000125668 001__ 125668
000125668 005__ 20240228143323.0
000125668 0247_ $$2doi$$a10.1016/j.ajpath.2015.10.020
000125668 0247_ $$2pmid$$apmid:26687818
000125668 0247_ $$2ISSN$$a0002-9440
000125668 0247_ $$2ISSN$$a1525-2191
000125668 0247_ $$2altmetric$$aaltmetric:4869260
000125668 037__ $$aDKFZ-2017-01794
000125668 041__ $$aeng
000125668 082__ $$a610
000125668 1001_ $$aD'Asti, Esterina$$b0
000125668 245__ $$aTissue Factor Regulation by miR-520g in Primitive Neuronal Brain Tumor Cells: A Possible Link between Oncomirs and the Vascular Tumor Microenvironment.
000125668 260__ $$aNew York [u.a.]$$bElsevier$$c2016
000125668 3367_ $$2DRIVER$$aarticle
000125668 3367_ $$2DataCite$$aOutput Types/Journal article
000125668 3367_ $$0PUB:(DE-HGF)16$$2PUB:(DE-HGF)$$aJournal Article$$bjournal$$mjournal$$s1521723398_2109
000125668 3367_ $$2BibTeX$$aARTICLE
000125668 3367_ $$2ORCID$$aJOURNAL_ARTICLE
000125668 3367_ $$00$$2EndNote$$aJournal Article
000125668 520__ $$aPediatric embryonal brain tumors with multilayered rosettes demonstrate a unique oncogenic amplification of the chromosome 19 miRNA cluster, C19MC. Because oncogenic lesions often cause deregulation of vascular effectors, including procoagulant tissue factor (TF), this study explores whether there is a link between C19MC oncogenic miRNAs (oncomirs) and the coagulant properties of cancer cells, a question previously not studied. In a pediatric embryonal brain tumor tissue microarray, we observed an association between C19MC amplification and reduced fibrin content and TF expression, indicative of reduced procoagulant activity. In medulloblastoma cell lines (DAOY and UW228) engineered to express miR-520g, a biologically active constituent of the C19MC cluster, we observed reduced TF expression, procoagulant and TF signaling activities (responses to factor VIIa stimulation), and diminished TF emission as cargo of extracellular vesicles. Antimir and luciferase reporter assays revealed a specific and direct effect of miR-520g on the TF 3 untranslated region. Although the endogenous MIR520G locus is methylated in differentiated cells, exposure of DAOY cells to 5-aza-2-deoxycytidine or their growth as stem cell-like spheres up-regulated endogenous miR-520g with a coincident reduction in TF expression. We propose that the properties of tumors harboring oncomirs may include unique alterations of the vascular microenvironment, including deregulation of TF, with a possible impact on the biology, therapy, and hemostatic adverse effects of both disease progression and treatment.
000125668 536__ $$0G:(DE-HGF)POF3-312$$a312 - Functional and structural genomics (POF3-312)$$cPOF3-312$$fPOF III$$x0
000125668 588__ $$aDataset connected to CrossRef, PubMed,
000125668 650_7 $$2NLM Chemicals$$aMIRN520 microRNA, human
000125668 650_7 $$2NLM Chemicals$$aMicroRNAs
000125668 650_7 $$09035-58-9$$2NLM Chemicals$$aThromboplastin
000125668 7001_ $$aHuang, Annie$$b1
000125668 7001_ $$0P:(DE-He78)4c28e2aade5f44d8eca9dd8e97638ec8$$aKool, Marcel$$b2$$udkfz
000125668 7001_ $$aMeehan, Brian$$b3
000125668 7001_ $$aChan, Jennifer A$$b4
000125668 7001_ $$aJabado, Nada$$b5
000125668 7001_ $$0P:(DE-He78)8d9c904a6cea14d4c99c78ba46e41f93$$aKorshunov, Andrey$$b6$$udkfz
000125668 7001_ $$0P:(DE-He78)f746aa965c4e1af518b016de3aaff5d9$$aPfister, Stefan$$b7$$udkfz
000125668 7001_ $$aRak, Janusz$$b8
000125668 773__ $$0PERI:(DE-600)1480207-7$$a10.1016/j.ajpath.2015.10.020$$gVol. 186, no. 2, p. 446 - 459$$n2$$p446 - 459$$tThe American journal of pathology$$v186$$x0002-9440$$y2016
000125668 909CO $$ooai:inrepo02.dkfz.de:125668$$pVDB
000125668 9101_ $$0I:(DE-588b)2036810-0$$6P:(DE-He78)4c28e2aade5f44d8eca9dd8e97638ec8$$aDeutsches Krebsforschungszentrum$$b2$$kDKFZ
000125668 9101_ $$0I:(DE-588b)2036810-0$$6P:(DE-He78)8d9c904a6cea14d4c99c78ba46e41f93$$aDeutsches Krebsforschungszentrum$$b6$$kDKFZ
000125668 9101_ $$0I:(DE-588b)2036810-0$$6P:(DE-He78)f746aa965c4e1af518b016de3aaff5d9$$aDeutsches Krebsforschungszentrum$$b7$$kDKFZ
000125668 9131_ $$0G:(DE-HGF)POF3-312$$1G:(DE-HGF)POF3-310$$2G:(DE-HGF)POF3-300$$3G:(DE-HGF)POF3$$4G:(DE-HGF)POF$$aDE-HGF$$bGesundheit$$lKrebsforschung$$vFunctional and structural genomics$$x0
000125668 9141_ $$y2016
000125668 915__ $$0StatID:(DE-HGF)0100$$2StatID$$aJCR$$bAM J PATHOL : 2015
000125668 915__ $$0StatID:(DE-HGF)0200$$2StatID$$aDBCoverage$$bSCOPUS
000125668 915__ $$0StatID:(DE-HGF)0300$$2StatID$$aDBCoverage$$bMedline
000125668 915__ $$0StatID:(DE-HGF)0310$$2StatID$$aDBCoverage$$bNCBI Molecular Biology Database
000125668 915__ $$0StatID:(DE-HGF)0199$$2StatID$$aDBCoverage$$bThomson Reuters Master Journal List
000125668 915__ $$0StatID:(DE-HGF)0110$$2StatID$$aWoS$$bScience Citation Index
000125668 915__ $$0StatID:(DE-HGF)0150$$2StatID$$aDBCoverage$$bWeb of Science Core Collection
000125668 915__ $$0StatID:(DE-HGF)0111$$2StatID$$aWoS$$bScience Citation Index Expanded
000125668 915__ $$0StatID:(DE-HGF)1110$$2StatID$$aDBCoverage$$bCurrent Contents - Clinical Medicine
000125668 915__ $$0StatID:(DE-HGF)1030$$2StatID$$aDBCoverage$$bCurrent Contents - Life Sciences
000125668 915__ $$0StatID:(DE-HGF)1050$$2StatID$$aDBCoverage$$bBIOSIS Previews
000125668 915__ $$0StatID:(DE-HGF)9900$$2StatID$$aIF < 5
000125668 9201_ $$0I:(DE-He78)G380-20160331$$kG380$$lKKE Neuropathologie$$x0
000125668 9201_ $$0I:(DE-He78)B062-20160331$$kB062$$lPädiatrische Neuroonkologie$$x1
000125668 980__ $$ajournal
000125668 980__ $$aVDB
000125668 980__ $$aI:(DE-He78)G380-20160331
000125668 980__ $$aI:(DE-He78)B062-20160331
000125668 980__ $$aUNRESTRICTED