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https://www.selleckchem.com/btk.html r tissues to promote migration and invasion of breast cancer cells by up-regulating ARHGAP36 expression. To explore the effect of dibenzyl trisulfide (DTS) on cell proliferation and apoptosis in human head and neck squamous cell carcinoma (HNSCC) HN30 cells. The effects of DTS on proliferation of HNSCC cell lines HN30, HN12, and SCC25 were examined by assessing colony formation ability of the treated cells. The effect of different concentrations of DTS on viability of HN30 cells was assessed using MTT assay. HN30 cells were treated with 3, 10, or 30 μmol/L DTS for 24 h, and the cell apoptosis and mitochondrial membrane potential (MMP) were detected using flow cytometry with annexin Ⅴ-FITC/PI double staining and JC-1 fluorescent probe staining. Western blotting was performed to determine the protein expressions of caspase-3, cleaved caspase-3 and Bcl-2 in the treated cells. The phosphorylation levels of Akt and p53 in HN30 cells were detected using Western blotting after treatment with 10 μmol/L DTS for 0.5, 1, 2, 4, 8, or 16 h. DTS at 1 μmol/L significantly inhibited the proliferation of HN30, HN12 and SCC25 cells as shown by colony formation assay. MTT assay showed that DTS dose-dependently decreased HN30 cell viability as compared with the solvent control group, and 100 μmol/L DTS produced the strongest inhibitory effect ( < 0.0001). Treatment with DTS below 30 μmol/L concentrationdependently promoted apoptosis ( < 0.01) and lowered the MMP ( < 0.01) of HN30 cells, and after treatment for 24 h, the cells showed significantly increased cleaved caspase-3 ( < 0.01) and decreased Bcl-2 expression ( < 0.01). Treatment with 10 μmol/L DTS for 16 h significantly inhibited Akt phosphorylation ( < 0.001) and enhanced p53 phosphorylation ( < 0.01) in HN30 cells. DTS inhibits proliferation and induces apoptosis of HN30 cells possibly through mechanisms involving the inhibition of Akt and the activation of p53. DTS inhibits proliferation an

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