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

Increasing evidence suggests that is involved in colorectal carcinogenesis. Previous studies have explored whether may trigger colonic epithelial-mesenchymal transition. The results of the present study demonstrated that enhances the proliferation and invasion of NCM460 cells compared with that of normal control and DH5α cells. Furthermore, 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, 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 infection, whereas it increased inflammation in response to β-catenin silencing. infection could not increase the proportion of cells at S phase when E-cadherin was silenced. Nevertheless, 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 infection interacted with E-cadherin instead of β-catenin, which in turn enhances the malignant phenotype of colorectal cancer cells.