Objective To investigate the potentiation of radiosensitivity and mechanism by tetrandrine(Tet) in human esophageal carcinoma cell line Eca-109.Methods The impact of radiosensitivity of Tet on human esophageal carcinoma cell line Eca-109 was determined by clonogenic assay, the distribution of cell cycle after radiation therapy was tested by flow cytometry, the expression of related cell cycle protein was analyzed by Western blotting and the influence of radiosensitivity of Tet on cell division was examined by mitotic index.Results The data of clonogenic assay showed that Tet markedly sensitized Eca-109 cell to γ-rays, and the sensitization enhancement ratio (SER) of Tet was 1.43.Flow cytometry assay showed that exposure of Eca-109 cells to γ-rays caused cells to arrest in G2 phase, whereas Tet was able to lower the number of cells arrested at G2 phase.Furthermore, the results showed that the levels of Cyclin B1 and Cdc2 expression decreased after γ-irradiance, and the mitotic index was lower too.Tet could reverse this decrease and induce γ-ray-irradiated cells to enter mitosis.Conclusion Tet markedly enhances the cytotoxicity of γ-irradiation.The mechanism is possibly associated with the abrogation of G2/M arrest in human esophageal carcinoma cell line Eca-109.%目的 研究汉防己甲素(Tet)在γ射线照射人食管癌细胞株Eca-109中的放射增敏作用,并探讨其机制.方法 采用克隆形成分析法测定Tet对人食管癌细胞株Eca-109放射敏感性的影响,流式细胞术分析Eca-109细胞经放射线照射后细胞周期的再分布情况,Western blotting法分析周期相关蛋白表达以及分裂指数法分析Tet对照射后细胞分裂的影响.结果 在Eca-109细胞中,Tet显著增加γ射线的杀伤作用,其增敏比为1.43;在γ射线照射后,细胞明显阻滞于G2期,Tet可以降低这种阻滞.Eca-109细胞在受到γ射线照射后其Cyclin B1与Cdc2蛋白表达水平明显降低,Tet可以逆转γ射线对Cyclin B1与Cdc2蛋白的表达的抑制作用.Tet可以促使阻滞于G2期的Eca-109细胞进人M期.结论 Tet能显著增加γ射线对人食管癌细胞的杀伤作用,其作用机制可能与Tet去除放射引起的G2/M期阻滞有关.
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