The Role of Fusobacterium nucleatum in Colorectal Cancer Cell Proliferation and Migration

Simple Summary Although the promoting roles of the epithelial-mesenchymal transition (EMT), tumor microenvironment (TME), and oncogenic ncRNAs in tumor metastasis have been fully verified, the mechanisms by which Fusobacterium nucleatum (Fn) contributes to the progression of colorectal cancer (CRC) remain poorly understood. The main scope of the current work is to summarize the potential molecular mechanisms by which Fn promotes the proliferation and migration of CRC cells by affecting biological processes, such as EMT, TME, and oncogenic ncRNAs. The ultimate goal is to provide a possible strategy for effective CRC treatment in the near future. Colorectal cancer (CRC) is a common cancer worldwide with poor prognosis. The presence of Fusobacterium nucleatum (Fn) in the intestinal mucosa is associated with the progression of CRC. In this review, we explore the mechanisms by which Fn contributes to proliferation and migration of CRC cells from the following four aspects: induction of the epithelial-mesenchymal transition (EMT), regulation of the tumor microenvironment (TME), expression of oncogenic noncoding RNAs, and DNA damage. This review outlines the scientific basis for the use of Fn as a biomarker and therapeutic target in CRC.

Automated summary

This review summarizes the potential molecular mechanisms by which Fusobacterium nucleatum (Fn) promotes the proliferation and migration of colorectal cancer (CRC) cells, such as induction of epithelial-mesenchymal transition, regulation of the tumor microenvironment, expression of oncogenic noncoding RNAs, and DNA damage.