Objective The aim of this study was to investigate the effect of NLRP3/IL-1β pathway in macrophages on the migration and invasion of oral squamous cell carcinoma cells and the regulatory role of Carnosol on this process.Methods qRT-PCR,Western Blot and ELISA were used to detect the effects of Carnosol between oral squamous cell carcinoma cells and macrophages on NLRP3 inflammasome activation and IL-1β release in macrophages.Transwell and qRT-PCR assays were used to determine the effects of IL-1β on the migration and invasion of oral squamous cell cells.The effect of carnol on the activation of NLRP3 inflammasome and the release of IL-1β in macrophages induced by crosstalk was detected by ELISA.The transwell assay was used to detect the changes in the migration and invasion ability of oral squamous cell carcinoma cells caused by the effect of the crosstalk.CCK8 assay was used to detect the toxic effects of Carnosol cultured oral squamous cell carcinoma cell line Cal-27 and monocyte macrophage cell line THP-1.Results Crosstalk between oral squamous cell carcinoma cells and macrophages leads to NLRP3 inflammasome activation and IL-1β release from macrophages.Transwell assay results suggest that IL-1βpromotes oral squamous cell migration and invasion in a dose-dependent manner.Carnosol inhibits crosstalk-induced NLRP3 inflammasome activation and IL-1β release in a dose-dependent manner,and a concentration of 40 μM Carnosol effectively inhibits the increased migration and invasion of oral squamous cell carcinoma cells enhanced by the crosstalk;The results of CCK8 experiments show that Carnosol at concentrations of 0-100 μM is not toxic to both Cal-27 and THP-1 cells.Conclusion This study demonstrated that the crosstalk between oral squamous cell carcinoma cells and macrophages could promote NLRP3 inflammasome activation and IL-1β release from macrophages,thereby significantly enhancing the migration and invasion ability of oral squamous cell carcinoma cells.Carnosol inhibits the migration and invasion of oral squamous cell carcinoma cells by inhibiting the activation of NLRP3/IL-1β pathway and the release of IL-1β in macrophages.
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