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Approximately 8 years ago, two groups independently reported enrichment of Fusobacterium nucleatum (Fn) in human colorectal cancer (CRC) tissues compared with adjacent normal tissues.1 2 Since this discovery, intense research interests have been drawn to the bacterium in the context of CRC. The association between Fn and CRC has been confirmed in numerous studies, and several Fn-driven pro-oncogenic mechanisms have been proposed based on observations from preclinical models.3 Notably, much of our knowledge regarding the involvement of Fn is at the primary CRC development stage. How Fn might impact CRC metastasis—the late stage of carcinogenesis that really determines poor prognosis in patients—is relatively unexplored, despite detection of the bacterium in CRC metastases to the liver and lymph nodes.1 2 4
The first evidence that Fn is important for CRC metastasis emerged in 2017, when it was shown that Fn presence correlated with successful establishment of CRC patients-derived xenografts in mice.4 Yet, the molecular process underlying Fn-dependent metastatic tumour formation was undefined. Earlier this year, three research groups, using a similar in vitro experimental design, reported that Fn infection enhanced migration of human CRC-derived HCT116 cells, although each group proposes distinct mechanisms.5–7 These include induction of interleukin-8 (IL-8) and C-X-C Motif Chemokine Ligand 1 (CXCL1),5 upregulation of caspase …
Contributors Both author contributed to review of the literature and the writing of the article.
Funding This research was supported by the National Institutes of Health grants R01DK073338 and from the University of Florida, Department of Medicine Gatorade Fund to CJ.
Competing interests None declared.
Patient consent for publication Not required.
Provenance and peer review Commissioned; internally peer reviewed.
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