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@ARTICLE{Fabian:125790,
      author       = {J. Fabian$^*$ and D. M. I. Opitz$^*$ and K. Althoff and M.
                      Lodrini$^*$ and B. Hero and R. Volland and A. Beckers and K.
                      de Preter and A. Decock and N. Patil and M. Abba and A.
                      Kopp-Schneider$^*$ and K. Astrahantseff and J. Wünschel$^*$
                      and S. Pfeil and M. Ercu and A. Künkele and J. Hu$^*$ and
                      T. Thole$^*$ and L. Schweizer and G. Mechtersheimer and D.
                      Carter and B. B. Cheung and O. Popanda and A. von
                      Deimling$^*$ and J. Koster and R. Versteeg and M. Schwab and
                      G. M. Marshall and F. Speleman and U. Erb and M. Zoeller and
                      H. Allgayer and T. Simon and M. Fischer and A. E. Kulozik
                      and A. Eggert and O. Witt$^*$ and J. H. Schulte and H. E.
                      Deubzer$^*$},
      title        = {{MYCN} and {HDAC}5 transcriptionally repress {CD}9 to
                      trigger invasion and metastasis in neuroblastoma.},
      journal      = {OncoTarget},
      volume       = {7},
      number       = {41},
      issn         = {1949-2553},
      address      = {[S.l.]},
      publisher    = {Impact Journals LLC},
      reportid     = {DKFZ-2017-01916},
      pages        = {66344 - 66359},
      year         = {2016},
      abstract     = {The systemic and resistant nature of metastatic
                      neuroblastoma renders it largely incurable with current
                      multimodal treatment. Clinical progression stems mainly from
                      the increasing burden of metastatic colonization.
                      Therapeutically inhibiting the migration-invasion-metastasis
                      cascade would be of great benefit, but the mechanisms
                      driving this cycle are as yet poorly understood. In-depth
                      transcriptome analyses and ChIP-qPCR identified the cell
                      surface glycoprotein, CD9, as a major downstream player and
                      direct target of the recently described GRHL1 tumor
                      suppressor. CD9 is known to block or facilitate cancer cell
                      motility and metastasis dependent upon entity. High-level
                      CD9 expression in primary neuroblastomas correlated with
                      patient survival and established markers for favorable
                      disease. Low-level CD9 expression was an independent risk
                      factor for adverse outcome. MYCN and HDAC5 colocalized to
                      the CD9 promoter and repressed transcription. CD9 expression
                      diminished with progressive tumor development in the TH-MYCN
                      transgenic mouse model for neuroblastoma, and CD9 expression
                      in neuroblastic tumors was far below that in ganglia from
                      wildtype mice. Primary neuroblastomas lacking MYCN
                      amplifications displayed differential CD9 promoter
                      methylation in methyl-CpG-binding domain sequencing
                      analyses, and high-level methylation was associated with
                      advanced stage disease, supporting epigenetic regulation.
                      Inducing CD9 expression in a SH-EP cell model inhibited
                      migration and invasion in Boyden chamber assays. Enforced
                      CD9 expression in neuroblastoma cells transplanted onto
                      chicken chorioallantoic membranes strongly reduced
                      metastasis to embryonic bone marrow. Combined treatment of
                      neuroblastoma cells with HDAC/DNA methyltransferase
                      inhibitors synergistically induced CD9 expression despite
                      hypoxic, metabolic or cytotoxic stress. Our results show CD9
                      is a critical and indirectly druggable suppressor of the
                      invasion-metastasis cycle in neuroblastoma.},
      cin          = {G340 / C060 / C010 / L101 / L201},
      ddc          = {610},
      cid          = {I:(DE-He78)G340-20160331 / I:(DE-He78)C060-20160331 /
                      I:(DE-He78)C010-20160331 / I:(DE-He78)L101-20160331 /
                      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:27572323},
      pmc          = {pmc:PMC5341807},
      doi          = {10.18632/oncotarget.11662},
      url          = {https://inrepo02.dkfz.de/record/125790},
}