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dc.contributor.authorFerrer-Mayorga, Gemmaes_ES
dc.contributor.authorLarriba, María Jesúses_ES
dc.contributor.authorCrespo, Pieroes_ES
dc.contributor.authorMuñoz Terol, Albertoes_ES
dc.date.accessioned2019-08-22T11:07:24Z-
dc.date.available2019-08-22T11:07:24Z-
dc.date.issued2019-
dc.identifier.citationJournal of Steroid Biochemistry and Molecular Biology 185: 1-6 (2019)es_ES
dc.identifier.issn0960-0760-
dc.identifier.urihttp://hdl.handle.net/10261/188881-
dc.description.abstractColorectal cancer (CRC) is the neoplasia that is most frequently associated with vitamin D deficiency in epidemiological and observational studies in terms of incidence and mortality. Many mechanistic studies show that the active vitamin D metabolite (1α,25-dihydroxyvitamin D3 or calcitriol) inhibits proliferation and promotes epithelial differentiation of human colon carcinoma cell lines that express vitamin D receptor (VDR) via the regulation of a high number of genes. A key action underlining this effect is the multilevel inhibition of the Wnt/β-catenin signaling pathway, whose abnormal activation in colon epithelial cells initiates and promotes CRC. Recently, our group has shown that calcitriol modulates gene expression and inhibits protumoral properties of patient-derived colon cancer-associated fibroblasts (CAFs). Accordingly, high VDR expression in tumor stromal fibroblasts is associated with longer survival of CRC patients. Moreover, many types of immune cells express VDR and are regulated by calcitriol, which probably contributes to its action against CRC. Given the role attributed to the intestinal microbiota in CRC and the finding that it is altered by vitamin D deficiency, an indirect antitumoral effect of calcitriol is also plausible at this level. In summary, calcitriol has an array of potential protective effects against CRC by acting on carcinoma cells, CAFs, immune cells and probably also the gut microbiota.es_ES
dc.description.sponsorshipThe work in the authors' laboratories is supported by the Ministerio de Economía y Competitividad of Spain-Fondo Europeo de Desarrollo Regional (FEDER) (SAF2016-76377-R, SAF2017-90604-REDT/Nurcamein) and the Instituto de Salud Carlos III-FEDER (CIBERONC, CB16/12/00273 and CB16/12/00436).es_ES
dc.language.isoenges_ES
dc.publisherElsevieres_ES
dc.relationMINECO/ICTI2013-2016/SAF2016-76377-Res_ES
dc.relationMICIU/ICTI2017-2020/SAF2017-90604-REDTes_ES
dc.relation.isversionofPostprint-
dc.rightsopenAccesses_ES
dc.subjectVitamin Des_ES
dc.subjectVitamin D receptores_ES
dc.subjectColorectal canceres_ES
dc.subjectCalcitrioles_ES
dc.subjectWnt/β-catenines_ES
dc.subjectCancer-associated fibroblastses_ES
dc.subjectGutes_ES
dc.subjectMicrobiotaes_ES
dc.titleMechanisms of action of vitamin D in colon canceres_ES
dc.typeartículoes_ES
dc.identifier.doi10.1016/j.jsbmb.2018.07.002-
dc.description.peerreviewedPeer reviewedes_ES
dc.relation.publisherversionhttps://doi.org/10.1016/j.jsbmb.2018.07.002es_ES
dc.identifier.e-issn1879-1220-
dc.contributor.funderMinisterio de Economía y Competitividad (España)es_ES
dc.contributor.funderMinisterio de Ciencia, Innovación y Universidades (España)es_ES
dc.contributor.funderInstituto de Salud Carlos IIIes_ES
dc.contributor.funderEuropean Commissiones_ES
dc.relation.csices_ES
oprm.item.hasRevisionno ko 0 false*
dc.identifier.funderhttp://dx.doi.org/10.13039/501100000780es_ES
dc.identifier.funderhttp://dx.doi.org/10.13039/501100003329es_ES
dc.identifier.funderhttp://dx.doi.org/10.13039/501100004587es_ES
dc.identifier.pmid29981368-
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