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@ARTICLE{Bure:141250,
      author       = {I. Bure and S. Geer and J. Knopf and M. Roas and S.
                      Henze$^*$ and P. Ströbel and A. Agaimy and S. Wiemann$^*$
                      and J. Hoheisel$^*$ and A. Hartmann and F. Haller and E. A.
                      Moskalev},
      title        = {{L}ong noncoding {RNA} {HOTAIR} is upregulated in an
                      aggressive subgroup of gastrointestinal stromal tumors
                      ({GIST}) and mediates the establishment of gene-specific
                      {DNA} methylation patterns.},
      journal      = {Genes, chromosomes $\&$ cancer},
      volume       = {57},
      number       = {11},
      issn         = {1045-2257},
      address      = {New York, NY},
      publisher    = {Wiley-Liss},
      reportid     = {DKFZ-2018-01770},
      pages        = {584 - 597},
      year         = {2018},
      abstract     = {Aberrant alterations of DNA methylation are common events
                      in oncogenesis. The origin of cancer-associated epigenetic
                      defects is of interest for mechanistic understanding of
                      malignant transformation and-in the long run-therapeutic
                      modulation of DNA methylation in a locus-specific manner.
                      Given the ability of certain long noncoding RNAs to operate
                      as an interface between DNA and the epigenetic modification
                      machinery which can interact with DNA methyltransferases, we
                      hypothesized-considering HOTAIR as an example-that this
                      transcript may contribute to gene specificity of DNA
                      methylation. Using gastrointestinal stromal tumors (GISTs,
                      n = 67) as a model, we confirmed upregulation of HOTAIR
                      in tumors with high risk of recurrence and showed high
                      abundance of the transcript in GIST cell lines. HOTAIR
                      knockdown in GIST-T1 cells triggered transcriptional
                      response of genes involved in the organization and
                      disassembly of the extracellular matrix and, notably,
                      induced global locus-specific alterations of DNA methylation
                      patterns. Hypomethylation was induced at a total of 507 CpG
                      sites, whereas 382 CpG dinucleotides underwent gain of
                      methylation upon HOTAIR depletion. Importantly, orchestrated
                      gain or loss of methylation at multiple individual CpG sites
                      was shown for cancer-related DPP4, RASSF1, ALDH1A3, and
                      other targets. Collectively, our data indicate that HOTAIR
                      enables target specificity of DNA methylation in GIST and is
                      capable of dual (hypo- and hypermethylation) regulation by a
                      yet to be defined mechanism. The results further suggest the
                      feasibility of manipulating DNA methylation in a targeted
                      manner and are of interest in the context of epigenetic
                      cancer therapy.},
      cin          = {W110 / B050 / B070},
      ddc          = {610},
      cid          = {I:(DE-He78)W110-20160331 / I:(DE-He78)B050-20160331 /
                      I:(DE-He78)B070-20160331},
      pnm          = {312 - Functional and structural genomics (POF3-312)},
      pid          = {G:(DE-HGF)POF3-312},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:30248209},
      doi          = {10.1002/gcc.22672},
      url          = {https://inrepo02.dkfz.de/record/141250},
}