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Kim, S.E.* ; Zhang, L.* ; Ma, K.* ; Riegman, M.* ; Chen, F.* ; Ingold, I. ; Conrad, M. ; Turker, M.Z.* ; Gao, M.* ; Jiang, X.* ; Monette, S.* ; Pauliah, M.* ; Gonen, M.* ; Zanzonico, P.* ; Quinn, T.* ; Wiesner, U.* ; Bradbury, M.S.* ; Overholtzer, M.*

Ultrasmall nanoparticles induce ferroptosis in nutrient-deprived cancer cells and suppress tumour growth.

Nat. Nanotechnol. 11, 977-985 (2016)
Verlagsversion Postprint Forschungsdaten DOI
Open Access Green
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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Publikationstyp Artikel: Journalartikel
Dokumenttyp Wissenschaftlicher Artikel
ISSN (print) / ISBN 1748-3387
e-ISSN 1748-3395
Zeitschrift Nature Nanotechnology
Quellenangaben Band: 11, Heft: , Seiten: 977-985 Artikelnummer: , Supplement: ,
Verlag Nature Publishing Group
Verlagsort London
Begutachtungsstatus Peer reviewed