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BRG1 and NPM-ALK Are Co-Regulated in Anaplastic Large-Cell Lymphoma; BRG1 Is a Potential Therapeutic Target in ALCL.

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cam.issuedOnline2021-12-29
dc.contributor.authorGarland, Gavin D
dc.contributor.authorDucray, Stephen P
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 J
dc.contributor.authorTurner, Suzanne D
dc.contributor.orcidDucray, Stephen P [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 J [0000-0002-6312-4436]
dc.contributor.orcidTurner, Suzanne D [0000-0002-8439-4507]
dc.date.accessioned2022-01-07T16:53:05Z
dc.date.available2022-01-07T16:53:05Z
dc.date.issued2021-12-29
dc.date.updated2022-01-07T16:53:05Z
dc.description.abstractAnaplastic 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.
dc.identifier.doi10.17863/CAM.79867
dc.identifier.eissn2072-6694
dc.identifier.issn2072-6694
dc.identifier.urihttps://www.repository.cam.ac.uk/handle/1810/332421
dc.languageen
dc.language.isoeng
dc.publisherMDPI AG
dc.publisher.urlhttp://dx.doi.org/10.3390/cancers14010151
dc.subjectALCL
dc.subjectBrg1
dc.subjectNPM-ALK
dc.titleBRG1 and NPM-ALK Are Co-Regulated in Anaplastic Large-Cell Lymphoma; BRG1 Is a Potential Therapeutic Target in ALCL.
dc.typeArticle
dcterms.dateAccepted2021-12-28
prism.issueIdentifier1
prism.publicationNameCancers (Basel)
prism.volume14
pubs.funder-project-idEuropean Commission Horizon 2020 (H2020) Marie Sk?odowska-Curie actions (675712)
pubs.funder-project-idCancer Research UK (A25117)
pubs.funder-project-idCancer Research UK (C6946/A24843)
pubs.funder-project-idWellcome Trust (203144/A/16/Z)
rioxxterms.licenseref.urihttps://creativecommons.org/licenses/by/4.0/
rioxxterms.versionVoR
rioxxterms.versionofrecord10.3390/cancers14010151

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