Objective To investigate the mechanism of ropivacaine inhibiting the proliferation, migration and invasion of gastric cancer cell NCI-N87 through the Wnt signaling pathway.
Methods Gastric cancer cells NCI-N87 were cultured by ropivacaine cell culture fluid and were divided into control group (0 μg/mL ropivacaine), ROP-L group (160 μg/mL ropivacaine), ROP-M group (320 μg/mL ropivacaine), ROP-H group (640 μg/mL ropivacaine) and ROP-H+Licl (640 μg/mL ropivacaine, Wnt signal activator Licl) group. MTT assay was used to detect cell proliferation activity. Transwell assay was used to detect the changes in ability of cell migration and invasion. The protein expression levels of matrix metalloproteinase 9 (MMP-9), matrix metalloproteinase 2 (MMP-2), E-cadherin, β-catenin, N-cadherin and Wnt1 were analyzed by western blot.
Results Compared with the control group, the number of migration and invasion of gastric cancer cells in the ROP-L, ROP-M, and ROP-H groups gradually decreased, the proliferation activity decreased, the expression levels of MMP-2 and MMP-9 proteins in the cells gradually decreased, and the protein expression level of E-cadherin in the cells gradually increased, and the N-cadherin, Wnt1, and β-catenin protein expression levels gradually decreased (P < 0.05). Compared with the ROP-H group, the number of migration and invasion of gastric cancer cells in the ROP-H+Licl group increased, the protein levels of MMP-9, MMP-2, N-cadherin, Wnt1 and β-catenin increased, and the protein level of E-cadherin decreased (P < 0.05).
Conclusion Ropivacaine inhibits the proliferation, migration, invasion and epithelial-mesenchymal transition (EMT) of gastric cancer cell NCI-N87 by down-regulating the Wnt signaling pathway.
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