Three specific gut bacteria in the occurrence and development of colorectal cancer: a concerted effort

Abstract

Colorectal cancer (CRC), which develops from the gradual evolution of tubular adenomas and serrated polyps in the colon and rectum, has a poor prognosis and a high mortality rate. In addition to genetics, lifestyle, and chronic diseases, intestinal integrity and microbiota (which facilitate digestion, metabolism, and immune regulation) could promote CRC development. For example, enterotoxigenic Bacteroides fragilis, genotoxic Escherichia coli (pks+ E. coli), and Fusobacterium nucleatum, members of the intestinal microbiota, are highly correlated in CRC. This review describes the roles and mechanisms of these three bacteria in CRC development. Their interaction during CRC initiation and progression has also been proposed. Our view is that in the precancerous stage of colorectal cancer, ETBF causes inflammation, leading to potential changes in intestinal ecology that may provide the basic conditions for pks+ E. coli colonization and induction of oncogenic mutations, when cancerous intestinal epithelial cells can further recruit F. nucleatum to colonise the lesion site and F. nucleatum may contribute to CRC advancement by primarily the development of cancer cells, stemization, and proliferation, which could create new and tailored preventive, screening and therapeutic interventions. However, there is the most dominant microbiota in each stage of CRC development, not neglecting the possibility that two or even all three bacteria could be engaged at any stage of the disease. The relationship between the associated gut microbiota and CRC development may provide important information for therapeutic strategies to assess the potential use of the associated gut microbiota in CRC studies, antibiotic therapy, and prevention strategies.

Application of Fusobacterium nucleatum as a biomarker in gastrointestinal malignancies

“…To investigate bacterial symbiosis and its potential interactions, Tran et al [ 41 ] constructed a correlation network using the gut microbiomes of CRC patients and identified that multiple subspecies of Fusobacterium cluster in the tumor microbiome, and furthermore, that genes encoding key virulence factors (Fap2 and RadD) may undergo frequent horizontal gene transfer or recombination. Gong et al [ 42 ] postulated that in the early stages of CRC, Bacteroides fragilis-mediated inflammation induced intestinal epithelial degradation and intestinal mucosal injury, leading to an imbalance in intestinal ecology and providing the basic conditions for PKS + E. coli colonization and induction of oncogenic mutations. Cancerous intestinal epithelial cells can further recruit F. nucleatum to colonize the lesion site, and F. nucleatum in turn was shown to promote cancer cell proliferation through Fap2-mediated immune evasion.…”

The histologic features, molecular features, detection and management of serrated polyps: a review

“…Specifically, miRNA-31 expression has been found to be associated with CIMP status in serrated lesions with BRAF mutation. However, the precise role of miRNA in this process remains unclear (11,(31)(32)(33).…”