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dc.contributor.authorNeves, Maria 
dc.contributor.authorMarolda, Viviana
dc.contributor.authorMayor Menéndez, Federico 
dc.contributor.authorPenela Márquez, Petronila 
dc.contributor.otherUAM. Departamento de Biología Moleculares_ES
dc.date.accessioned2023-03-07T12:11:49Z
dc.date.available2023-03-07T12:11:49Z
dc.date.issued2022-10-01
dc.identifier.citationInternational Journal of Molecular Sciences 23.19 (2022): 11887es_ES
dc.identifier.issn1661-6596 (print)es_ES
dc.identifier.issn1422-0067 (online)es_ES
dc.identifier.urihttp://hdl.handle.net/10486/706569
dc.description.abstractA better understanding of the complex crosstalk among key receptors and signaling pathways involved in cancer progression is needed to improve current therapies. We have investigated in cell models representative of the major subtypes of breast cancer (BC) the interplay between the chemokine CXCL12/CXCR4/ACKR3 and EGF receptor (EGFR) family signaling cascades. These cell lines display a high heterogeneity in expression profiles of CXCR4/ACKR3 chemokine receptors, with a predominant intracellular localization and different proportions of cell surface CXCR4+, ACKR3+ or double-positive cell subpopulations, and display an overall modest activation of oncogenic pathways in response to exogenous CXCL12 alone. Interestingly, we find that in MDA-MB-361 (luminal B subtype, Her2-overexpressing), but not in MCF7 (luminal A) or MDA-MB-231 (triple negative) cells, CXCR4/ACKR3 and EGFR receptor families share signaling components and crosstalk mechanisms to concurrently promote ERK1/2 activation, with a key involvement of the G protein-coupled receptor kinase 2 (GRK2) signaling hub and the cytosolic tyrosine kinase Src. Our findings suggest that in certain BC subtypes, a relevant cooperation between CXCR4/ACKR3 and growth factor receptors takes place to integrate concurrent signals emanating from the tumor microenvironment and foster cancer progressiones_ES
dc.format.extent18 pag.es_ES
dc.format.mimetypeapplication/pdfes_ES
dc.language.isoenges_ES
dc.publisherMDPIes_ES
dc.relation.ispartofInternational Journal of Molecular Scienceses_ES
dc.rights© 2022 by the authorses_ES
dc.subject.otherChemokine Receptor CXCR4es_ES
dc.subject.otherChemokine Receptor CXCR7es_ES
dc.subject.otherG Protein Coupled Receptor Kinase 2es_ES
dc.subject.otherMitogen Activated Protein Kinase 1es_ES
dc.subject.otherStromal Cell Derived Factor 1es_ES
dc.titleCrosstalk between CXCR4/ACKR3 and EGFR signaling in breast cancer cellses_ES
dc.typearticlees_ES
dc.subject.ecienciaBiología y Biomedicina / Biologíaes_ES
dc.relation.publisherversionhttps://doi.org/10.3390/ijms231911887es_ES
dc.identifier.doi10.3390/ijms231911887es_ES
dc.identifier.publicationfirstpage11887-1es_ES
dc.identifier.publicationissue19es_ES
dc.identifier.publicationlastpage11887-18es_ES
dc.identifier.publicationvolume23es_ES
dc.relation.projectIDinfo:eu-repo/grantAgreement/EC/H2020/860229/EU//ONCORNET2.0es_ES
dc.relation.projectIDGobierno de España. PID2020-117218RB-I00es_ES
dc.relation.projectIDComunidad de Madrid. S2017/BMD-3671/INFLAMUNE-CMes_ES
dc.type.versioninfo:eu-repo/semantics/publishedVersiones_ES
dc.rights.ccReconocimientoes_ES
dc.rights.accessRightsopenAccesses_ES
dc.facultadUAMFacultad de Cienciases_ES
dc.institutoUAMCentro de Biología Molecular Severo Ochoa (CBMSO)es_ES
dc.institutoUAMInstituto de Investigación Sanitaria Hospital Universitario de La Princesa (IIS-Princesa)es_ES


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