EGCG通过抑制SIRT1表达抑制鼻咽癌细胞增殖

摘要

Objective To examine the effect of epigallocatechin gallate (EGCG) at different concentration (0,10,25, 50 and 100μmol/L ) on proliferation rate and apoptosis of nasopharyngeal carcinoma cell line C666-1 in vitro, and elucidate the role of silent information regulator 1 (SIRT1). Methods The proliferation rate in vitro of C666-1 cells stimulated by EGCG at increasing concentrations (0,10,25,50,and 100 μmol/L)for 24 h or at concentration of 50μmol/L for 0,6,12 h and 24 h were detected by cell counting kit-8 (CCK-8) assays. Cell were treated with EGCG at concentration of 0,25, 50 and 100 μmol/L for 24 h, cell apoptosis was anylysed by TUNEL assay and expression levels of SIRT1 protein was detected by western blotting. Results EGCG suppressed cell proliferation of C666-1 cell line in a concentration-dependent manner at concentration of 0 ,10,25,50,and 100μmol/L, and in a time-dependently when treated with 50 μmol/L for 12 to 24 h(P<0.05). After treated for 24 h with different concentration of EGCG at 0、25、50、100 μmol/L, cell apoptosis increased at concentration of 50 to 100μmol/L and expression of SIRT1 decreased in a concentration-dependently (P<0.05). Conclusion EGCG induced cell apoptosis of C666-1 cells by down-regulating SIRT1 expression.%目的：观察不同浓度（0、10、25、50、100μmol/L）表没食子儿茶素没食子酸酯（EGCG）对鼻咽癌细胞株C666-1的增殖及凋亡的影响，明确沉默信息调节因子（SIRT）1在其中的作用。方法：不同浓度（0、10、25、50、100μmol/EGCG作用C666-1细胞24 h后或50μmol/L的EGCG作用不同时间（0，6，12，24 h）， Cell Counting Kit-8（CCK-8）法检测其增殖情况；0、25、50、100μmol/L的EGCG作用24 h后，TUNEL法检测的细胞凋亡情况，Western blotting检测细胞内SIRT1蛋白表达情况。结果：0、10、25、50、100μmol/L的EGCG处理C666-1细胞24 h后，细胞增殖明显受到抑制，并呈剂量依赖性（P＜0．05）；而50μmol/L EGCG分别作用0、6、12、24 h时，12 h～24 h细胞增殖抑制明显被抑制（P＜0．05）。0、25、50、100μmol/L的EGCG处理C666-1细胞24 h后，50μmol/L的EGCG即可引起明显的细胞凋亡（P＜0．05），细胞内SIRT1的表达亦被明显抑制，且具有剂量依赖性（P＜0．05）。结论： EGCG通过诱导鼻咽癌细胞C666-1凋亡抑制其增殖， SIRT1可能参与该过程。