CAJ | 학술논문

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。
목적：연구 AMPK 신호통로재 ECG 유도인비인암세포주 C666-1조망중적작용。방법인비인암 C666-1세포급여 AMPK 특이성억제제 compound C 혹불동농도 ECG 처리후，분별채용 CCK-8법화 TUNEL 염색법검측세포증식정황화조망；채용 Western blotting 법검측 AMPK、p70S6K、S6등상관단백린산화수평。결과 ECG 가제량의뢰성지증가 C666-1세포중 AMPK 적린산화수평병억제 p70S6K 화 S6적린산화；급여 compound C 예처리지후가현저역전 ECG 대 C666-1세포증식화조망적영향，병역전 ECG 대 AMPK、p70S6K 화 S6등린산화수평적영향。결론ECG 통과조공 AMPK 의뢰적통로억제인비인암세포주 C666-1증식，병유도기조망。
Objective:To study whether AMPK participate in the effect of ECG on the apoptosis of nasopharyngeal car-cinoma 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 C666-1 cells. Western blotting was performed to detect the expression levels of p-AMPK,p-p70S6K and p-S6. Results:ECG in-creased the protein expression of p-AMPK and inhibited the expression level of p-p70S6K and p-S6 in C666-1 cells. Pre-treated with compound C abrogated the effect of ECG on the proliferation,apoptosis and the protein expression of p-AMPK, p-p70S6K and p-S6 in nasopharyngeal carcinoma cell line C666-1. Conclusion:ECG inhibits proliferation and induces ap-optosis of nasopharyngeal carcinoma cell line C666-1 by regulating AMPK-dependent signaling pathway.