自噬
PI3K/AKT/mTOR通路
细胞凋亡
赫拉
安普克
细胞生物学
蛋白激酶B
化学
RPTOR公司
癌症研究
人参皂甙
癌细胞
程序性细胞死亡
细胞生长
磷酸化
细胞
生物
癌症
医学
蛋白激酶A
生物化学
病理
替代医学
遗传学
人参
作者
Shuai Bian,Meichen Liu,Yang Song,Shuyan Lu,Siming Wang,Xueyuan Bai,Daqing Zhao,Jiawen Wang
摘要
20(S)-Ginsenoside Rh2 (GRh2) has various biological activities including anticancer effects. However, no reports have investigated the connection between autophagy and apoptosis in HeLa cells treated with 20(S)-GRh2. In this study, we found that 20(S)-GRh2 suppressed proliferation and induced apoptosis in HeLa cells by activating the intrinsic apoptotic pathway and causing mitochondrial dysfunction. 20(S)-GRh2 enhanced cell autophagy through promoting the phosphorylation of AMPK, depressed the phosphorylation of AKT, and suppressed mTOR activity. Furthermore, treatment with the autophagy inhibitor 3-methyladenine (3-MA) enhanced 20(S)-GRh2-induced apoptosis, while the autophagy inducer rapamycin promoted cell survival. Moreover, the apoptosis inhibitor Z-VAD-FMK significantly restrained the apoptosis and autophagy induced by 20(S)-GRh2 in HeLa cells. We found that 20(S)-ginsenoside Rh2-induced protective autophagy promotes apoptosis of cervical cancer cells by inhibiting AMPK/mTOR pathway.
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