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Por favor, use este identificador para citar o enlazar a este item: http://hdl.handle.net/10261/124905
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dc.contributor.authorCebola, Inês-
dc.contributor.authorPrieto, Patricia-
dc.contributor.authorBoscá, Lisardo-
dc.contributor.authorMoreno, Víctor-
dc.contributor.authorPeinado, Miguel A.-
dc.date.accessioned2015-11-12T11:03:30Z-
dc.date.available2015-11-12T11:03:30Z-
dc.date.issued2015-
dc.identifierdoi: 10.1186/s13148-015-0110-4-
dc.identifierissn: 1868-7075-
dc.identifiere-issn: 1868-7083-
dc.identifier.citationClinical Epigenetics 7: 74 (2015)-
dc.identifier.urihttp://hdl.handle.net/10261/124905-
dc.descriptionThis is an Open Access article distributed under the terms of the Creative Commons Attribution License.-- et al.-
dc.description.abstract[Background]: Misregulation of the PTGS (prostaglandin endoperoxide synthase, also known as cyclooxygenase or COX) pathway may lead to the accumulation of pro-inflammatory signals, which constitutes a hallmark of cancer. To get insight into the role of this signaling pathway in colorectal cancer (CRC), we have characterized the transcriptional and epigenetic landscapes of the PTGS pathway genes in normal and cancer cells. [Results]: Data from four independent series of CRC patients (502 tumors including adenomas and carcinomas and 222 adjacent normal tissues) and two series of colon mucosae from 69 healthy donors have been included in the study. Gene expression was analyzed by real-time PCR and Affymetrix U219 arrays. DNA methylation was analyzed by bisulfite sequencing, dissociation curves, and HumanMethylation450K arrays. Most CRC patients show selective transcriptional deregulation of the enzymes involved in the synthesis of prostanoids and their receptors in both tumor and its adjacent mucosa. DNA methylation alterations exclusively affect the tumor tissue (both adenomas and carcinomas), redirecting the transcriptional deregulation to activation of prostaglandin E 2 (PGE 2 ) function and blockade of other biologically active prostaglandins. In particular, PTGIS, PTGER3, PTGFR, and AKR1B1 were hypermethylated in more than 40 % of all analyzed tumors. [Conclusions]: The transcriptional and epigenetic profiling of the PTGS pathway provides important clues on the biology of the tumor and its microenvironment. This analysis renders candidate markers with potential clinical applicability in risk assessment and early diagnosis and for the design of new therapeutic strategies.-
dc.description.sponsorshipIC was funded by Fundação para a Ciência e a Tecnologia (SFRH/BD/28464/2006); JC was funded by a FPI fellowship. ADV was supported in part by a contract from the Ministerio de Economía y Competitividad (MINECO) (PTC2011-1091). This work was supported by the MINECO(SAF2011/23638, SAF2014/52492), the Catalan Institute of Oncology and the Instituto de Salud Carlos III (grant PI11-01439, RD12/0042/0019 and CIBERESP CB06/02/2005), the Generalitat de Catalunya (grant 2014SGR647), and the Asociación Española Contra el Cáncer (AECC).-
dc.publisherBioMed Central-
dc.relationinfo:eu-repo/grantAgreement/MINECO/Plan Estatal de Investigación Científica y Técnica y de Innovación 2013-2016/SAF2014-52492-R-
dc.relation.isversionofPublisher's version-
dc.rightsopenAccess-
dc.titleEpigenetics override pro-inflammatory PTGS transcriptomic signature towards selective hyperactivation of PGE 2 in colorectal cancer-
dc.typeartículo-
dc.identifier.doi10.1186/s13148-015-0110-4-
dc.relation.publisherversionhttp://dx.doi.org/10.1186/s13148-015-0110-4-
dc.date.updated2015-11-12T11:03:30Z-
dc.description.versionPeer Reviewed-
dc.language.rfc3066eng-
dc.rights.licensehttp://creativecommons.org/licenses/by/4.0-
dc.contributor.funderAsociación Española Contra el Cáncer-
dc.contributor.funderInstituto de Salud Carlos III-
dc.contributor.funderInstitut Català d'Oncologia-
dc.contributor.funderFundação para a Ciência e a Tecnologia (Portugal)-
dc.contributor.funderMinisterio de Economía y Competitividad (España)-
dc.contributor.funderGeneralitat de Catalunya-
dc.relation.csicSí-
dc.identifier.funderhttp://dx.doi.org/10.13039/501100004587es_ES
dc.identifier.funderhttp://dx.doi.org/10.13039/501100001871es_ES
dc.identifier.funderhttp://dx.doi.org/10.13039/501100003329es_ES
dc.identifier.funderhttp://dx.doi.org/10.13039/501100002809es_ES
dc.identifier.pmid26207152-
dc.type.coarhttp://purl.org/coar/resource_type/c_6501es_ES
item.fulltextWith Fulltext-
item.openairecristypehttp://purl.org/coar/resource_type/c_18cf-
item.cerifentitytypePublications-
item.grantfulltextopen-
item.openairetypeartículo-
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