Background: Lidocaine, an amide local anesthetic, has recently been found to have anticancer action in various cancer cells. However, the role of lidocaine in epithelial ovarian cancer (EOC) remains largely unknown. In the present study, we investigated how lidocaine regulates the progression of EOC.
Methods: Real-time polymerase chain reaction was used to examine the expression of Snail, Wnt, β-catenin, E-cadherin, vimentin, matrix metalloproteinase (MMP)-7, MMP-9, and vascular endothelial growth factor in lidocaine-treated cells. Cell proliferation assays, cell apoptosis assays, and cell migration assays were employed to verify the function of lidocaine in EOC cells. Cell proliferation and cell migration assays were employed to verify the function of Wnt/β-catenin signaling in lidocaine-treated EOC cells together with Wnt-overexpressing plasmids or inhibitor NVP-XAV939.
Results: Lidocaine could inhibit proliferation, migration, and invasion, and induce apoptosis in ovarian cancer cells lines in a dose-dependent manner. Wnt/β-catenin signaling was involved in the suppression of epithelial-mesenchymal transition progression of ovarian cancer cells, which resulted in the downregulation of Snail and vimentin, as well as the upregulation of E-cadherin. Furthermore, overexpressed Wnt could reverse the carcinostatic effect of lidocaine, while Wnt inhibitor XAV-939 synergistically enhanced the antitumor effect of lidocaine.
Conclusions: Mechanistically, lidocaine could inhibit the proliferation and metastasis of EOC by the Wnt/β-catenin pathway to regulate the progression of EOC.
Keywords: Lidocaine; Wnt/β-catenin; epithelial ovarian cancer (EOC); metastasis.
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