Abstract
Lung cancer is one of the most frequent cancers in the world and the main cause of cancer related deaths. Among them, non-small cell lung cancer (NSCLC) accounts for about 85% of lung cancer. Myristicin (1-allyl-5-methoxy-3,4-methylenedioxybenzene), an active aromatic compound, has been proved to have anti-cancer effects. However, the effects of myristicin on NSCLC are not fully illustrated. Our research aimed to elucidate the roles and explain the potential mechanism of myristicin in NSCLC. A549 and H1975 cells were exposed to 0.5, 1, 5mM myristicin for 48 h, EdU, flow cytometry, Transwell and wound healing migration assay were applied for analyzing cell proliferation, apoptosis, cycle, migration and invasion, respectively. Caspase 3 activity and cleaved-Caspase3 expression were determined by relevant kits and western blotting, respectively. Besides, the Epithelial-Mesenchymal Transition (EMT) related genes levels and Wnt/β-catenin pathway related genes expressions, including E-cadherin, N-cadherin, Wnt3a and β-catenin, were assessed by qRT-PCR, and western blot assays. The nuclear translocation of β-catenin in NSCLC cells was analyzed by immunofluorescence staining. Our data revealed that myristicin suppressed NSCLC proliferation, migration and invasion in a dose-dependent manner. Besides, myristicin led to cell apoptotic and G0/G1 arrest and enhancing Caspase3 activity in NSCLC. Moreover, myristicin inhibited NSCLC EMT and blocked Wnt/β-Catenin signaling pathway in a dose-dependent manner, as confirmed by enhanced E-cadherin expression, suppressed N-cadherin level, inhibited Wnt3a and β-catenin levels, and reduced nuclear translocation of β-catenin. Myristicin blocked the development of NSCLC via regulating cells proliferation, migration, invasion and EMT through deactivating the Wnt/β-catenin pathway, which provide a new therapeutic treatment for NSCLC in clinical. Supplementary information: The online version contains supplementary material available at 10.1007/s10616-026-00893-0.