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@ARTICLE{DAsti:125668,
      author       = {E. D'Asti and A. Huang and M. Kool$^*$ and B. Meehan and J.
                      A. Chan and N. Jabado and A. Korshunov$^*$ and S.
                      Pfister$^*$ and J. Rak},
      title        = {{T}issue {F}actor {R}egulation by mi{R}-520g in {P}rimitive
                      {N}euronal {B}rain {T}umor {C}ells: {A} {P}ossible {L}ink
                      between {O}ncomirs and the {V}ascular {T}umor
                      {M}icroenvironment.},
      journal      = {The American journal of pathology},
      volume       = {186},
      number       = {2},
      issn         = {0002-9440},
      address      = {New York [u.a.]},
      publisher    = {Elsevier},
      reportid     = {DKFZ-2017-01794},
      pages        = {446 - 459},
      year         = {2016},
      abstract     = {Pediatric 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.},
      keywords     = {MIRN520 microRNA, human (NLM Chemicals) / MicroRNAs (NLM
                      Chemicals) / Thromboplastin (NLM Chemicals)},
      cin          = {G380 / B062},
      ddc          = {610},
      cid          = {I:(DE-He78)G380-20160331 / I:(DE-He78)B062-20160331},
      pnm          = {312 - Functional and structural genomics (POF3-312)},
      pid          = {G:(DE-HGF)POF3-312},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:26687818},
      doi          = {10.1016/j.ajpath.2015.10.020},
      url          = {https://inrepo02.dkfz.de/record/125668},
}