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dc.contributor.authorHernández-Sánchez, Marta-
dc.contributor.authorPoch, Enric-
dc.contributor.authorGuasch, Rosa M.-
dc.contributor.authorOrtega, Joaquín-
dc.contributor.authorLópez-Almela, Inmaculada-
dc.contributor.authorPalmero, Ignacio-
dc.contributor.authorPérez-Roger, Ignacio-
dc.date.accessioned2015-11-16T12:10:44Z-
dc.date.available2015-11-16T12:10:44Z-
dc.date.issued2015-
dc.identifierdoi: 10.18632/oncotarget.4127-
dc.identifiere-issn: 1949-2553-
dc.identifier.citationOncotarget 6(19): 17479-17490 (2015)-
dc.identifier.urihttp://hdl.handle.net/10261/125104-
dc.descriptionThis is an open-access article distributed under the terms of the Creative Commons Attribution License.-
dc.description.abstractRhoE is a small GTPase involved in the regulation of actin cytoskeleton dynamics, cell cycle and apoptosis. The role of RhoE in cancer is currently controversial, with reports of both oncogenic and tumor-suppressive functions for RhoE. Using RhoE-deficient mice, we show here that the absence of RhoE blunts contact-inhibition of growth by inhibiting p27Kip1 nuclear translocation and cooperates in oncogenic transformation of mouse primary fibroblasts. Heterozygous RhoE+/gt mice are more susceptible to chemically induced skin tumors and RhoE knock-down results in increased metastatic potential of cancer cells. These results indicate that RhoE plays a role in suppressing tumor initiation and progression.-
dc.description.sponsorshipThis work was supported by grants from the Instituto de Salud Carlos III (to IPR and RMG), MINECO SAF2013-49176-C2-1-R and SAF2012-32117 (to IPR and IP, respectively) and Universidad CEU Cardenal Herrera Santander-Copernicus (to IPR). The work was also supported by fellowships from the Generalitat Valenciana (to MHS).-
dc.publisherImpact Journals-
dc.relationinfo:eu-repo/grantAgreement/MINECO/Plan Estatal de Investigación Científica y Técnica y de Innovación 2013-2016/SAF2013-49176-C2-1-R-
dc.relation.isversionofPublisher's version-
dc.rightsopenAccess-
dc.titleRhoE is required for contact inhibition and negatively regulates tumor initiation and progression-
dc.typeartículo-
dc.identifier.doi10.18632/oncotarget.4127-
dc.relation.publisherversionhttp://dx.doi.org/10.18632/oncotarget.4127-
dc.date.updated2015-11-16T12:10:44Z-
dc.description.versionPeer Reviewed-
dc.language.rfc3066eng-
dc.rights.licensehttp://creativecommons.org/licenses/by/3.0/-
dc.contributor.funderGeneralitat Valenciana-
dc.contributor.funderMinisterio de Economía y Competitividad (España)-
dc.contributor.funderUniversidad CEU Cardenal Herrera-
dc.contributor.funderInstituto de Salud Carlos III-
dc.contributor.funderFundación Banco Santander-
dc.relation.csic-
dc.identifier.funderhttp://dx.doi.org/10.13039/501100003359es_ES
dc.identifier.funderhttp://dx.doi.org/10.13039/501100003329es_ES
dc.identifier.funderhttp://dx.doi.org/10.13039/501100004587es_ES
dc.identifier.funderhttp://dx.doi.org/10.13039/100008049es_ES
dc.identifier.pmid26036260-
dc.type.coarhttp://purl.org/coar/resource_type/c_6501es_ES
item.openairetypeartículo-
item.cerifentitytypePublications-
item.grantfulltextopen-
item.openairecristypehttp://purl.org/coar/resource_type/c_18cf-
item.fulltextWith Fulltext-
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