Plumbagin induces apoptotic and autophagic cell death through inhibition of the PI3K/Akt/mTOR pathway in human non-small cell lung cancer cells
Plumbagin induces apoptotic and autophagic cell death through inhibition of the PI3K/Akt/mTOR pathway in human non-small cell lung cancer cells
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DOI：
10.1016/j.canlet.2013.11.001
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发表时间：
2014-03-28
期刊：
影响因子：
9.7
通讯作者：
Zhou, Shu-Feng
中科院分区：
文献类型：
--
作者：
Li, Yan-Cong;He, Shu-Ming;Zhou, Shu-Feng
白花丹素（PLB）已显示出抗癌活性，但其机制尚不清楚。本研究发现 PLB 对 A549 和 H23 细胞具有有效的促凋亡和促自噬作用。 PLB 将细胞阻滞在 G2/M 期，并增加两种细胞系中活性氧的细胞内水平。 PLB 剂量依赖性地通过抑制 PI3K/Akt/mTOR 通路诱导自噬，Akt 和 mTOR 磷酸化减少表明这一点。抑制或诱导自噬可增强 PLB 诱导的细胞凋亡。 PLB 诱导的细胞凋亡和自噬之间存在串扰。这些发现表明 PLB 通过协调途径启动 NSCLC 细胞的凋亡和自噬。 (C) 2013 Elsevier Ireland Ltd. 保留所有权利。
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. (C) 2013 Elsevier Ireland Ltd. All rights reserved.