研究紫铆因对人食管鳞癌细胞增殖和存活的影响。通过MTS和软琼脂集落实验检测紫铆因对食管鳞癌增殖的抑制, 生化分析仪检测紫铆因对食管鳞癌糖酵解的影响, 并利用免疫印迹检测紫铆因对食管鳞癌细胞增殖和凋亡激活相关蛋白分子的表达。结果发现紫铆因剂量依赖性抑制KYSE150和Eca109细胞增殖, 下调EGFR信号通路活化, 抑制HK2的表达及糖酵解。一定浓度的紫铆因能诱导食管鳞癌细胞发生凋亡, caspase3和PARP被剪切, Bcl-2和Mcl-1表达下调, 但Bcl-XL未见明显改变。结果证明紫铆因抑制食管鳞癌的增殖, 可能与EGFR信号通路和糖酵解被抑制, 及促存活蛋白Bcl-2和Mcl-1的表达下调有关。

To investigate the effects of butein on proliferation and apoptosis of human esophageal squamous cell carcinoma cells. The proliferation of KYSE150 and Eca109 cells was tested by MTS and soft agar assay. Glycolysis was evaluated through measurement of glucose uptake and lactate production. Meanwhile, the signaling transduction pathway after butein treatment and the expression of the protein which was involved in proliferation and apoptosis were tested via immunoblotting. We found that butein inhibited the proliferation of KYSE150 and Eca109 cells in a dose-dependent manner. The effects of butein mediated proliferation inhibition of human esophageal squamous cell carcinoma cells was related to the suppression of EGFR signaling pathway and down-regulation of glycolysis. A certain concentration of butein can directly induce apoptosis in human esophageal squamous cell carcinoma cells, which result in the activation of caspase3/PARP and down-regulation of the expression of Bcl-2 and Mcl-1. Our primary data demonstrated that the suppression of EGFR signaling pathway and glycolysis, as well as down-regulation of Bcl-2 and Mcl-1 expression are involved in butein mediated proliferation inhibition and apoptosis in human esophageal squamous cell carcinoma.