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dc.contributor.authorHernández, Marita-
dc.contributor.authorMartín, Rubén-
dc.contributor.authorGarcía-Cubillas, Miriam Daniela-
dc.contributor.authorMaeso, Patricia-
dc.contributor.authorNieto, María Luisa-
dc.date.accessioned2012-05-08T11:26:21Z-
dc.date.available2012-05-08T11:26:21Z-
dc.date.issued2010-10-
dc.identifier.citationNeuro-Oncology 12(10): 1014-1023 (2010)es_ES
dc.identifier.issn1522-8517-
dc.identifier.urihttp://hdl.handle.net/10261/49373-
dc.description10 páginas, 5 figuras.es_ES
dc.description.abstractWe have investigated mechanisms that contribute to reinforce the relationship between inflammation and cancer. Secreted phospholipase A2 group IIA (sPLA2-IIA) is a molecule relevant in inflammatory events and has been proposed as a marker for some of these. Previously, we reported the mitogenic properties of this sPLA2 in the human astrocytoma cell line 1321N1. Here, we go deeper into the mechanisms that link this inflammatory protein with proliferation in one of the most aggressive types of tumors. We found that phosphorylation of the extracellular regulated kinase (ERK) was preceded by the activation of the small GTPase Ras, and both failed to be activated by inhibiting protein kinase C (PKC). Fractionation and immunofluorescence studies revealed translocation of PKC alpha, delta, and epsilon to the membrane fraction upon stimulation with sPLA2-IIA. Immunoprecipitation analysis showed that sPLA2-IIA induces phosphorylation of the epidermal growth factor receptor (EGFR) through a PKC-dependent pathway. We found that phosphorylation of this receptor contributed to Ras and ERK activation and that inhibition of ERK, PKC, and EGFR blocked the mitogenic response induced by sPLA2-IIA. This study showed that sPLA2-IIA is able to bring into play EGFR to trigger its signaling and that PKC leads the distribution of resources. Interestingly, we found that this is not a cell-specific response, because sPLA2-IIA was also able to transactivate EGFR in MCF7 human breast cancer cells. Therefore, this mechanism could contribute to worsen the prognosis of a tumor in an inflammatory microenvironment. We also present more links of the tumor chain possibly susceptible to targeting.es_ES
dc.description.sponsorshipThis work was supported by the Ramón y Cajal Program (to M.H.), F.P.I. Program from the Autonomous Government of Castilla y León. (to R.M.), both cofunded by F.S.E and by the ISCIII, Red de Centros RECAVA, C03/01 (to P.M.H. and M.D.G.C.), and by grants SAF2005-01242 and SAF2009-08407 from the Spanish Ministry of Science and Innovation, and CSI11A08 from the Autonomous Government of Castilla y León.es_ES
dc.language.isoenges_ES
dc.publisherOxford University Presses_ES
dc.relation.isversionofPublisher's version-
dc.rightsopenAccesses_ES
dc.subjectCanceres_ES
dc.subjectEpidermal growth factor receptores_ES
dc.subjectInflammationes_ES
dc.subjectSecreted phospholipase A2-IIAes_ES
dc.subjectSignal transductiones_ES
dc.titleSecreted PLA2 induces proliferation in astrocytoma through the EGF receptor: another inflammation-cancer linkes_ES
dc.typeArtículoes_ES
dc.identifier.doi10.1093/neuonc/noq078-
dc.description.peerreviewedPeer reviewedes_ES
dc.relation.publisherversionhttp://dx.doi.org/10.1093/neuonc/noq078es_ES
dc.identifier.e-issn1523-5866-
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