Objective. To explore the possible mechanisms of Tanshinone IIA (TanllA) on esophageal carcinoma cell lines. Methods. Two human esophageal carcinoma cell lines (EC-1 cells and ECa-109 cells) were treated with different concentrations of TanllA. Cell proliferation was measured by CCK-8, colony-forming efficiency was calculated, cell cycle and apoptosis were measured, and changes in cell cycle- and apoptosis-related gene expression were measured by Western blotting. Results. The CCK-8 and colony formation assay indicated that TanllA inhibited the cell proliferation of human esophageal cancer cells (IC50 below 1 mug/mL) at 48 h. Hoechst 33258 and flow cytometry showed that TanllA induced apoptosis in both esophageal cancer cell lines. Flow cytometry showed that TanllA arrested cell cycle in S phase and G2/M phase. Western blotting analysis showed that Akt1 and its phosphorylation were inhibited, the Bax/Bcl-2 ratio increased, and both caspase-9 and caspase-3 were activated after treatment with 1.3 mug/mL TanllA at 48 h. Meanwhile, p53 and p21 protein levels increased, whereas cyclin B1, CDC2, and CDC2 phosphorylation were inhibited. Conclusion. TanllA inhibits the growth of esophageal cancer cells and induces apoptosis in a time-dependent and concentration-dependent manner, possibly by affecting cell cycle- and apoptosis-related signaling pathways.
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