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dc.contributor.authorGarland, Gavin D
dc.contributor.authorDucray, Stephen
dc.contributor.authorJahangiri, Leila
dc.contributor.authorPucci, Perla
dc.contributor.authorAmos Burke, GA
dc.contributor.authorMonahan, Jack
dc.contributor.authorLai, Raymond
dc.contributor.authorMerkel, Olaf
dc.contributor.authorSchiefer, Ana-Iris
dc.contributor.authorKenner, Lukas
dc.contributor.authorBannister, Andrew
dc.contributor.authorTurner, Suzanne
dc.date.accessioned2022-01-05T00:31:20Z
dc.date.available2022-01-05T00:31:20Z
dc.date.issued2021-12-29
dc.identifier.issn2072-6694
dc.identifier.urihttps://www.repository.cam.ac.uk/handle/1810/331950
dc.description.abstract<jats:p>Anaplastic large-cell lymphoma (ALCL) is a T-cell malignancy driven in many cases by the product of a chromosomal translocation, nucleophosmin–anaplastic lymphoma kinase (NPM-ALK). NPM-ALK activates a plethora of pathways that drive the hallmarks of cancer, largely signalling pathways normally associated with cytokine and/or T-cell receptor-induced signalling. However, NPM-ALK is also located in the nucleus and its functions in this cellular compartment for the most part remain to be determined. We show that ALCL cell lines and primary patient tumours express the transcriptional activator BRG1 in a NPM-ALK-dependent manner. NPM-ALK regulates expression of BRG1 by post-translational mechanisms dependent on its kinase activity, protecting it from proteasomal degradation. Furthermore, we show that BRG1 drives a transcriptional programme associated with cell cycle progression. In turn, inhibition of BRG1 expression with specific shRNA decreases cell viability, suggesting that it may represent a key therapeutic target for the treatment of ALCL.</jats:p>
dc.publisherMDPI AG
dc.rightsAttribution 4.0 International
dc.rights.urihttps://creativecommons.org/licenses/by/4.0/
dc.titleBRG1 and NPM-ALK Are Co-Regulated in Anaplastic Large-Cell Lymphoma; BRG1 Is a Potential Therapeutic Target in ALCL
dc.typeArticle
dc.publisher.departmentDepartment of Pathology
dc.date.updated2021-12-28T09:12:50Z
prism.publicationNameCancers
dc.identifier.doi10.17863/CAM.79399
dcterms.dateAccepted2021-12-28
rioxxterms.versionofrecord10.3390/cancers14010151
rioxxterms.versionVoR
dc.contributor.orcidDucray, Stephen [0000-0001-6407-1906]
dc.contributor.orcidJahangiri, Leila [0000-0003-0235-8447]
dc.contributor.orcidPucci, Perla [0000-0003-1264-3487]
dc.contributor.orcidLai, Raymond [0000-0002-6963-2407]
dc.contributor.orcidSchiefer, Ana-Iris [0000-0003-3555-8672]
dc.contributor.orcidKenner, Lukas [0000-0003-2184-1338]
dc.contributor.orcidBannister, Andrew [0000-0002-6312-4436]
dc.contributor.orcidTurner, Suzanne [0000-0002-8439-4507]
dc.identifier.eissn2072-6694
rioxxterms.typeJournal Article/Review
pubs.funder-project-idEuropean Commission Horizon 2020 (H2020) Marie Sk?odowska-Curie actions (675712)
pubs.funder-project-idCancer Research UK (A25117)
cam.issuedOnline2021-12-29
cam.depositDate2021-12-28
pubs.licence-identifierapollo-deposit-licence-2-1
pubs.licence-display-nameApollo Repository Deposit Licence Agreement


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Attribution 4.0 International
Except where otherwise noted, this item's licence is described as Attribution 4.0 International