesis in vivo and reducing the DNA damage response of cells and intestinal organs.
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