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dc.contributor.authorButton, RW
dc.contributor.authorLin, F
dc.contributor.authorErcolano, E
dc.contributor.authorVincent, JH
dc.contributor.authorHu, B
dc.contributor.authorHanemann, CO
dc.contributor.authorLuo, S
dc.contributor.editorFimia GM
dc.date.accessioned2016-05-18T10:54:19Z
dc.date.available2016-05-18T10:54:19Z
dc.date.issued2014-10
dc.identifier.issn2041-4889
dc.identifier.issn2041-4889
dc.identifier.othere1466
dc.identifier.urihttp://hdl.handle.net/10026.1/4649
dc.description.abstract

<jats:title>Abstract</jats:title><jats:p>Established as a potent anti-malaria medicine, artemisinin-based drugs have been suggested to have anti-tumour activity in some cancers. Although the mechanism is poorly understood, it has been suggested that artemisinin induces apoptotic cell death. Here, we show that the artemisinin analogue artesunate (ART) effectively induces cell death in RT4 schwannoma cells and human primary schwannoma cells. Interestingly, our data indicate for first time that the cell death induced by ART is largely dependent on necroptosis. ART appears to inhibit autophagy, which may also contribute to the cell death. Our data in human schwannoma cells show that ART can be combined with the autophagy inhibitor chloroquine (CQ) to potentiate the cell death. Thus, this study suggests that artemisinin-based drugs may be used in certain tumours where cells are necroptosis competent, and the drugs may act in synergy with apoptosis inducers or autophagy inhibitors to enhance their anti-tumour activity.</jats:p>

dc.format.extent0-0
dc.format.mediumElectronic
dc.languageen
dc.language.isoen
dc.publisherSpringer Science and Business Media LLC
dc.subjectApoptosis
dc.subjectArtemisinins
dc.subjectArtesunate
dc.subjectAutophagy
dc.subjectCell Line, Tumor
dc.subjectChloroquine
dc.subjectDrug Synergism
dc.subjectFree Radical Scavengers
dc.subjectHumans
dc.subjectNecrosis
dc.subjectNeurilemmoma
dc.subjectNuclear Pore Complex Proteins
dc.subjectRNA-Binding Proteins
dc.subjectReactive Oxygen Species
dc.titleArtesunate induces necrotic cell death in schwannoma cells
dc.typejournal-article
dc.typeArticle
plymouth.author-urlhttps://www.ncbi.nlm.nih.gov/pubmed/25321473
plymouth.issue10
plymouth.volume5
plymouth.publisher-urlhttp://dx.doi.org/10.1038/cddis.2014.434
plymouth.publication-statusPublished online
plymouth.journalCell Death & Disease
dc.identifier.doi10.1038/cddis.2014.434
plymouth.organisational-group/Plymouth
plymouth.organisational-group/Plymouth/Faculty of Health
plymouth.organisational-group/Plymouth/Faculty of Health/Peninsula Dental School
plymouth.organisational-group/Plymouth/Faculty of Health/Peninsula Medical School
plymouth.organisational-group/Plymouth/REF 2021 Researchers by UoA
plymouth.organisational-group/Plymouth/REF 2021 Researchers by UoA/UoA01 Clinical Medicine
plymouth.organisational-group/Plymouth/REF 2021 Researchers by UoA/UoA03 Allied Health Professions, Dentistry, Nursing and Pharmacy
plymouth.organisational-group/Plymouth/Research Groups
plymouth.organisational-group/Plymouth/Research Groups/Institute of Translational and Stratified Medicine (ITSMED)
plymouth.organisational-group/Plymouth/Research Groups/Institute of Translational and Stratified Medicine (ITSMED)/CBR
plymouth.organisational-group/Plymouth/Users by role
plymouth.organisational-group/Plymouth/Users by role/Academics
plymouth.organisational-group/Plymouth/Users by role/Researchers in ResearchFish submission
dc.publisher.placeEngland
dcterms.dateAccepted2014-09-08
dc.identifier.eissn2041-4889
dc.rights.embargoperiodNot known
rioxxterms.versionofrecord10.1038/cddis.2014.434
rioxxterms.licenseref.urihttp://www.rioxx.net/licenses/all-rights-reserved
rioxxterms.licenseref.startdate2014-10
rioxxterms.typeJournal Article/Review


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