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dc.contributor.authorHernández Garrido, Marita 
dc.contributor.authorMartín Martín, Rubén
dc.contributor.authorGarcía Cubillas, Miriam Daniela
dc.contributor.authorMaeso Hernández, Patricia
dc.contributor.authorNieto Callejo, María Luisa
dc.date.accessioned2021-06-22T11:22:40Z
dc.date.available2021-06-22T11:22:40Z
dc.date.issued2010
dc.identifier.citationNeuro-Oncology, 2010, vol. 12, n. 10. p. 1014-1023es
dc.identifier.issn1522-8517es
dc.identifier.urihttps://uvadoc.uva.es/handle/10324/47000
dc.descriptionProducción Científicaes
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
dc.format.mimetypeapplication/pdfes
dc.language.isoenges
dc.publisherOxford University Presses
dc.rights.accessRightsinfo:eu-repo/semantics/openAccesses
dc.rights.urihttp://creativecommons.org/licenses/by-nc-nd/4.0/*
dc.titleSecreted PLA2 induces proliferation in astrocytoma through the EGF receptor: another inflammation-cancer linkes
dc.typeinfo:eu-repo/semantics/articlees
dc.rights.holder© 2010 Oxford University Presses
dc.identifier.doi10.1093/neuonc/noq078es
dc.relation.publisherversionhttps://academic.oup.com/neuro-oncology/article/12/10/1014/1079585es
dc.peerreviewedSIes
dc.description.otherAnexo: Erratum: Secreted PLA 2 induces proliferation in astrocytoma through the EGF receptor: another inflammation-cancer
dc.description.projectMinisterio de Ciencia, Innovación y Universidades (grants SAF2005-01242 and SAF2009-08407)es
dc.description.projectJunta de Castilla y León (grant CSI11A08)es
dc.rightsAttribution-NonCommercial-NoDerivatives 4.0 Internacional*
dc.type.hasVersioninfo:eu-repo/semantics/publishedVersiones
dc.subject.unesco3201.01 Oncologíaes


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