Targeted production of reactive oxygen species in mitochondria to overcome cancer drug resistance

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dc.contributor.authorWang, Hai
dc.contributor.authorGao, Zan
dc.contributor.authorLiu, Xuanyou
dc.contributor.authorAgarwal, Pranay
dc.contributor.authorZhao, Shuting
dc.contributor.authorConroy, Daniel W.
dc.contributor.authorJi, Guang
dc.contributor.authorYu, Jianhua
dc.contributor.authorJaroniec, Christopher P.
dc.contributor.authorLiu, Zhenguo
dc.contributor.authorLu, Xiongbin
dc.contributor.authorLi, Xiaodong
dc.contributor.authorHe, Xiaoming
dc.date.accessioned2018-06-29T17:00:47Z
dc.date.available2018-06-29T17:00:47Z
dc.date.issued2018-02-08
dc.descriptionPartial funding for Open Access provided by the UMD Libraries' Open Access Publishing Fund.en_US
dc.description.abstractMultidrug resistance is a major challenge to cancer chemotherapy. The multidrug resistance phenotype is associated with the overexpression of the adenosine triphosphate (ATP)-driven transmembrane efflux pumps in cancer cells. Here, we report a lipid membrane-coated silica-carbon (LSC) hybrid nanoparticle that targets mitochondria through pyruvate, to specifically produce reactive oxygen species (ROS) in mitochondria under near-infrared (NIR) laser irradiation. The ROS can oxidize the NADH into NAD+ to reduce the amount of ATP available for the efflux pumps. The treatment with LSC nanoparticles and NIR laser irradiation also reduces the expression and increases the intracellular distribution of the efflux pumps. Consequently, multidrug-resistant cancer cells lose their multidrug resistance capability for at least 5 days, creating a therapeutic window for chemotherapy. Our in vivo data show that the drug-laden LSC nanoparticles in combination with NIR laser treatment can effectively inhibit the growth of multidrug-resistant tumors with no evident systemic toxicity.en_US
dc.identifierhttps://doi.org/10.13016/M2513TZ9H
dc.identifier.citationNature Communications, (2018) 9:562; DOI: 10.1038/s41467-018-02915-8en_US
dc.identifier.urihttp://hdl.handle.net/1903/20696
dc.language.isoen_USen_US
dc.publisherNature Publishing Groupen_US
dc.relation.isAvailableAtA. James Clark School of Engineeringen_us
dc.relation.isAvailableAtFischell Department of Bioengineeringen_us
dc.relation.isAvailableAtDigital Repository at the University of Marylanden_us
dc.relation.isAvailableAtUniversity of Maryland (College Park, MD)en_us
dc.titleTargeted production of reactive oxygen species in mitochondria to overcome cancer drug resistanceen_US
dc.typeArticleen_US

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