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dc.contributor.authorNogués, Laura-
dc.contributor.authorReglero, Clara-
dc.contributor.authorRivas, Verónica-
dc.contributor.authorSalcedo, Alicia-
dc.contributor.authorLafarga, Vanesa-
dc.contributor.authorNeves, María-
dc.contributor.authorRamos, Paula-
dc.contributor.authorStamatakis, Konstantinos-
dc.contributor.authorMayor Menéndez, Federico-
dc.contributor.authorPenela, Petronila-
dc.date.accessioned2017-06-16T08:39:12Z-
dc.date.available2017-06-16T08:39:12Z-
dc.date.issued2016-10-01-
dc.identifierdoi: 10.1016/j.ebiom.2016.09.030-
dc.identifierissn: 2352-3964-
dc.identifier.citationEBioMedicine 13: 132- 145 (2016)-
dc.identifier.urihttp://hdl.handle.net/10261/151531-
dc.description.abstractIn addition to oncogenic drivers, signaling nodes can critically modulate cancer-related cellular networks to strength tumor hallmarks. We identify G-protein-coupled receptor kinase 2 (GRK2) as a relevant player in breast cancer. GRK2 is up-regulated in breast cancer cell lines, in spontaneous tumors in mice, and in a proportion of invasive ductal carcinoma patients. Increased GRK2 functionality promotes the phosphorylation and activation of the Histone Deacetylase 6 (HDAC6) leading to de-acetylation of the Prolyl Isomerase Pin1, a central modulator of tumor progression, thereby enhancing its stability and functional interaction with key mitotic regulators. Interestingly, a correlation between GRK2 expression and Pin1 levels and de-acetylation status is detected in breast cancer patients. Activation of the HDAC6-Pin1 axis underlies the positive effects of GRK2 on promoting growth factor signaling, cellular proliferation and anchorage-independent growth in both luminal and basal breast cancer cells. Enhanced GRK2 levels promote tumor growth in mice, whereas GRK2 down-modulation sensitizes cells to therapeutic drugs and abrogates tumor formation. Our data suggest that GRK2 acts as an important onco-modulator by strengthening the functionality of key players in breast tumorigenesis such as HDAC6 and Pin1.-
dc.publisherElsevier-
dc.relation.isversionofPublisher's version-
dc.rightsopenAccess-
dc.subjectBreast transformation-
dc.subjectAcetylation-
dc.subjectPin1-
dc.subjectHDAC6-
dc.subjectGRK2-
dc.subjectCancer-
dc.titleG Protein-coupled Receptor Kinase 2 (GRK2) Promotes Breast Tumorigenesis Through a HDAC6-Pin1 Axis-
dc.typeartículo-
dc.identifier.doi10.1016/j.ebiom.2016.09.030-
dc.date.updated2017-06-16T08:39:12Z-
dc.description.versionPeer Reviewed-
dc.language.rfc3066eng-
dc.rights.licensehttps://creativecommons.org/licenses/by-nc-nd/4.0/-
dc.relation.csic-
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