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dc.contributor.author
Castillo, Lilian Fedra
dc.contributor.author
Rivero, Ezequiel Mariano
dc.contributor.author
Goffin, Vincent
dc.contributor.author
Luthy, Isabel Alicia
dc.date.available
2018-10-25T16:02:26Z
dc.date.issued
2017-06
dc.identifier.citation
Castillo, Lilian Fedra; Rivero, Ezequiel Mariano; Goffin, Vincent; Luthy, Isabel Alicia; Alpha2-adrenoceptor agonists trigger prolactin signaling in breast cancer cells; Elsevier Science Inc; Cellular Signalling; 34; 6-2017; 76-85
dc.identifier.issn
0898-6568
dc.identifier.uri
http://hdl.handle.net/11336/63048
dc.description.abstract
Breast cancer is the most frequent malignancy among women worldwide. We have described the expression of α2-adrenoceptors in breast cancer cell lines, associated with increased cell proliferation and tumor growth. A mitogenic autocrine/paracrine loop of prolactin (Prl) has been described in breast cancer cells. We hypothesized that the α2-adrenergic enhancement of proliferation could be mediated, at least in part, by this Prl loop. In both T47D and MCF-7 cell lines, the incubation with the α2-adrenergic agonist dexmedetomidine significantly increased Prl release into the culture medium (measured by the Nb2 bioassay), this effect being reversed by the α2-adrenergic antagonist rauwolscine. No change in Prl receptors (PrlR) was observed by RT-qPCR in these cell lines. In IBH-6 cells a decrease in Prl secretion was observed at the lower dexmedetomidine concentration. The signaling pathways involved in ovine Prl (oPrl) and dexmedetomidine action were also assessed. Both compounds significantly activated STAT5 and ERK in all three cell lines. In T47D and MCF-7 cell lines also AKT was activated by both Prl and dexmedetomidine. We therefore describe the STAT5 phosphorylation by an α2-adrenergic agonist, dexmedetomidine. In T47D cells, the α2-adrenergic stimulation of cell proliferation is probably mediated, at least in part, by the Prl autocrine/paracrine loop, because this effect is abrogated by the specific PrlR antagonist Δ1?9-G129R-hPrl. The implication of Prl loop describes a novel mechanism of action of this GPCR.
dc.format
application/pdf
dc.language.iso
eng
dc.publisher
Elsevier Science Inc
dc.rights
info:eu-repo/semantics/restrictedAccess
dc.rights.uri
https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
dc.subject
Cell Signaling
dc.subject
Ibh-6
dc.subject
Mcf-7
dc.subject
T47d
dc.subject.classification
Biología Celular, Microbiología
dc.subject.classification
Ciencias Biológicas
dc.subject.classification
CIENCIAS NATURALES Y EXACTAS
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Anatomía y Morfología
dc.subject.classification
Medicina Básica
dc.subject.classification
CIENCIAS MÉDICAS Y DE LA SALUD
dc.subject.classification
Anatomía y Morfología
dc.subject.classification
Medicina Básica
dc.subject.classification
CIENCIAS MÉDICAS Y DE LA SALUD
dc.title
Alpha2-adrenoceptor agonists trigger prolactin signaling in breast cancer cells
dc.type
info:eu-repo/semantics/article
dc.type
info:ar-repo/semantics/artículo
dc.type
info:eu-repo/semantics/publishedVersion
dc.date.updated
2018-10-23T15:50:48Z
dc.journal.volume
34
dc.journal.pagination
76-85
dc.journal.pais
Estados Unidos
dc.description.fil
Fil: Castillo, Lilian Fedra. Instituto Angel H. Roffo; Argentina
dc.description.fil
Fil: Rivero, Ezequiel Mariano. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Biología y Medicina Experimental. Fundación de Instituto de Biología y Medicina Experimental. Instituto de Biología y Medicina Experimental; Argentina
dc.description.fil
Fil: Goffin, Vincent. Inserm; Francia. Universite de Paris; Francia
dc.description.fil
Fil: Luthy, Isabel Alicia. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Biología y Medicina Experimental. Fundación de Instituto de Biología y Medicina Experimental. Instituto de Biología y Medicina Experimental; Argentina
dc.journal.title
Cellular Signalling
dc.relation.alternativeid
info:eu-repo/semantics/altIdentifier/url/https://www.sciencedirect.com/science/article/pii/S0898656817300724
dc.relation.alternativeid
info:eu-repo/semantics/altIdentifier/doi/http://dx.doi.org/10.1016/j.cellsig.2017.03.003
dc.relation.alternativeid
info:eu-repo/semantics/altIdentifier/pmid/28302567


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