Author/Authors :
Li، نويسنده , , Yan-Cong and He، نويسنده , , Shu-Ming and He، نويسنده , , Zhi-Xu and Li، نويسنده , , Minghua and Yang، نويسنده , , Yinxue and Pang، نويسنده , , Jianxin and Zhang، نويسنده , , Xueji and Chow، نويسنده , , Kevin Zheng Zhou، نويسنده , , Qingyu and Duan، نويسنده , , Wei and Zhou، نويسنده , , Zhiwei and Yang، نويسنده , , Tianxin and Huang، نويسنده , , Gui-Hua and Liu، نويسنده , , Aibing and Qiu، نويسنده , , Jia-Xuan and Liu، نويسنده , , Jun-Ping and Zhou، نويسنده , , Shu-Feng، نويسنده ,
Abstract :
Plumbagin (PLB) has shown anti-cancer activity but the mechanism is unclear. This study has found that PLB has a potent pro-apoptotic and pro-autophagic effect on A549 and H23 cells. PLB arrests cells in G2/M phase, and increases the intracellular level of reactive oxygen species in both cell lines. PLB dose-dependently induces autophagy through inhibition of PI3K/Akt/mTOR pathway as indicated by reduced phosphorylation of Akt and mTOR. Inhibition or induction of autophagy enhances PLB-induced apoptosis. There is crosstalk between PLB-induced apoptosis and autophagy. These findings indicate that PLB initiates both apoptosis and autophagy in NSCLC cells through coordinated pathways.
Keywords :
Plumbagin , apoptosis , Non-small-cell lung cancer , Autophagy , PI3K/AKT/mTOR
