自噬
癌细胞
细胞生物学
A549电池
程序性细胞死亡
癌症研究
细胞凋亡
PI3K/AKT/mTOR通路
活力测定
细胞毒性T细胞
癌症
生物
化学
材料科学
信号转导
生物化学
体外
遗传学
作者
Mohd Shahnawaz Khan,Akbar Mohammad,Govil Patil,S.A.H. Naqvi,L. S. Chauhan,Iqbal Ahmad
出处
期刊:Biomaterials
[Elsevier]
日期:2012-02-01
卷期号:33 (5): 1477-1488
被引量:402
标识
DOI:10.1016/j.biomaterials.2011.10.080
摘要
Autophagy has attracted a great deal of research interest in tumor therapy in recent years. An attempt was made in this direction and now we report that iron oxide NPs synthesized by us selectively induce autophagy in cancer cells (A549) and not in normal cells (IMR-90). It was also noteworthy that autophagy correlated with ROS production as well as mitochondrial damage. Protection of NAC against ROS clearly suggested the implication of ROS in hyper-activation of autophagy and cell death. Pre-treatment of cancer cells with 3-MA also exhibited protection against autophagy and promote cellular viability. Results also showed involvement of classical mTOR pathway in autophagy induction by iron oxide NPs in A549 cells. Our results had shown that bare iron oxide NPs are significantly cytotoxic to human cancer cells (A549) but not to the normal human lung fibroblast cells (IMR-90).In other words our nanoparticles selectively kill cancerous cells. It is encouraging to conclude that iron oxide NPs bear the potential of its applications in biomedicine, such as tumor therapy specifically by inducing autophagy mediated cell death of cancer cells.
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