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@ARTICLE{Bhatia:126144,
      author       = {S. Bhatia and N. A. Baig and O. Timofeeva and E. B.
                      Pasquale and K. Hirsch and T. J. MacDonald and A. Dritschilo
                      and Y. C. Lee and M. Henkemeyer and B. Rood and M. Jung and
                      X.-J. Wang and M. Kool$^*$ and O. Rodriguez and C. Albanese
                      and S. D. Karam},
      title        = {{K}nockdown of {E}ph{B}1 receptor decreases medulloblastoma
                      cell growth and migration and increases cellular
                      radiosensitization.},
      journal      = {OncoTarget},
      volume       = {6},
      number       = {11},
      issn         = {1949-2553},
      address      = {[S.l.]},
      publisher    = {Impact Journals LLC},
      reportid     = {DKFZ-2017-02259},
      pages        = {8929 - 8946},
      year         = {2015},
      abstract     = {The expression of members of the Eph family of receptor
                      tyrosine kinases and their ephrin ligands is frequently
                      dysregulated in medulloblastomas. We assessed the expression
                      and functional role of EphB1 in medulloblastoma cell lines
                      and engineered mouse models. mRNA and protein expression
                      profiling showed expression of EphB1 receptor in the human
                      medulloblastoma cell lines DAOY and UW228. EphB1
                      downregulation reduced cell growth and viability, decreased
                      the expression of important cell cycle regulators, and
                      increased the percentage of cells in G1 phase of the cell
                      cycle. It also modulated the expression of proliferation,
                      and cell survival markers. In addition, EphB1 knockdown in
                      DAOY cells resulted in significant decrease in migration,
                      which correlated with decreased β1-integrin expression and
                      levels of phosphorylated Src. Furthermore, EphB1 knockdown
                      enhanced cellular radiosensitization of medulloblastoma
                      cells in culture and in a genetically engineered mouse
                      medulloblastoma model. Using genetically engineered mouse
                      models, we established that genetic loss of EphB1 resulted
                      in a significant delay in tumor recurrence following
                      irradiation compared to EphB1-expressing control tumors.
                      Taken together, our findings establish that EphB1 plays a
                      key role in medulloblastoma cell growth, viability,
                      migration, and radiation sensitivity, making EphB1 a
                      promising therapeutic target.},
      keywords     = {Antigens, CD29 (NLM Chemicals) / Cell Cycle Proteins (NLM
                      Chemicals) / Neoplasm Proteins (NLM Chemicals) / RNA, Small
                      Interfering (NLM Chemicals) / Receptor, EphB1 (NLM
                      Chemicals) / Proto-Oncogene Proteins pp60(c-src) (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:25879388},
      pmc          = {pmc:PMC4496193},
      doi          = {10.18632/oncotarget.3369},
      url          = {https://inrepo02.dkfz.de/record/126144},
}