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

Abstract

Increasing evidence suggests that <i>Fusobacterium nucleatum</i> is involved in colorectal carcinogenesis. Previous studies have explored whether <i>F. nucleatum</i> may trigger colonic epithelial-mesenchymal transition. The results of the present study demonstrated that <i>F. nucleatum</i> enhances the proliferation and invasion of NCM460 cells compared with that of normal control and DH5α cells. Furthermore, <i>F. nucleatum</i> significantly increased the phosphorylation of p65 (a subunit of nuclear factor-κB), as well as the expression of interleukin (IL)-6, IL-1β and matrix metalloproteinase (MMP)-13. Additionally, <i>F. nucleatum</i> infection did not affect the expression levels of epithelial (E-)cadherin and β-catenin. E-cadherin knockdown in NCM460 cells did not induce the activation of inflammatory responses in response to <i>F. nucleatum</i> infection, whereas it increased inflammation in response to β-catenin silencing. <i>F. nucleatum</i> infection could not increase the proportion of cells at S phase when E-cadherin was silenced. Nevertheless, <i>F. nucleatum</i> infection enhanced the proportion of NCM460 cells at S phase when transfected with small interfering RNAs to knock down β-catenin expression. In conclusion, the results of the present study demonstrated that <i>F. nucleatum</i> infection interacted with E-cadherin instead of β-catenin, which in turn enhances the malignant phenotype of colorectal cancer cells.