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dc.contributor.authorMontenegro Arce, María Fernanda-
dc.contributor.authorSánchez del Campo Ferrer, Luis-
dc.contributor.authorGonzalez Guerrero, Rebeca-
dc.contributor.authorMartínez Barba, Enrique-
dc.contributor.authorPiñero Madrona, Antonio-
dc.contributor.authorCabezas Herrera, Juan-
dc.contributor.authorRodríguez Lopez, José Neptuno-
dc.date.accessioned2024-12-10T09:14:06Z-
dc.date.available2024-12-10T09:14:06Z-
dc.date.issued2016-05-02-
dc.identifier.citationOncogene, 2016, Vol. 35, pp. 6143–6152es
dc.identifier.issnElectronic: 1476-5594-
dc.identifier.issnPrint: 0950-9232-
dc.identifier.urihttp://hdl.handle.net/10201/147267-
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.2016.154es
dc.description.abstractDuring the course of cancer progression, neoplastic cells undergo dynamic and reversible transitions between multiple phenotypic states, and this plasticity is enabled by underlying shifts in epigenetic regulation. Our results identified a negative feedback loop in which SET9 controls DNA methyltransferase-1 protein stability, which represses the transcriptional activity of the SET9 promoter in coordination with Snail. The modulation of SET9 expression in breast cancer cells revealed a connection with E2F1 and the silencing of SET9 was sufficient to complete an epigenetic program that favored epithelial–mesenchymal transition and the generation of cancer stem cells, indicating that SET9 plays a role in modulating breast cancer metastasis. SET9 expression levels were significantly higher in samples from patients with pathological complete remission than in samples from patients with disease recurrence, which indicates that SET9 acts as a tumor suppressor in breast cancer and that its expression may serve as a prognostic marker for malignancyes
dc.formatapplication/pdfes
dc.format.extent33es
dc.languageenges
dc.publisherSpringer Naturees
dc.relationThis work was supported by grants from Ministerio de Economia y Competitividad (MINECO; Co-financing with Fondos FEDER) (SAF2013-48375-C2-1-R) to JNR-L and Fundación Séneca, Región de Murcia (FS-RM) (15230/PI/10 and 19304/PI/14) to JNR-L, JC-H, and AP-M. JC-H is contracted by the FFIS. MFM is contracted by Fundación de la Asociación Española contra el Cáncer (FAECC). LS-d-C is supported by the Ludwig Institute for Cancer Research and FAECC.es
dc.relation.isreplacedbyhttps://doi.org/10.1038/onc.2016.154es
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.subjectSET9es
dc.subjectEpigenetices
dc.subjectDNA methyltransferase 1es
dc.titleTumor suppressor SET9 guides the epigenetic plasticity of breast cancer cells and serves as an early-stage biomarker for predicting metastasises
dc.typeinfo:eu-repo/semantics/articlees
dc.relation.publisherversionhttps://www.nature.com/articles/onc2016154es
dc.identifier.doihttps://doi.org/10.1038/onc.2016.154-
dc.contributor.departmentDepartamento de Bioquímica y Biología Molecular Aes
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