目的：研究去甲斑蝥素对人食管鳞癌Ec9706细胞的致凋亡作用及其可能的作用机制，为去甲斑蝥素应用于临床抗癌治疗提供实验依据。 方法：不同质量浓度去甲斑蝥素 (0、5、10、20、40 μg/ml)分别作用Ec9706细胞不同时间(12、24和48 h)后，MTT方法检测细胞增殖抑制率，流式细胞术检测细胞凋亡及Caspase-3和Survivin蛋白表达的变化。结果：去甲斑蝥素作用后Ec9706细胞呈现不同程度的增殖抑制，而且细胞增殖抑制程度随作用剂量及时间增加不断增强，40 μg/ml去甲斑蝥素作用48 h时，Ec9706细胞增殖抑制率达（80.00±2.15）%。去甲斑蝥素显著诱导Ec9706细胞凋亡，其20 μg/ml作用48 h时，Ec9706细胞的凋亡率达（38.57±1.76）%。去甲斑蝥素作用后，Ec9706细胞中Caspase-3蛋白水平显著增高，而Survivin蛋白水平显著降低(P<0.05)。结论：去甲斑蝥素明显诱导食管癌Ec9706细胞凋亡，其作用机制可能与下调细胞Survivin蛋白及上调Caspase-3蛋白表达有关。

Objective: To study the effect of norcantharidin on apoptosis of esophageal cancer Ec9706 cells and the putative mechanism(s) underlying the effect. Methods: Ec9706 cells were treated with norcantharidin at 0, 5, 10, 20 or 40 μg/ml. Cell viability was determined by MTT assays and apoptosis, caspase-3 and survivin protein levels in the treated Ec9706 cells were assessed by flow cytometry, respectively, at 12, 24 and 48 h after treatment. Results: Norcantharidin inhibited the growth of Ec9706 cells in a dose- and time-dependent manner; the growth inhibition rate was (80.00±215)% at 40 μg/ml for 48 h. Norcantharidin induced apoptosis, significantly increased caspase-3 protein level (P<0.05) and significantly decreased survivin protein level (P<0.05) in Ec9706 cells in a dose- and time-dependent manner; the apoptosis rate was 38.57±1.76%at 20 μg/ml for 48h. Conclusion: Norcantharidin may induce apoptosis of esophageal cancer Ec9706 cells through downregulation of survivin expression and upregulation of caspase-3 expression.

河北省自然科学基金资助项目(No. H2012206107)，河北省普通高等学校强势特色学科肿瘤学建设经费(No. \[2005\]52) 。