Sulindac inhibits the proliferation and promotes apoptosis of laryngeal cancer cells by down-regulating the AKT/β-catenin pathway

Background: Laryngeal cancer is one of the most common tumors in the head and neck. Uncertainty of targets, mechanisms, and lack of effective drugs largely limit laryngeal cancer prevention and clinical treatment. Therefore, there is an urgent need to develop new drug candidates to prevent and treat laryngeal cancer. Methods: : In this study, laryngeal cancer Tu212 and Tu686 cells were treated with different concentrations of sulindac, and their effects on the proliferation, cell cycle, and apoptosis of laryngeal cancer cells were detected by CCK-8, clone formation assay, and flow cytometry; Western-blot was used to detect the effects of sulindac on proliferation and apoptosis-related proteins. Results: : Sulindac can dose-dependently block the G1/S phase of the laryngeal cancer Tu686 and Tu212 cell cycle to inhibit cell proliferation and significantly induce laryngeal cancer cell apoptosis. Besides, Western blotting also confirmed that the relative expressions of cell cycle-related proteins CyclinD1 and c-Myc were down-regulated; apoptosis-related proteins Bcl-2, Caspase-3, and Survivin were down-regulated, Bax and Cleaved caspase-3 were up-regulated. In addition, sulindac can down-regulate the expression of p-Akt and β-catenin. Conclusion: Our study found that sulindac can inhibit the proliferation of laryngeal cancer cells and induce apoptosis by down-regulating the expression of the AKT/β-catenin pathway. Research on the anti-laryngeal cancer properties of sulindac is still very scarce. Our research provides an important theoretical basis for the clinical application of sulindac in the prevention and treatment of laryngeal cancer.