Liu Liang, Ju Yingchao, Wang Jing, Zhou Rongmiao
Tumor Institute, The Fourth Hospital of Hebei Medical University, Shijiazhuang, Hebei, 050011, PR China.
Animal Experimental Center, The Fourth Hospital of Hebei Medical University, Shijiazhuang, Hebei, 050011, PR China.
Pathol Res Pract. 2017 Oct;213(10):1242-1250. doi: 10.1016/j.prp.2017.09.006. Epub 2017 Sep 12.
Evidence for demonstrating the role of the green tea component epigallocatechin-3-gallate (EGCG) in esophageal squamous cell carcinoma cells is limited. In this study, we investigated apoptosis induced by EGCG and the underlying molecular mechanisms in human esophageal squamous cell carcinoma cells. The growth-inhibitory effects of EGCG on esophageal cancer cell (Eca109 and Ec9706) were detected by MTT. Using flow cytometry, we determined the cellular apoptosis, bcl-2, bax and caspase-3 protein expression in Eca109 and Ec9706 cells following treatment with EGCG for 24h. After treatment of Eca109/ABCG2 (an esophageal cancer multidrug resistance cell line) cells with adriamycin (ADM) combined with EGCG for 24h, the cellular apoptosis, mitochondrial membrane potential, ADM concentration in cells and ABCG2 protein expression were detected by flow cytometry. EGCG inhibited the growth of Eca109 and Ec9706 cells in a dose- and time- dependent manner. EGCG induced apoptosis, decreased the bcl-2 protein expression and increased the expression of bax and caspase-3 protein. The rate of apoptosis and ADM concentration in the Eca109/ABCG2 cells following treatment with ADM and EGCG were higher than that with ADM treatment alone, although the mitochondrial membrane potential was significantly lower (P<0.01). EGCG reduced the ABCG2 expression of Eca109/ABCG2 cells. Our data indicated that EGCG inhibited cell growth and induced esophageal cancer cell apoptosis. It reduced the bcl-2 protein expression and increased the bax and caspase-3 protein expression. EGCG reversed multi-drug resistance by reducing ABCG2 expression and increasing the anticancer drug concentration in cancer cells.
关于绿茶成分表没食子儿茶素-3-没食子酸酯（EGCG）在食管鳞状细胞癌细胞中作用的证据有限。在本研究中，我们调查了EGCG诱导的人食管鳞状细胞癌细胞凋亡及其潜在的分子机制。通过MTT检测EGCG对食管癌细胞（Eca109和Ec9706）的生长抑制作用。使用流式细胞术，我们测定了用EGCG处理24小时后Eca109和Ec9706细胞中的细胞凋亡、bcl-2、bax和caspase-3蛋白表达。用阿霉素（ADM）联合EGCG处理Eca109/ABCG2（一种食管癌多药耐药细胞系）细胞24小时后，通过流式细胞术检测细胞凋亡、线粒体膜电位、细胞内ADM浓度和ABCG2蛋白表达。EGCG以剂量和时间依赖性方式抑制Eca109和Ec9706细胞的生长。EGCG诱导细胞凋亡，降低bcl-2蛋白表达，并增加bax和caspase-3蛋白的表达。用ADM和EGCG处理后，Eca109/ABCG2细胞中的凋亡率和ADM浓度高于单独用ADM处理，尽管线粒体膜电位显著降低（P<0.01）。EGCG降低了Eca109/ABCG2细胞的ABCG2表达。我们的数据表明，EGCG抑制细胞生长并诱导食管癌细胞凋亡。它降低bcl-2蛋白表达并增加bax和caspase-3蛋白表达。EGCG通过降低ABCG2表达和增加癌细胞中的抗癌药物浓度来逆转多药耐药性。
