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dc.contributor.authorBee, A
dc.contributor.authorBrewer, D
dc.contributor.authorBeesley, C
dc.contributor.authorDodson, A
dc.contributor.authorForootan, S
dc.contributor.authorDickinson, T
dc.contributor.authorGerard, P
dc.contributor.authorLane, B
dc.contributor.authorYao, S
dc.contributor.authorCooper, CS
dc.contributor.authorDjamgoz, MBA
dc.contributor.authorGosden, CM
dc.contributor.authorKe, Y
dc.contributor.authorFoster, CS
dc.date.accessioned2018-08-13T11:31:41Z
dc.date.issued2011-07-22
dc.identifier7
dc.identifier.citationPLOS ONE, 2011, 6
dc.identifier.issn1932-6203
dc.identifier.urihttps://repository.icr.ac.uk/handle/internal/2323
dc.identifier.doi10.1371/journal.pone.0022672
dc.description.abstractWe provide novel functional data that posttranscriptional silencing of gene RPL19 using RNAi not only abrogates the malignant phenotype of PC-3M prostate cancer cells but is selective with respect to transcription and translation of other genes. Reducing RPL19 transcription modulates a subset of genes, evidenced by gene expression array analysis and Western blotting, but does not compromise cell proliferation or apoptosis in-vitro. However, growth of xenografted tumors containing the knocked-down RPL19 in-vivo is significantly reduced. Analysis of the modulated genes reveals induction of the non-malignant phenotype principally to involve perturbation of networks of transcription factors and cellular adhesion genes. The data provide evidence that extra-ribosomal regulatory functions of RPL19, beyond protein synthesis, are critical regulators of cellular phenotype. Targeting key members of affected networks identified by gene expression analysis raises the possibility of therapeutically stabilizing a benign phenotype generated by modulating the expression of an individual gene and thereafter constraining a malignant phenotype while leaving non-malignant tissues unaffected.
dc.languageeng
dc.language.isoeng
dc.publisherPUBLIC LIBRARY SCIENCE
dc.rights.urihttps://creativecommons.org/licenses/by/4.0
dc.titlesiRNA Knockdown of Ribosomal Protein Gene RPL19 Abrogates the Aggressive Phenotype of Human Prostate Cancer
dc.typeJournal Article
rioxxterms.versionofrecord10.1371/journal.pone.0022672
rioxxterms.licenseref.urihttps://creativecommons.org/licenses/by/4.0
rioxxterms.licenseref.startdate2011-07-22
rioxxterms.typeJournal Article/Review
dc.relation.isPartOfPLOS ONE
pubs.notesaffiliation: Bee, A (Reprint Author), Univ Liverpool, Inst Translat Med, Dept Mol & Clin Canc Med, Sect Cellular Pathol & Mol Genet, Liverpool L69 3BX, Merseyside, England. Bee, Alix; Beesley, Carol; Dodson, Andrew; Forootan, Shiva; Dickinson, Timothy; Gerard, Patricia; Yao, Sheng; Gosden, Christine M.; Ke, Youqiang; Foster, Christopher S., Univ Liverpool, Inst Translat Med, Dept Mol & Clin Canc Med, Sect Cellular Pathol & Mol Genet, Liverpool L69 3BX, Merseyside, England. Brewer, Daniel; Cooper, Colin S., Inst Canc Res, Mol Carcinogenesis Grp, Sutton, Surrey, England. Lane, Brian, Univ Liverpool, Ctr Genom Res, Liverpool Microarray Facil, Liverpool L69 3BX, Merseyside, England. Djamgoz, Mustafa B. A., Univ London Imperial Coll Sci Technol & Med, Div Cell & Mol Biol, London, England. article-number: e22672 keywords-plus: DIAMOND-BLACKFAN ANEMIA; EPITHELIAL-STROMAL INTERACTIONS; HIGH-LEVEL EXPRESSION; CELL-LINE PC-3; BREAST-CANCER; SIALIC-ACID; DIFFERENTIAL EXPRESSION; EUKARYOTIC RIBOSOME; COLORECTAL-CANCER; MESSENGER-RNA research-areas: Science & Technology - Other Topics web-of-science-categories: Multidisciplinary Sciences author-email: [email protected] researcherid-numbers: Brewer, Daniel/D-6201-2018 orcid-numbers: Brewer, Daniel/0000-0003-4753-9794 funding-acknowledgement: North West Cancer Research Fund (UK); Cancer Research-UK; National Cancer Research Institute (MRC-UK); US National Cancer Institute (USA); Grand Charity of Freemasons; Rosetrees Trust; Bob Champion Cancer Trust; Orchid Appeal and David Koch Foundation funding-text: This work was funded by the North West Cancer Research Fund (UK), Cancer Research-UK, the National Cancer Research Institute (MRC-UK), a Specialized Program of Research Excellence (SPORE) grant from the US National Cancer Institute (USA), Grand Charity of Freemasons, Rosetrees Trust, The Bob Champion Cancer Trust, The Orchid Appeal and David Koch Foundation. Funding bodies had no involvement in the design and conduct of the study, in collection management, analysis and interpretation of the data, or in preparation, review and approval of the paper. number-of-cited-references: 119 times-cited: 25 usage-count-last-180-days: 0 usage-count-since-2013: 6 journal-iso: PLoS One doc-delivery-number: 797BJ unique-id: ISI:000293097300079 oa: gold da: 2018-08-13
pubs.notesNot known
pubs.organisational-group/ICR
pubs.organisational-group/ICR/Primary Group
pubs.organisational-group/ICR/Primary Group/ICR Divisions
pubs.organisational-group/ICR/Primary Group/ICR Divisions/Closed research teams
pubs.organisational-group/ICR/Primary Group/ICR Divisions/Closed research teams/Cell Transformation
pubs.organisational-group/ICR
pubs.organisational-group/ICR/Primary Group
pubs.organisational-group/ICR/Primary Group/ICR Divisions
pubs.organisational-group/ICR/Primary Group/ICR Divisions/Closed research teams
pubs.organisational-group/ICR/Primary Group/ICR Divisions/Closed research teams/Cell Transformation
pubs.volume6
pubs.embargo.termsNot known
icr.researchteamCell Transformationen_US
dc.contributor.icrauthorCooper, Colinen


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