Fusobacterium nucleatum promotes the progression of colorectal cancer by interacting with E-cadherin

Increasing evidence suggests that Fusobacterium nucleatum is involved in colorectal carcinogenesis. Previous studies have explored whether F. nucleatum may trigger colonic epithelial-mesenchymal transition. The results of the present study demonstrated that F. nucleatum enhances the proliferation and invasion of NCM460 cells compared with that of normal control and DH5 alpha cells. Furthermore, F. nucleatum significantly increased the phosphorylation of p65 (a subunit of nuclear factor-kappa B), as well as the expression of interleukin (IL)-6, IL-1 beta and matrix metalloproteinase (MMP)-13. Additionally, F. nucleatum infection did not affect the expression levels of epithelial (E-)cadherin and beta-catenin. E-cadherin knockdown in NCM460 cells did not induce the activation of inflammatory responses in response to F. nucleatum infection, whereas it increased inflammation in response to beta-catenin silencing. F. nucleatum infection could not increase the proportion of cells at S phase when E-cadherin was silenced. Nevertheless, F. nucleatum infection enhanced the proportion of NCM460 cells at S phase when transfected with small interfering RNAs to knock down beta-catenin expression. In conclusion, the results of the present study demonstrated that F. nucleatum infection interacted with E-cadherin instead of beta-catenin, which in turn enhances the malignant phenotype of colorectal cancer cells.