Please use this identifier to cite or link to this item: http://hdl.handle.net/2445/44737
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dc.contributor.authorSánchez Tena, Susana-
dc.contributor.authorReyes-Zurita, Fernando J.-
dc.contributor.authorDiaz Moralli, Santiago-
dc.contributor.authorVinardell Martínez-Hidalgo, Ma. Pilar-
dc.contributor.authorReed, Michelle A. C.-
dc.contributor.authorGarcía-García, Francisco-
dc.contributor.authorDopazo, Joaquín-
dc.contributor.authorLupiáñez, José A.-
dc.contributor.authorGünther, Ulrich L.-
dc.contributor.authorCascante i Serratosa, Marta-
dc.date.accessioned2013-07-11T13:49:35Z-
dc.date.available2013-07-11T13:49:35Z-
dc.date.issued2013-03-18-
dc.identifier.issn1932-6203-
dc.identifier.urihttp://hdl.handle.net/2445/44737-
dc.description.abstractChemoprevention is a pragmatic approach to reduce the risk of colorectal cancer, one of the leading causes of cancerrelated death in western countries. In this regard, maslinic acid (MA), a pentacyclic triterpene extracted from wax-like coatings of olives, is known to inhibit proliferation and induce apoptosis in colon cancer cell lines without affecting normal intestinal cells. The present study evaluated the chemopreventive efficacy and associated mechanisms of maslinic acid treatment on spontaneous intestinal tumorigenesis in ApcMin/+ mice. Twenty-two mice were randomized into 2 groups: control group and MA group, fed with a maslinic acid-supplemented diet for six weeks. MA treatment reduced total intestinal polyp formation by 45% (P,0.01). Putative molecular mechanisms associated with suppressing intestinal polyposis in ApcMin/+ mice were investigated by comparing microarray expression profiles of MA-treated and control mice and by analyzing the serum metabolic profile using NMR techniques. The different expression phenotype induced by MA suggested that it exerts its chemopreventive action mainly by inhibiting cell-survival signaling and inflammation. These changes eventually induce G1-phase cell cycle arrest and apoptosis. Moreover, the metabolic changes induced by MA treatment were associated with a protective profile against intestinal tumorigenesis. These results show the efficacy and underlying mechanisms of MA against intestinal tumor development in the ApcMin/+ mice model, suggesting its chemopreventive potential against colorectal cancer.-
dc.format.extent11 p.-
dc.format.mimetypeapplication/pdf-
dc.language.isoeng-
dc.publisherPublic Library of Science (PLoS)-
dc.relationinfo:eu-repo/semantics/altIdentifier/doi/10.1371/journal.pone.0059392-
dc.relation.isformatofReproducció del document publicat a: http://dx.doi.org/10.1371/journal.pone.0059392-
dc.relation.ispartofPLoS One, 2013, vol. 8, num. 3, p. e59392-
dc.relation.urihttp://dx.doi.org/10.1371/journal.pone.0059392-
dc.rightscc-by (c) Sánchez Tena, Susana et al., 2013-
dc.rights.urihttp://creativecommons.org/licenses/by/3.0/es-
dc.sourceArticles publicats en revistes (Bioquímica i Fisiologia)-
dc.subject.classificationTumors-
dc.subject.classificationCàncer colorectal-
dc.subject.classificationMedicaments antineoplàstics-
dc.subject.classificationMetabolisme-
dc.subject.otherTumors-
dc.subject.otherColorectal cancer-
dc.subject.otherAntineoplastic agents-
dc.subject.otherMetabolism-
dc.titleMaslinic acid-enriched diet decreases intestinal tumorigenesis in ApcMin/+ mice through transcriptomic and metabolomic reprogramming-
dc.typeinfo:eu-repo/semantics/article-
dc.typeinfo:eu-repo/semantics/publishedVersion-
dc.identifier.idgrec622879-
dc.date.updated2013-07-11T13:49:35Z-
dc.relation.projectIDinfo:eu-repo/grantAgreement/EC/FP7/222639/EU//ETHERPATHS-
dc.relation.projectIDinfo:eu-repo/grantAgreement/EC/FP7/261863/EU//BIO-NMR-
dc.rights.accessRightsinfo:eu-repo/semantics/openAccess-
dc.identifier.pmid23527181-
Appears in Collections:Articles publicats en revistes (Bioquímica i Biomedicina Molecular)
Articles publicats en revistes (Bioquímica i Fisiologia)
Publicacions de projectes de recerca finançats per la UE

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