Please use this identifier to cite or link to this item: http://hdl.handle.net/10553/43484
DC FieldValueLanguage
dc.contributor.authorRubio Sánchez, Saraen_US
dc.contributor.authorQuintana Aguiar, José Martínen_US
dc.contributor.authorEiroa, José L.en_US
dc.contributor.authorTriana, Jorgeen_US
dc.contributor.authorEstévez Rosas, Francisco Jesúsen_US
dc.contributor.otherRubio, Sara-
dc.contributor.otherQuintana, Jose-
dc.contributor.otherEstevez, Francisco-
dc.contributor.otherRubio Sánchez, Sara-
dc.date.accessioned2018-11-21T15:31:49Z-
dc.date.available2018-11-21T15:31:49Z-
dc.date.issued2007en_US
dc.identifier.issn0143-3334en_US
dc.identifier.urihttp://hdl.handle.net/10553/43484-
dc.description.abstractFlavonoids are polyphenolic compounds that are ubiquitously in plants and display a vast array of biological activities. Here we have studied the effect of the phenylbenzo-γ-pyrone-derivative quercetin 3-methyl ether tetracetate (QD), obtained by acetylation of the natural product quercetin 3-methyl ether, on cell viability of human leukemia HL-60 and U937 cell lines. The results show that QD was cytotoxic and induced G 2 –M phase cell cycle arrest on both cell lines and it was a potent apoptotic inducer on HL-60 cells. QD-induced apoptosis is (i) mediated by caspase activation, since it was prevented by the non-specific caspase inhibitor z-VAD-fmk, (ii) associated with cytochrome c release and (iii) triggered in Bcl-2 over-expressing U937 cells. The treatment of HL-60 and U937 cells with QD also induces the activation of the mitogen-activated protein kinases (MAPKs) pathway, including c-Jun N-terminal kinase, p38 mitogen-activated protein kinase and extracellular signal-regulated kinases (ERK) 1/2. Inhibition of c-Jun N-terminal kinase by SP600125 and of p38 mitogen-activated protein kinase by SB203580 had no influence on QD-mediated apoptosis. In contrast, inhibition of ERK1/2 with the pharmacologic inhibitors U0126 or PD98059, together with QD, resulted in an important enhancement of apoptosis. Cells are sensitized to QD-mediated apoptosis after blocking ERK1/2, which suggests that inhibition of this pathway is a valuable strategy to increase the sensitivity of human leukemia HL-60 cells toward QD.en_US
dc.languageengen_US
dc.publisher0143-3334-
dc.relationNuevos Compuestos Antileucémicosen_US
dc.relation.ispartofCarcinogenesisen_US
dc.sourceCarcinogenesis [ISSN 0143-3334], v. 28, p. 2105-2113en_US
dc.subject32 Ciencias médicasen_US
dc.subject.otherActivated Protein-Kinase
dc.subject.otherP38 Map Kinase
dc.subject.otherInduced Apoptosis
dc.subject.otherCancer-Therapy
dc.subject.otherMolecular-Mechanisms
dc.subject.otherConverting Enzyme
dc.subject.otherHl-60 Cells
dc.subject.otherPathway
dc.subject.otherBcl-2
dc.subject.otherCaspases
dc.titleAcetyl derivative of quercetin 3-methyl ether-induced cell death in human leukemia cells is amplified by the inhibition of ERKen_US
dc.typeinfo:eu-repo/semantics/Articleen_US
dc.typeArticleen_US
dc.identifier.doi10.1093/carcin/bgm131en_US
dc.identifier.scopus35148878657-
dc.identifier.isi000250676400007-
dcterms.isPartOfCarcinogenesis-
dcterms.sourceCarcinogenesis[ISSN 0143-3334],v. 28 (10), p. 2105-2113-
dc.contributor.authorscopusid22635323400-
dc.contributor.authorscopusid8681043500-
dc.contributor.authorscopusid6507583429-
dc.contributor.authorscopusid6602859915-
dc.contributor.authorscopusid7003810011-
dc.description.lastpage2113en_US
dc.description.firstpage2105en_US
dc.relation.volume28en_US
dc.investigacionCiencias de la Saluden_US
dc.type2Artículoen_US
dc.identifier.wosWOS:000250676400007-
dc.contributor.daisngid4276242-
dc.contributor.daisngid128315-
dc.contributor.daisngid2831014-
dc.contributor.daisngid1400733-
dc.contributor.daisngid384944-
dc.identifier.investigatorRIDK-4656-2013-
dc.identifier.investigatorRIDK-5709-2014-
dc.identifier.investigatorRIDK-5125-2014-
dc.identifier.investigatorRIDNo ID-
dc.contributor.wosstandardWOS:Rubio, S-
dc.contributor.wosstandardWOS:Quintana, J-
dc.contributor.wosstandardWOS:Eiroa, JL-
dc.contributor.wosstandardWOS:Triana, J-
dc.contributor.wosstandardWOS:Estevez, F-
dc.date.coverdateOctubre 2007en_US
dc.identifier.ulpgces
dc.description.jcr5,406
dc.description.jcrqQ1
item.fulltextSin texto completo-
item.grantfulltextnone-
crisitem.author.deptBioquímica y Biología Molecular, Fisiología, Genética e Inmunología.-
crisitem.author.deptBioquímica Farmacológica-
crisitem.author.deptIU de Investigaciones Biomédicas y Sanitarias-
crisitem.author.deptBioquímica y Biología Molecular, Fisiología, Genética e Inmunología.-
crisitem.author.deptBioquímica Farmacológica-
crisitem.author.deptIU de Investigaciones Biomédicas y Sanitarias-
crisitem.author.deptQuímica-
crisitem.author.deptBioquímica Farmacológica-
crisitem.author.deptIU de Investigaciones Biomédicas y Sanitarias-
crisitem.author.deptBioquímica y Biología Molecular, Fisiología, Genética e Inmunología.-
crisitem.author.orcid0000-0001-7633-1285-
crisitem.author.orcid0000-0001-8225-4538-
crisitem.author.orcid0000-0002-4986-8332-
crisitem.author.orcid0000-0002-9728-2774-
crisitem.author.parentorgIU de Investigaciones Biomédicas y Sanitarias-
crisitem.author.parentorgIU de Investigaciones Biomédicas y Sanitarias-
crisitem.author.parentorgIU de Investigaciones Biomédicas y Sanitarias-
crisitem.author.fullNameRubio Sánchez, Sara-
crisitem.author.fullNameQuintana Aguiar, José Martín-
crisitem.author.fullNameEiroa Martínez, José Luis-
crisitem.author.fullNameEstévez Rosas, Francisco Jesús-
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