AMPK信号通路在ECG诱导人鼻咽癌细胞株C666-1凋亡中的作用研究  

ECG-induced cell apoptosis through AMPK signaling pathways in human nasopharyngeal carcinoma cell line C666-1

作　　者：蔡轶[1] 赵莉[1] 

机构地区：[1]广州医科大学药学院蛇毒研究所,广东广州511436

出　　处：《泰山医学院学报》2015年第7期721-724,共4页Journal of Taishan Medical College

基　　金：国家自然科学基金青年项目(81300085);广东省自然科学基金博士启动项目(S2013040013895);广东省科技计划项目-广东省高科技发展专项资金项目(2013B010403024);广州市教育局市属高校科技计划项目(1201430926);广州医科大学博士启动项目(2012C03)

摘　　要：目的研究AMPK信号通路在ECG诱导人鼻咽癌细胞株C666-1凋亡中的作用。方法人鼻咽癌C666-1细胞给予AMPK特异性抑制剂compound C或不同浓度ECG处理后,分别采用CCK-8法和TUNEL染色法检测细胞增殖情况和凋亡;采用Western blotting法检测AMPK、p70S6K、S6等相关蛋白磷酸化水平。结果 ECG可剂量依赖性地增加C666-1细胞中AMPK的磷酸化水平并抑制p70S6K和S6的磷酸化;给予compound C预处理之后可显著逆转ECG对C666-1细胞增殖和凋亡的影响,并逆转ECG对AMPK、p70S6K和S6等磷酸化水平的影响。结论ECG通过调控AMPK依赖的通路抑制人鼻咽癌细胞株C666-1增殖,并诱导其凋亡。Objective： To study whether AMPK participate in the effect of ECG on the apoptosis of nasopharyngeal carcinoma cell line C666-1. Methods： C666-1 cells were treated with different concentrations（ 0 - 100 μM） ECG or compound C,CCK-8 assay was used to evaluate the proliferation and Tunel assay was used to investigate the apoptosis of C666-1cells. Western blotting was performed to detect the expression levels of p-AMPK,p-p70S6 K and p-S6. Results： ECG increased the protein expression of p-AMPK and inhibited the expression level of p-p70S6 K and p-S6 in C666-1 cells. Pretreated with compound C abrogated the effect of ECG on the proliferation,apoptosis and the protein expression of p-AMPK,p-p70S6 K and p-S6 in nasopharyngeal carcinoma cell line C666-1. Conclusion： ECG inhibits proliferation and induces apoptosis of nasopharyngeal carcinoma cell line C666-1 by regulating AMPK-dependent signaling pathway.

关 键 词：表儿茶素没食子酸酯 AMP激活的蛋白激酶 C666-1 

分 类 号：R739.63[医药卫生—肿瘤]