E7050对肺癌细胞EBC-1抗增殖作用及其机制的研究

Study on antiproliferative effect and mechanism of E7050 on EBC-1 lung cancer cells

目的研究E7050对人肺癌细胞系EBC-1的生长抑制作用及分子机制。方法人肺癌EBC-1细胞经不同剂量E7050作用后,应用四甲基偶氮唑蓝(MTT)法测定E7050对肺癌细胞系EBC-1的增殖抑制率;蛋白印迹法观察相关蛋白的表达;流式细胞术及Hoechst33342染色法检测E7050对EBC-1细胞的凋亡诱导作用。结果 E7050可有效抑制肺癌细胞的生长,且抑制率具有剂量效应依赖性。E7050还可以通过诱导EBC-1细胞凋亡抑制其增殖;同时,E7050可明显下调EBC-1细胞p-Met的表达,而c-Met基因没有变化。结论E7050可以通过诱导凋亡和下调p-Met表达体外抑制EBC-1肺癌细胞增殖。

[Objective] To investigate the effect of e-Met inhibitor E7050 on the growth inhibition of hu- man cancer line EBC-1. [Methods] The inhibitory effect of E7050 on EBC-1 proliferation was determined by MTT assay. Western Blot assay was used to detect the expression of related protein. Apoptotic features in EBC-1 cells treated with E7050 were analyzed by FCM and Hoechst 33342 dying method. [Results] E7050 can effectively inhibit the growth of human lung cancer EBC-1, which was in a dose-dependent manner. E7050 also can suppress the proliferation of EBC-1 cells by apoptotic induction. Meanwhile, E7050 could significantly reduce the expression of p-Met in EBC-1 cells. However, the expression of c-met was not de- creased. [Conclusion] E7050 could inhibit cell proliferation of EBC-1 cells by apoptotic induction and downregulation of p-met expression in vitro.