纳米医学
程序性细胞死亡
乙二醇
癌细胞
纳米颗粒
癌症研究
化学
癌症
细胞凋亡
生物物理学
纳米技术
材料科学
生物
生物化学
遗传学
有机化学
作者
Sung Eun Kim,Li Zhang,Kai Ma,Michelle Riegman,Feng Chen,Irina Ingold,Marcus Conrad,Melik Z. Turker,Minghui Gao,Xuejun Jiang,Sébastien Monette,Mohan Pauliah,Mithat Gönen,Pat Zanzonico,Thomas P. Quinn,Ulrich Wiesner,Michelle S. Bradbury,Michael Overholtzer
标识
DOI:10.1038/nnano.2016.164
摘要
The design of cancer-targeting particles with precisely tuned physicochemical properties may enhance the delivery of therapeutics and access to pharmacological targets. However, a molecular-level understanding of the interactions driving the fate of nanomedicine in biological systems remains elusive. Here, we show that ultrasmall (<10 nm in diameter) poly(ethylene glycol)-coated silica nanoparticles, functionalized with melanoma-targeting peptides, can induce a form of programmed cell death known as ferroptosis in starved cancer cells and cancer-bearing mice. Tumour xenografts in mice intravenously injected with nanoparticles using a high-dose multiple injection scheme exhibit reduced growth or regression, in a manner that is reversed by the pharmacological inhibitor of ferroptosis, liproxstatin-1. These data demonstrate that ferroptosis can be targeted by ultrasmall silica nanoparticles and may have therapeutic potential.
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