Abstract: Objective: To investigate the effect of lipopolysaccharide (LPS) on the expressions of epithelial-mesenchymal transition (EMT) markers and β-catenin in the breast cancer MDA-MB-231 cells, and to clarify its possible mechanism. Methods: The breast cancer MDA-MB-231 cells were divided into control group and different concentrations (5, 10, 20, and 40 mg·L^-1) of LPS groups. Inverted microscope was used to observe the morphology of MDA-MB-231 cells in various groups. Immunofluorescence test was used to detect the β-catenin expression and location in the MDA-MB-231 cells in various groups. Real-time quantitative PCR(RT-qPCR) and Western blotting methods were used to detect the expression levels of the EMT markers E-cadherin, Vimentin and β-catenin mRNA and proteins in the MDA-MB-231 cells in various groups. Results: The morphology of MDA-MB-231 cells in control group was epithelial phenotype, and the morphology of MDA-MB-231 cells in different concentrations of LPS groups were the phenotype of mesenchymal cells. The results of immunofluorescence staining showed that the expression of β-catenin was mainly located in the nucleus. Compared with control group, the expression levels of Vimentin and β-catenin mRNA and proteins in the MDA-MB-231 cells in different concentrations of LPS groups were increased (P<0.05 or P<0.01), especially in 20 mg·L^-1 LPS group. Compared with control group, the expression levels of E-cadherin mRNA and proteins in the MDA-MB-231 cells in different concentrations of LPS groups were decreased (P<0.05 or P<0.01), especially in 20 mg·L^-1 LPS group. Conclusion: LPS could promote the EMT, invasion and metastasis of the breast cancer MDA-MB-231 cells by down-regulating the E-cadherin expression and up-regulating the Vimentin expression, and its mechanism may be related to Wnt/β-catenin signaling pathway.

Key words: breast neoplasms, lipopolysaccharide, epithelial mesenchymal transition, Wnt/β-catenin signaling pathway