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Modulating the unfolded protein response with ONC201 to impact on radiation response in prostate cancer cells

2021-12Artigo científico Acesso aberto
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dc.contributor.authorAmoroso, Francesca
dc.contributor.authorGlass, Kimberley
dc.contributor.authorSingh, Reema
dc.contributor.authorLiberal, Francisco
dc.contributor.authorSteele, Rebecca E.
dc.contributor.authorMaguire, Sarah
dc.contributor.authorTarapore, Rohinton
dc.contributor.authorAllen, Joshua E.
dc.contributor.authorVan Schaeybroeck, Sandra
dc.contributor.authorButterworth, Karl T.
dc.contributor.authorPrise, Kevin
dc.contributor.authorO’Sullivan, Joe M.
dc.contributor.authorJain, Suneil
dc.contributor.authorWaugh, David J.
dc.contributor.authorMills, Ian G.
dc.contributor.institutionFaculdade de Ciências e Tecnologia (FCT)
dc.contributor.pblNature Publishing Group
dc.date.accessioned2022-12-02T22:13:25Z
dc.date.available2022-12-02T22:13:25Z
dc.date.issued2021-12
dc.descriptionFunding Information: This work was supported by Movember Prostate Cancer UK Centre of Excellence (CEO13_2-004) to JOS and DJW and also by a grant from the Norwegian Research Council (230559) to IGM. IGM is also supported by the John Black Charitable Research Foundation. The authors acknowledge the Genomic Core Technology Unit, CCRCB, Queen’s University Belfast that performed the RNA-Seq Sequencing; the support of Fundação para a Ciência e Tecnologia (FCT-MCTES), Radiation Biology and Biophysics Doctoral Training Programme (RaBBiT, PD/00193/2012); and scholarships grants number SFRH/BD/114448/2016 to (FL). Publisher Copyright: © 2021, The Author(s).
dc.description.abstractProstate cancer (PCa) is the most common non-cutaneous cancer in men and a notable cause of cancer mortality when it metastasises. The unfolded protein response (UPR) can be cytoprotective but when acutely activated can lead to cell death. In this study, we sought to enhance the acute activation of the UPR using radiation and ONC201, an UPR activator. Treating PCa cells with ONC201 quickly increased the expression of all the key regulators of the UPR and reduced the oxidative phosphorylation, with cell death occurring 72 h later. We exploited this time lag to sensitize prostate cancer cells to radiation through short-term treatment with ONC201. To understand how priming occurred, we performed RNA-Seq analysis and found that ONC201 suppressed the expression of cell cycle and DNA repair factors. In conclusion, we have shown that ONC201 can prime enhanced radiation response.en
dc.description.versionpublishersversion
dc.description.versionpublished
dc.format.extent2711541
dc.identifier.doi10.1038/s41598-021-83215-y
dc.identifier.issn2045-2322
dc.identifier.otherPURE: 45531474
dc.identifier.otherPURE UUID: 267d8978-7afe-4dea-9d76-673aaa9be745
dc.identifier.otherScopus: 85101207566
dc.identifier.otherPubMed: 33608585
dc.identifier.otherWOS: 000621514400002
dc.identifier.otherPubMedCentral: PMC7896060
dc.identifier.urihttp://hdl.handle.net/10362/145942
dc.identifier.urlhttps://www.scopus.com/pages/publications/85101207566
dc.language.isoeng
dc.peerreviewedyes
dc.subjectGeneral
dc.subjectSDG 3 - Good Health and Well-being
dc.titleModulating the unfolded protein response with ONC201 to impact on radiation response in prostate cancer cellsen
dc.typejournal article
degois.publication.issue1
degois.publication.titleScientific Reports
degois.publication.volume11
dspace.entity.typePublication
rcaap.rightsopenAccess

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