Abstract:OBJECTIVE: To investigate the key targets of curcumin against laryngeal cancer based on network pharmacology and to design experiments to verify them. METHODS: Curcumin targets were screened by Swiss Target Prediction, laryngeal cancer targets were screened by GeneCards, OMIM and TTD databases, shared targets were obtained by FunRich software, gene ontology biological processes and Kyoto Gene and Genome Encyclopedia pathways were performed on curcumin-laryngeal cancer shared targets using DAVID platform. The effect of curcumin on the migration ability of laryngeal cancer cells was observed by cell scratching assay, the effect of curcumin on cell proliferation ability and its chemotherapeutic potentiation effect on chemotherapeutic drug doxorubicin was detected by CCK-8 method, and the effect of curcumin on the expression level of P STAT3 protein expression level in laryngeal cancer cells. Results: Five targets were obtained, and KEGG pathway enrichment analysis revealed that the signaling pathways related to laryngeal cancer were proteoglycan pathway in cancer, TNF signaling pathway, pathway in cancer, HIF-1 signaling pathway, Jak-STAT signaling pathway, carbon metabolism pathway in cancer, and vascular endothelial growth factor signaling pathway, and it was found by molecular docking that: curcumin binds well to STAT3, P- STAT3, cell scratch assay observed that curcumin could inhibit the migration ability of laryngeal cancer cells, CCK-8 method found that curcumin could significantly inhibit the proliferation activity of laryngeal cancer cells in vitro, and curcumin had a chemotherapeutic potentiation effect on chemotherapeutic drug doxorubicin; Western blot assay found that as the concentration of curcumin increased to different degrees to inhibit the expression of P-STAT3 protein expression.Conclusion: Curcumin inhibited the proliferation and migration of laryngeal cancer cells in a dose-dependent manner; curcumin had a chemotherapeutic potentiation effect on the chemotherapeutic drug doxorubicin; curcumin inhibited laryngeal cancer tumor cells by regulating EGFR, STAT3, EP300 and P-STAT3, and the validated target was P-STAT3.