探讨C-Myc与有丝分裂期检查点蛋白BubR1的表达关系和对紫杉醇药物作用的可能影响。用免疫组化方法检测23例食管鳞癌组织标本中C-Myc和BubR1的表达水平,并通过免疫印迹的方法比较3株食管鳞癌细胞株ECA-109,KYSE150和KYSE180中C-Myc和BubR1的表达高低,分析相关性;将人BUB1b基因启动子上游约2000bp片段插入pSEAP2分泌型碱性磷酸酶报告质粒中构建为pSEAP2-BubR1-P2000,分别转染至3株鳞癌细胞内,检测启动子激活效果;在ECA-109细胞内过表达C-Myc后再转染pSEAP2-BubR1-P2000后,检测启动子的激活效果;免疫印迹方法检测C-Myc抑制剂10058-F4对BubR1蛋白表达的影响;通过MTT检测10058-F4干扰C-Myc后ECA-109细胞在梯度紫杉醇浓度下的生存率变化;最后通过DAPI染色观察单用C-Myc抑制剂,单用低浓度紫杉醇(100nM)或联用10058-F4和紫杉醇组的凋亡比例。结果发现在临床食管鳞癌标本和食管鳞癌细胞株中C-Myc和BubR1的表达有相关一致性;C-Myc高表达的细胞株中BubR1启动子活性的激活程度更强,并且过表达C-Myc后能进一步上调启动子活性;C-Myc特异性抑制剂10058-F4可以有效下调BubR1表达,并减低细胞在梯度紫杉醇作用下的细胞生存率。DAPI染色结果显示联用10058-F4和低浓度紫杉醇能明显增加细胞处于有丝分裂期的比率。在食管鳞癌细胞中C-Myc能上调有丝分裂期检查点蛋白BuR1的水平,并与食管癌对紫杉醇的敏感性相关,C-Myc可能通过上调BubR1表达而减低食管鳞癌对紫杉醇的反应。 To investigate the relationship between the expression of C-Myc and the mitotic checkpoint protein BubR1 and its possible effect on paclitaxel drug effects. The expression of C-Myc and BubR1 in 23 cases of esophageal squamous cell carcinoma were detected by immunohistochemistry. The expressions of C-Myc and BubR1 in 3 esophageal squamous cell carcinoma cell lines ECA-109, KYSE150 and KYSE180 were compared by Western blotting The upstream of human BUB1b promoter about 2000bp was inserted into pSEAP2 secreting alkaline phosphatase reporter plasmids to construct pSEAP2-BubR1-P2000 and transfected into 3 squamous cell carcinoma cells respectively, The effect of promoter activation was detected after overexpression of C-Myc in ECA-109 cells and pSEAP2-BubR1-P2000. Western blotting was used to detect the expression of BubR1 in C-Myc inhibitor 10058-F4 The survival rate of ECA-109 cells after exposure to C-Myc with 10058-F4 was detected by MTT assay. The survival rate of ECA-109 cells was evaluated by DAPI staining with C-Myc inhibitor alone. Apoptosis ratio with 10058-F4 and paclitaxel groups. The results showed that there was a correlation between C-Myc and BubR1 expression in esophageal squamous cell carcinoma and esophageal squamous cell carcinoma; BubR1 promoter activity was more activated in C-Myc-overexpressing cell lines, and overexpression of C -Myc can further up-regulate the promoter activity; C-Myc-specific inhibitor 10058-F4 can effectively down-regulate the expression of BubR1 and decrease the cell viability under the action of gradient paclitaxel. DAPI staining showed that the combination of 10058-F4 and low concentration of paclitaxel significantly increased the cell mitosis ratio. C-Myc can upregulate the level of BuR1 at the mitotic checkpoint in esophageal squamous carcinoma cells and is correlated with the sensitivity of paclitaxel to esophageal cancer. C-Myc may reduce the response of paclitaxel to esophageal squamous carcinoma by up-regulating the expression of BubR1.