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dc.contributor.authorNoguera-Uclés, José Francisco
dc.contributor.authorBoyero, Laura
dc.contributor.authorSalinas, Ana
dc.contributor.authorCordero Varela, Juan Antonio
dc.contributor.authorBenedetti, Johana Cristina
dc.contributor.authorBernabé-Caro, Reyes
dc.contributor.authorSánchez-Gastaldo, Amparo
dc.contributor.authorAlonso, Miriam
dc.contributor.authorMolina-Pinelo, Sonia
dc.contributor.authorPaz Ares, Luis Gonzaga 
dc.date.accessioned2021-04-06T10:46:07Z
dc.date.available2021-04-06T10:46:07Z
dc.date.issued2020-07-27
dc.identifier.citationCancers (Basel). 2020;12(8):2075es_ES
dc.identifier.issn2072-6694es_ES
dc.identifier.urihttp://hdl.handle.net/20.500.12105/12522
dc.description.abstractGenomic imprinting is a process that involves one gene copy turned-off in a parent-of-origin-dependent manner. The regulation of imprinted genes is broadly dependent on promoter methylation marks, which are frequently associated with both oncogenes and tumor suppressors. The purpose of this study was to assess the DNA methylation patterns of the imprinted solute-carrier family 22 member 18 (SLC22A18) and SLC22A18 antisense (SLC22A18AS) genes in non-small cell lung cancer (NSCLC) patients to study their relevance to the disease. We found that both genes were hypomethylated in adenocarcinoma and squamous cell carcinoma patients. Due to this imprinting loss, SLC22A18 and SLC22A18AS were found to be overexpressed in NSCLC tissues, which is significantly more evident in lung adenocarcinoma patients. These results were validated through analyses of public databases of NSCLC patients. The reversed gene profile of both genes was achieved in vitro by treatment with ademetionine. We then showed that high SLC22A18 and SLC22A18AS expression levels were significantly associated with worsening disease progression. In addition, low levels of SLC22A18AS were also correlated with better overall survival for lung adenocarcinoma patients. We found that SLC22A18 and SLC22A18AS knockdown inhibits cell proliferation in vitro. All these results suggest that both genes may be useful as diagnostic and prognostic biomarkers in NSCLC, revealing novel therapeutic opportunities.es_ES
dc.description.sponsorshipThis research was funded by the Ministry of Health and Social Welfare of Junta de Andalucia (PI-0046-2012, Nicolas Monardes Program C-0040-2016), and Instituto de Salud Carlos III though the project PI17/00033 (Co-funded by European Regional Development Fund) "A way to make Europe"es_ES
dc.language.isoenges_ES
dc.publisherMPDIes_ES
dc.relation.isversionofPublisher's versiones_ES
dc.rights.urihttp://creativecommons.org/licenses/by-nc-sa/4.0/*
dc.subjectTUMOR-SUPPRESSORes_ES
dc.subjectSLC22A18es_ES
dc.subjectIGF2es_ES
dc.subjectEPIGENETICSes_ES
dc.subjectTRANSPORTERSes_ES
dc.subjectGAINes_ES
dc.titleThe Roles of Imprinted SLC22A18 and SLC22A18AS Gene Overexpression Caused by Promoter CpG Island Hypomethylation as Diagnostic and Prognostic Biomarkers for Non-Small Cell Lung Cancer Patients.es_ES
dc.typeArtículoes_ES
dc.rights.licenseAtribución-NoComercial-CompartirIgual 4.0 Internacional*
dc.identifier.pubmedID32726996es_ES
dc.format.volume12es_ES
dc.format.number8es_ES
dc.identifier.doi10.3390/cancers12082075es_ES
dc.contributor.funderJunta de Andalucía (España)
dc.contributor.funderInstituto de Salud Carlos III - ISCIII
dc.description.peerreviewedes_ES
dc.relation.publisherversionhttps://doi.org/10.3390/cancers12082075.es_ES
dc.identifier.journalCancerses_ES
dc.repisalud.institucionCNIOes_ES
dc.repisalud.orgCNIOCNIO::Unidades técnicas::Unidad de Investigación Clínica de Cáncer Pulmón H12O-CNIOes_ES
dc.relation.projectIDinfo:eu-repo/grantAgreement/ES/PI-0046-2012es_ES
dc.relation.projectIDinfo:eu-repo/grantAgreement/ES/C-0040-2016es_ES
dc.relation.projectIDinfo:eu-repo/grantAgreement/ES/PI17/00033es_ES
dc.rights.accessRightsinfo:eu-repo/semantics/openAccesses_ES


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Atribución-NoComercial-CompartirIgual 4.0 Internacional
This item is licensed under a: Atribución-NoComercial-CompartirIgual 4.0 Internacional