Fusobacterium spp. and colorectal cancer: cause or consequence?

Abstract

Although increasing evidence suggests a relationship between bacterial dysbiosis and colorectal cancer (CRC), few studies have identified specific microbial etiologic factors. Recent studies have implicated overabundance of Fusobacterium in association with colorectal adenomas and cancer. Two articles published in Cell Host & Microbe provide insights into the Fusobacterium-CRC relationship.

Figure 1

Potential mechanisms by which Fusobacterium promotes colorectal carcinogenesis. In the presence of APC mutation, F. nucleatum promotes oncogenesis in the colon via adhesin FadA through attachment, phosphorylation and invasion (A). FadA binds to E-cadherin on the surface of the cell, inhibiting its tumor-suppressor activity and activating β-catenin signaling (B). β-catenin phosphorylation is decreased, resulting in increased β-catenin in the cytoplasm and translocation into the nucleus where it modulates increased expression of LEF, TCF, NF-κβ and other oncogenes (C). F. nucleatum invades the cell via internalization of E-cadherin by clathrin (D) and stimulates expression of inflammatory genes.