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@ARTICLE{Li:129046,
      author       = {P. Li and E. H. Lee and F. Du and R. E. Gordon and L. W.
                      Yuelling and Y. Liu and J. M. Y. Ng and H. Zhang and J. Wu
                      and A. Korshunov$^*$ and S. Pfister$^*$ and T. Curran and
                      Z.-J. Yang},
      title        = {{N}estin {M}ediates {H}edgehog {P}athway {T}umorigenesis.},
      journal      = {Cancer research},
      volume       = {76},
      number       = {18},
      issn         = {1538-7445},
      address      = {Philadelphia, Pa.},
      publisher    = {AACR},
      reportid     = {DKFZ-2017-05051},
      pages        = {5573 - 5583},
      year         = {2016},
      abstract     = {The intermediate filament protein Nestin serves as a
                      biomarker for stem cells and has been used to identify
                      subsets of cancer stem-like cells. However, the mechanistic
                      contributions of Nestin to cancer pathogenesis are not
                      understood. Here, we report that Nestin binds the hedgehog
                      pathway transcription factor Gli3 to mediate the development
                      of medulloblastomas of the hedgehog subtype. In a mouse
                      model system, Nestin levels increased progressively during
                      medulloblastoma formation, resulting in enhanced tumor
                      growth. Conversely, loss of Nestin dramatically inhibited
                      proliferation and promoted differentiation. Mechanistic
                      investigations revealed that the tumor-promoting effects of
                      Nestin were mediated by binding to Gli3, a zinc finger
                      transcription factor that negatively regulates hedgehog
                      signaling. Nestin binding to Gli3 blocked Gli3
                      phosphorylation and its subsequent proteolytic processing,
                      thereby abrogating its ability to negatively regulate the
                      hedgehog pathway. Our findings show how Nestin drives
                      hedgehog pathway-driven cancers and uncover in Gli3 a
                      therapeutic target to treat these malignancies. Cancer Res;
                      76(18); 5573-83. ©2016 AACR.},
      keywords     = {Gli3 protein, mouse (NLM Chemicals) / Hedgehog Proteins
                      (NLM Chemicals) / Kruppel-Like Transcription Factors (NLM
                      Chemicals) / Nerve Tissue Proteins (NLM Chemicals) / Nes
                      protein, mouse (NLM Chemicals) / Nestin (NLM Chemicals)},
      cin          = {G380 / B062 / L101},
      ddc          = {610},
      cid          = {I:(DE-He78)G380-20160331 / I:(DE-He78)B062-20160331 /
                      I:(DE-He78)L101-20160331},
      pnm          = {317 - Translational cancer research (POF3-317)},
      pid          = {G:(DE-HGF)POF3-317},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:27496710},
      pmc          = {pmc:PMC5091083},
      doi          = {10.1158/0008-5472.CAN-16-1547},
      url          = {https://inrepo02.dkfz.de/record/129046},
}