趋化因子CXCL11激活NF-κB信号通路促进胰腺癌的侵袭转移及上皮间质转换

Objective： To investigate the important role of NF-κB pathway in CXCL11-induced invasion and epithelial-mesenchymal transition (EMT) of pancreatic cancer cell line Panc-1. Methods： Panc-1 cultured in vitro was harvested and divided into control group, CXCL11 group, and BAY 11-7082 group (NF-κB inhibitor). Transwell invasion assay was applied to analyze the invasive ability of tumor cells in different groups. The expressions of p65, P-p65, E-cadherin, N-cadherin, and Vimentin were determined by Western blot. The intracellular localization of p65 was detected by immunofluorescence staining. Results： CXCL11 significantly induced the invasion of Panc-1 cells, promoted p65 nuclear translocation of Panc-1 cells, upregulated the expressions of P-p65, N-cadherin and Vimentin, and downregulated the expression of E-cadherin. Furthermore, the inhibition of NF-κB pathway obviously abrogated CXCL11-induced invasion of Panc-1 cells and enhanced the p65 nuclear translocation. Conclusion： CXCL11 induces epithelial-mesenchymal transition and enhances invasion of pancreatic cancer cells through the activation of NF-κB pathway.