Publication:
Targeting the epigenetic machinery of cancer cells

dc.contributor.authorFernández Pérez, María Piedad
dc.contributor.authorSáez Ayala, Magalí
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.accessioned2024-12-10T09:12:03Z
dc.date.available2024-12-10T09:12:03Z
dc.date.issued2014-01-27
dc.description© 2014, The authors. This manuscript version is made available under the CC-BY-NC-ND 4.0 license http://creativecommons.org/licenses/by-nc-nd/4.0/ This document is the Accepted version of a Published Work that appeared in final form in Oncogene. To access the final edited and published work see https://doi.org/10.1038/onc.2013.605es
dc.description.abstractCancer is characterised by uncontrolled cell growth and the acquisition of metastatic properties. In most cases, the activation of oncogenes and/or deactivation of tumour suppressor genes lead to uncontrolled cell cycle progression and inactivation of apoptotic mechanisms. Although the underlying mechanisms of carcinogenesis remain unknown, increasing evidence links aberrant regulation of methylation to tumourigenesis. In addition to the methylation of DNA and histones, methylation of non-histone proteins, such as transcription factors, is also implicated in the biology and development of cancer. Because the metabolic cycling of methionine is a key pathway for many of these methylating reactions, strategies to target the epigenetic machinery of cancer cells could result in novel and efficient anti-cancer therapies. The application of these new epigenetic therapies could be of utility to promote E2F1-dependent apoptosis in cancer cells, avoid metastatic pathways and/or sensitise tumour cells to radiotherapy.es
dc.formatapplication/pdfes
dc.format.extent29es
dc.identifier.citationOncogene, 2015, Vol. 34, pp. 135–143
dc.identifier.doihttps://doi.org/10.1038/onc.2013.605
dc.identifier.issnPrint: 0950-9232
dc.identifier.issnElectronic: 1476-5594
dc.identifier.urihttp://hdl.handle.net/10201/147266
dc.languageenges
dc.publisherSpringer Naturees
dc.relationThis work was supported by grants from the Ministerio de Ciencia e Innovación (MICINN) (SAF2009-12043-C02-01) and Fundación Séneca (FS) (15230/PI/10). MFM is contracted by the Fundación de la Asociación Española contra el Cáncer (FAECC).es
dc.relation.isreplacedbyhttps://doi.org/10.1038/onc.2013.605es
dc.relation.publisherversionhttps://www.nature.com/articles/onc2013605#article-infoes
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.subjectEpigenetices
dc.subjectCanceres
dc.subjectMethylationes
dc.subjectAntifolateses
dc.subjectNon histone proteinses
dc.titleTargeting the epigenetic machinery of cancer cellses
dc.typeinfo:eu-repo/semantics/articlees
dspace.entity.typePublicationes
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relation.isAuthorOfPublication.latestForDiscovery2d4e44e6-9dda-4146-8aef-fe0c6b5a8b8f
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