Publication:
Hsa-miR-584-5p as a novel candidate biomarker in Turkish men with severe coronary artery disease

dc.contributor.authorÇoban, Neslihan
dc.contributor.authorPirim, Dilek
dc.contributor.authorErkan, Ayçan Fahri
dc.contributor.authorDoğan, Berkcan
dc.contributor.authorEkici, Berkay
dc.contributor.buuauthorPİRİM, DİLEK
dc.contributor.buuauthorDOĞAN, BERKCAN
dc.contributor.departmentTıp Fakültesi
dc.contributor.departmentTıbbi Genetik Ana Bilim Dalı
dc.contributor.orcid0000-0002-0522-9432
dc.contributor.orcid0000-0001-8061-8131
dc.contributor.researcheridHTP-6233-2023
dc.contributor.researcheridAAD-5249-2020
dc.contributor.researcheridABA-4957-2020
dc.date.accessioned2024-07-24T11:40:52Z
dc.date.available2024-07-24T11:40:52Z
dc.date.issued2019-12-21
dc.description.abstractCoronary artery disease (CAD) is still the preliminary cause of mortality and morbidity in the developed world. Identification of novel predictive and therapeutic biomarkers is crucial for accurate diagnosis, prognosis and treatment of the CAD. The aim of this study was to detect novel candidate miRNA biomarker that may be used in the management of CAD. We performed miRNA profiling in whole blood samples of angiographically confirmed Turkish men with CAD and non-CAD controls with insignificant coronary stenosis. Validation of microarray results was performed by qRT-PCR in a larger cohort of 62 samples. We subsequently assessed the diagnostic value of the miRNA and correlations of miRNA with clinical parameters. miRNA-target identification and network analyses were conducted by Ingenuity Pathway Analysis (IPA) software. Hsa-miR-584-5p was one of the top significantly dysregulated miRNA observed in miRNA microarray. Men-specific down-regulation (p = 0.040) of hsa-miR-584-5p was confirmed by qRT-PCR. ROC curve analysis highlighted the potential diagnostic value of hsa-miR-584-5p with a power area under the curve (AUC) of 0.714 and 0.643 in men and in total sample, respectively. The expression levels of hsa-miR-584-5p showed inverse correlation with stenosis and Gensini scores. IPA revealed CDH13 as the only CAD related predicted target for the miRNA with biological evidence of its involvement in CAD. This study suggests that hsa-miR-584-5p, known to be tumor suppressor miRNA, as a candidate biomarker for CAD and highlighted its putative role in the CAD pathogenesis. The validation of results in larger samples incorporating functional studies warrant further research.
dc.description.sponsorshipİstanbul Üniversitesi - 51865- 47372
dc.identifier.doi10.1007/s11033-019-05235-2
dc.identifier.eissn1573-4978
dc.identifier.endpage1369
dc.identifier.issn0301-4851
dc.identifier.issue2
dc.identifier.startpage1361
dc.identifier.urihttps://doi.org/10.1007/s11033-019-05235-2
dc.identifier.urihttps://link.springer.com/article/10.1007/s11033-019-05235-2
dc.identifier.urihttps://hdl.handle.net/11452/43417
dc.identifier.volume47
dc.identifier.wos000503711500001
dc.indexed.wosWOS.SCI
dc.language.isoen
dc.publisherSpringer
dc.relation.journalMolecular Biology Reports
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi
dc.rightsinfo:eu-repo/semantics/closedAccess
dc.subjectMolecule t-cadherin
dc.subjectCirculating micrornas
dc.subjectMirna expression
dc.subjectCdh13 variants
dc.subjectCell-adhesion
dc.subjectAssociation
dc.subjectTargets
dc.subjectBlood
dc.subjectIdentification
dc.subjectRoles
dc.subjectAtherosclerosis
dc.subjectMirna
dc.subjectMicroarray
dc.subjectIpa
dc.subjectT-cadherin
dc.subjectStenosis
dc.subjectScience & technology
dc.subjectLife sciences & biomedicine
dc.subjectBiochemistry & molecular biology
dc.titleHsa-miR-584-5p as a novel candidate biomarker in Turkish men with severe coronary artery disease
dc.typeArticle
dspace.entity.typePublication
local.contributor.departmentFen Edebiyat Fakültesi/Moleküler Biyoloji ve Genetik Bölümü
local.contributor.departmentTıp Fakültesi/Tıbbi Genetik Ana Bilim Dalı
relation.isAuthorOfPublication4fe8e2a8-6667-4c54-9c39-a4059fcb6657
relation.isAuthorOfPublication2619712d-96a4-43ce-a680-666e68d6560f
relation.isAuthorOfPublication.latestForDiscovery4fe8e2a8-6667-4c54-9c39-a4059fcb6657

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