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PRMT1-dependent methylation of BRCA1 contributes to the epigenetic defense of breast cancer cells against ionizing radiation

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dc.contributor.authorGonzález Guerrero, Rebeca
dc.contributor.authorPiñero Madrona, Antonio
dc.contributor.authorCabezas Herrera, Juan
dc.contributor.authorMontenegro Arce, María Fernanda
dc.contributor.authorRodríguez López, José Neptuno
dc.contributor.authorSánchez del Campo Ferrer, Luis
dc.contributor.departmentBioquímica y Biología Molecular Aes
dc.date.accessioned2024-02-01T11:35:35Z
dc.date.available2024-02-01T11:35:35Z
dc.date.issued2020-08-06
dc.description©2020. This manuscript version is made available under the CC-BY 4.0 license http://creativecommons.org/licenses/by-nc-nd/4.0/ This document is the Published Manuscript version of a Published Work that appeared in final form in Scientific Reports. To access the final edited and published work see https://doi.org/10.1038/s41598-020-70289-3es
dc.description.abstractThe therapeutic effect of irradiation is thought to come from DNA damage that affects rapidly proliferating cancer cells; however, resistant cells rapidly initiate mechanisms to repair such damage. While DNA repair mechanisms responsible for cancer cell survival following DNA damage are understood, less is known about the epigenetic mechanisms resulting in resistance to radiotherapy. Although changes in DNA methylation are related to mechanisms of long-term resistance, it is more likely that the methylation state of a series of proteins could be responsible for the first-line of defense of cancer cells against irradiation. In this study, we observed that irradiation of breast cancer cells was accompanied by an overproduction in S-adenosylmethionine, which increases the activity of cellular methylases. We found that by activating PRMT1, irradiation triggers a BRCA1-dependent program that results in efficient DNA repair and inhibition of apoptosis. Depletion of PRMT1 in irradiated cells resulted in a switch of BRCA1 functions from repair and survival in the nucleus to activation of cell death signals in the cytoplasm. We conclude that by modulating the cellular localization of BRCA1, PRMT1 is an important regulator of the oncogenic functions of BRCA1, contributing to the epigenetic defense of breast cancer cells against ionizing radiation.es
dc.formatapplication/pdfes
dc.format.extent14es
dc.identifier.citationScientific Reports, Volumen 10 ,nº 13275, 2020
dc.identifier.doi10.1038/s41598-020-70289-3
dc.identifier.issn2045-2322
dc.identifier.urihttp://hdl.handle.net/10201/138354
dc.languageenges
dc.publisherSpringer Naturees
dc.relationÁmbito del proyecto: Nacional y regional - Agencia financiadora: Ministerio de Economía y Competitividad (MINECO; Co-financing with Fondos FEDER) y Fundación Séneca, the Región de Murcia (FS-RM) - Código o número del acuerdo de subvención: SAF2016-77241-R y 20809/PI/18es
dc.relation.isreplacedby10.1038/s41598-020-70289-3es
dc.relation.publisherversionhttps://doi.org/10.1038/s41598-020-70289-3es
dc.rightsinfo:eu-repo/semantics/openAccesses
dc.rightsAttribution-NonCommercial-NoDerivatives 4.0 Internacional*
dc.rights.urihttp://creativecommons.org/licenses/by-nc-nd/4.0/*
dc.subjectBreast canceres
dc.subjectMethylationes
dc.subjectSAMes
dc.subjectPRMT1es
dc.subjectEpigenetices
dc.subject.otherCDU::5 - Ciencias puras y naturales::57 - Biología::577 - Bioquímica. Biología molecular. Biofísicaes
dc.titlePRMT1-dependent methylation of BRCA1 contributes to the epigenetic defense of breast cancer cells against ionizing radiationes
dc.typeinfo:eu-repo/semantics/articlees
dspace.entity.typePublicationes
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relation.isAuthorOfPublication36d7ac7e-b9a7-477c-8f7e-f03d4cc834c1
relation.isAuthorOfPublicationf702e5be-3f82-4512-b2a2-6c69a5cb98ff
relation.isAuthorOfPublication.latestForDiscovery2d4e44e6-9dda-4146-8aef-fe0c6b5a8b8f
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