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@ARTICLE{Wirthschaft:143640,
      author       = {P. Wirthschaft$^*$ and J. Bode$^*$ and H. Soni$^*$ and F.
                      Dietrich$^*$ and T. Krüwel$^*$ and B. Fischer$^*$ and C. B.
                      Knobbe-Thomsen and G. Rossetti and A. Hentschel and N.
                      Mack$^*$ and K. Schönig and M. O. Breckwoldt$^*$ and A.
                      Schmandke and S. Pusch$^*$ and J. Medenbach and M. Bendszus
                      and M. E. Schwab and A. von Deimling$^*$ and M. Kool$^*$ and
                      C. Herold-Mende and G. Reifenberger$^*$ and R. Ahrends and
                      B. Tews$^*$},
      title        = {{R}ho{A} regulates translation of the {N}ogo-{A} decoy
                      {SPARC} in white matter-invading glioblastomas.},
      journal      = {Acta neuropathologica},
      volume       = {138},
      number       = {2},
      issn         = {1432-0533},
      address      = {Heidelberg},
      publisher    = {Springer},
      reportid     = {DKFZ-2019-01217},
      pages        = {275-293},
      year         = {2019},
      abstract     = {Glioblastomas strongly invade the brain by infiltrating
                      into the white matter along myelinated nerve fiber tracts
                      even though the myelin protein Nogo-A prevents cell
                      migration by activating inhibitory RhoA signaling. The
                      mechanisms behind this long-known phenomenon remained
                      elusive so far, precluding a targeted therapeutic
                      intervention. This study demonstrates that the prevalent
                      activation of AKT in gliomas increases the ER
                      protein-folding capacity and enables tumor cells to utilize
                      a side effect of RhoA activation: the perturbation of the
                      IRE1α-mediated decay of SPARC mRNA. Once translation is
                      initiated, glioblastoma cells rapidly secrete SPARC to block
                      Nogo-A from inhibiting migration via RhoA. By advanced
                      ultramicroscopy for studying single-cell invasion in whole,
                      undissected mouse brains, we show that gliomas require SPARC
                      for invading into white matter structures. SPARC depletion
                      reduces tumor dissemination that significantly prolongs
                      survival and improves response to cytostatic therapy. Our
                      finding of a novel RhoA-IRE1 axis provides a druggable
                      target for interfering with SPARC production and underscores
                      its therapeutic value.},
      cin          = {V077 / B062 / D170 / B300 / L401 / L101},
      ddc          = {610},
      cid          = {I:(DE-He78)V077-20160331 / I:(DE-He78)B062-20160331 /
                      I:(DE-He78)D170-20160331 / I:(DE-He78)B300-20160331 /
                      I:(DE-He78)L401-20160331 / I:(DE-He78)L101-20160331},
      pnm          = {319H - Addenda (POF3-319H)},
      pid          = {G:(DE-HGF)POF3-319H},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:31062076},
      doi          = {10.1007/s00401-019-02021-z},
      url          = {https://inrepo02.dkfz.de/record/143640},
}