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@ARTICLE{Buss:126217,
      author       = {M. C. Buss and M. Remke and J. Lee and K. Gandhi and M. J.
                      Schniederjan and M. Kool$^*$ and P. A. Northcott$^*$ and S.
                      Pfister$^*$ and M. D. Taylor and R. C. Castellino},
      title        = {{T}he {WIP}1 oncogene promotes progression and invasion of
                      aggressive medulloblastoma variants.},
      journal      = {Oncogene},
      volume       = {34},
      number       = {9},
      issn         = {1476-5594},
      address      = {Basingstoke},
      publisher    = {Nature Publ. Group},
      reportid     = {DKFZ-2017-02332},
      pages        = {1126 - 1140},
      year         = {2015},
      abstract     = {Recent studies suggest that medulloblastoma, the most
                      common malignant brain tumor of childhood, is comprised of
                      four disease variants. The WIP1 oncogene is overexpressed in
                      Group 3 and 4 tumors, which contain medulloblastomas with
                      the most aggressive clinical behavior. Our data demonstrate
                      increased WIP1 expression in metastatic medulloblastomas,
                      and inferior progression-free and overall survival of
                      patients with WIP1 high-expressing medulloblastoma.
                      Microarray analysis identified upregulation of genes
                      involved in tumor metastasis, including the G
                      protein-coupled receptor CXCR4, in medulloblastoma cells
                      with high WIP1 expression. Stimulation with the CXCR4 ligand
                      SDF1α activated PI-3 kinase signaling, and promoted growth
                      and invasion of WIP1 high-expressing medulloblastoma cells
                      in a p53-dependent manner. When xenografted into the
                      cerebellum of immunodeficient mice, medulloblastoma cells
                      with stable or endogenous high WIP1 expression exhibited
                      strong expression of CXCR4 and activated AKT in primary and
                      invasive tumor cells. WIP1 or CXCR4 knockdown inhibited
                      medulloblastoma growth and invasion. WIP1 knockdown also
                      improved the survival of mice xenografted with WIP1
                      high-expressing medulloblastoma cells. WIP1 knockdown
                      inhibited cell surface localization of CXCR4 by suppressing
                      expression of the G protein receptor kinase 5, GRK5.
                      Restoration of wild-type GRK5 promoted Ser339
                      phosphorylation of CXCR4 and inhibited the growth of
                      WIP1-stable medulloblastoma cells. Conversely, GRK5
                      knockdown inhibited Ser339 phosphorylation of CXCR4,
                      increased cell surface localization of CXCR4 and promoted
                      the growth of medulloblastoma cells with low WIP1
                      expression. These results demonstrate crosstalk among WIP1,
                      CXCR4 and GRK5, which may be important for the aggressive
                      phenotype of a subclass of medulloblastomas in children.},
      keywords     = {CXCL2 protein, human (NLM Chemicals) / CXCR4 protein, human
                      (NLM Chemicals) / Chemokine CXCL2 (NLM Chemicals) /
                      Receptors, CXCR4 (NLM Chemicals) / G-Protein-Coupled
                      Receptor Kinase 5 (NLM Chemicals) / GRK5 protein, human (NLM
                      Chemicals) / PPM1D protein, human (NLM Chemicals) /
                      Phosphoprotein Phosphatases (NLM Chemicals) / Ppm1d protein,
                      mouse (NLM Chemicals) / Protein Phosphatase 2C (NLM
                      Chemicals)},
      cin          = {B062},
      ddc          = {610},
      cid          = {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:24632620},
      pmc          = {pmc:PMC4722800},
      doi          = {10.1038/onc.2014.37},
      url          = {https://inrepo02.dkfz.de/record/126217},
}