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@ARTICLE{Linder:169388,
      author       = {B. Linder and C. Klein and M. E. Hoffmann and F. Bonn and
                      I. Dikic and D. Kögel$^*$},
      title        = {{BAG}3 is a negative regulator of ciliogenesis in
                      glioblastoma and triple-negative breast cancer cells.},
      journal      = {Journal of cellular biochemistry},
      volume       = {123},
      number       = {1},
      issn         = {1097-4644},
      address      = {New York, NY},
      publisher    = {Wiley-Liss},
      reportid     = {DKFZ-2021-01462},
      pages        = {77-90},
      year         = {2022},
      note         = {2022 Jan;123(1):77-90},
      abstract     = {By regulating several hallmarks of cancer, BAG3 exerts
                      oncogenic functions in a wide variety of malignant diseases
                      including glioblastoma (GBM) and triple-negative breast
                      cancer (TNBC). Here we performed global
                      proteomic/phosphoproteomic analyses of CRISPR/Cas9-mediated
                      isogenic BAG3 knockouts of the two GBM lines U343 and U251
                      in comparison to parental controls. Depletion of BAG3 evoked
                      major effects on proteins involved in ciliogenesis/ciliary
                      function and the activity of the related kinases
                      aurora-kinase A and CDK1. Cilia formation was significantly
                      enhanced in BAG3 KO cells, a finding that could be confirmed
                      in BAG3-deficient versus -proficient BT-549 TNBC cells, thus
                      identifying a completely novel function of BAG3 as a
                      negative regulator of ciliogenesis. Furthermore, we
                      demonstrate that enhanced ciliogenesis and reduced
                      expression of SNAI1 and ZEB1, two key transcription factors
                      regulating epithelial to mesenchymal transition (EMT) are
                      correlated to decreased cell migration, both in the GBM and
                      TNBC BAG3 knockout cells. Our data obtained in two different
                      tumor entities identify suppression of EMT and ciliogenesis
                      as putative synergizing mechanisms of BAG3-driven tumor
                      aggressiveness in therapy-resistant cancers.},
      keywords     = {BAG3 (Other) / cell migration (Other) / epithelial to
                      mesenchymal transition (Other) / glioblastoma (Other) /
                      primary cilium (Other) / triple-negative breast cancer
                      (Other)},
      cin          = {FM01},
      ddc          = {540},
      cid          = {I:(DE-He78)FM01-20160331},
      pnm          = {899 - ohne Topic (POF4-899)},
      pid          = {G:(DE-HGF)POF4-899},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:34180073},
      doi          = {10.1002/jcb.30073},
      url          = {https://inrepo02.dkfz.de/record/169388},
}