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@ARTICLE{Thole:120551,
      author       = {T. Thole$^*$ and M. Lodrini$^*$ and J. Fabian$^*$ and J.
                      Wuenschel$^*$ and S. Pfeil and T. Hielscher and A.
                      Kopp-Schneider$^*$ and U. Heinicke and S. Fulda and O.
                      Witt$^*$ and A. Eggert and M. Fischer and H. E. Deubzer$^*$},
      title        = {{N}euroblastoma cells depend on {HDAC}11 for mitotic cell
                      cycle progression and survival.},
      journal      = {Cell death $\&$ disease},
      volume       = {8},
      number       = {3},
      issn         = {2041-4889},
      address      = {London [u.a.]},
      publisher    = {Nature Publishing Group},
      reportid     = {DKFZ-2017-00980},
      pages        = {e2635},
      year         = {2017},
      abstract     = {The number of long-term survivors of high-risk
                      neuroblastoma remains discouraging, with 10-year survival as
                      low as $20\%,$ despite decades of considerable international
                      efforts to improve outcome. Major obstacles remain and
                      include managing resistance to induction therapy, which
                      causes tumor progression and early death in high-risk
                      patients, and managing chemotherapy-resistant relapses,
                      which can occur years after the initial diagnosis.
                      Identifying and validating novel therapeutic targets is
                      essential to improve treatment. Delineating and deciphering
                      specific functions of single histone deacetylases in
                      neuroblastoma may support development of targeted
                      acetylome-modifying therapeutics for patients with
                      molecularly defined high-risk neuroblastoma profiles. We
                      show here that HDAC11 depletion in MYCN-driven neuroblastoma
                      cell lines strongly induces cell death, mostly mediated by
                      apoptotic programs. Genes necessary for mitotic cell cycle
                      progression and cell division were most prominently enriched
                      in at least two of three time points in whole-genome
                      expression data combined from two cell systems, and all nine
                      genes in these functional categories were strongly
                      repressed, including CENPA, KIF14, KIF23 and RACGAP1.
                      Enforced expression of one selected candidate, RACGAP1,
                      partially rescued the induction of apoptosis caused by
                      HDAC11 depletion. High-level expression of all nine genes in
                      primary neuroblastomas significantly correlated with
                      unfavorable overall and event-free survival in patients,
                      suggesting a role in mediating the more aggressive
                      biological and clinical phenotype of these tumors. Our study
                      identified a group of cell cycle-promoting genes regulated
                      by HDAC11, being both predictors of unfavorable patient
                      outcome and essential for tumor cell viability. The data
                      indicate a significant role of HDAC11 for mitotic cell cycle
                      progression and survival of MYCN-amplified neuroblastoma
                      cells, and suggests that HDAC11 could be a valuable drug
                      target.},
      cin          = {G340 / C060 / L101 / L501 / L201},
      ddc          = {570},
      cid          = {I:(DE-He78)G340-20160331 / I:(DE-He78)C060-20160331 /
                      I:(DE-He78)L101-20160331 / I:(DE-He78)L501-20160331 /
                      I:(DE-He78)L201-20160331},
      pnm          = {317 - Translational cancer research (POF3-317)},
      pid          = {G:(DE-HGF)POF3-317},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:28252645},
      pmc          = {pmc:PMC5386552},
      doi          = {10.1038/cddis.2017.49},
      url          = {https://inrepo02.dkfz.de/record/120551},
}