Dioscin Enhances DNA Damage to Promote Apoptosis in Oral Squamous Cell Carcinoma Cells
Objective:To investigate the effects of Dioscin on DNA damage and apoptosis in SCC4 and SCC25 human OSCC cells and explore potential underlying mechanisms.Methods:SCC4 and SCC25 cells were treated with various concentrations of Dioscin(0.0,0.1,0.3,1.0,3.0,10.0 and 30.0 μmol/L)for 48 hours,and cell viability was assessed using the CCK-8 assay.Immunofluorescence was used to evaluate γH2AX expression in SCC4 cell nuclei after treatment with different Dioscin concentrations(0.0,1.0,2.0,4.0 μmol/L)for 48 hours.The expression of DNA damage repair proteins was examined by Western blotting.Flow cytometry was employed to measure apoptosis rates,and changes in the expression of apoptosis-related proteins were detected using Western blotting.Results:Dioscin exhibited a concentration-dependent inhibition of SCC4 and SCC25 cell activity(P＜0.05).It significantly increased the fluorescence intensity of γH2AX in SCC4 cell nuclei compared to the untreated group(P＜0.05)and activated the expression of DNA damage signal proteins,including P-ATM,P-CHK1,P-CHK2,and γH2AX.Dioscin also dose-dependently facilitated the activation of apoptosis-regulating proteins Cleaved-PARP and Cleaved-Caspase-3.Conclusion:Dioscin can suppress the activity of oral squamous cell carcinoma cells and promote apoptosis,and its mechanism may be linked to its induction of DNA damage in these cells.
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维普
