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@ARTICLE{Sundararajan:127584,
      author       = {V. Sundararajan and N. Gengenbacher$^*$ and M. P. Stemmler
                      and J. A. Kleemann and T. Brabletz and S. Brabletz},
      title        = {{T}he {ZEB}1/mi{R}-200c feedback loop regulates invasion
                      via actin interacting proteins {MYLK} and {TKS}5.},
      journal      = {OncoTarget},
      volume       = {6},
      number       = {29},
      issn         = {1949-2553},
      address      = {[S.l.]},
      publisher    = {Impact Journals LLC},
      reportid     = {DKFZ-2017-03607},
      pages        = {27083 - 27096},
      year         = {2015},
      abstract     = {Epithelial to mesenchymal transition (EMT) is a
                      developmental process which is aberrantly activated during
                      cancer invasion and metastasis. Elevated expression of
                      EMT-inducers like ZEB1 enables tumor cells to detach from
                      the primary tumor and invade into the surrounding tissue.
                      The main antagonist of ZEB1 in controlling EMT is the
                      microRNA-200 family that is reciprocally linked to ZEB1 in a
                      double negative feedback loop. Here, we further elucidate
                      how the ZEB1/miR-200 feedback loop controls invasion of
                      tumor cells. The process of EMT is attended by major changes
                      in the actin cytoskeleton. Via in silico screening of genes
                      encoding for actin interacting proteins, we identified two
                      novel targets of miR-200c - TKS5 and MYLK (MLCK).
                      Co-expression of both genes with ZEB1 was observed in
                      several cancer cell lines as well as in breast cancer
                      patients and correlated with low miR-200c levels. Depletion
                      of TKS5 or MYLK in breast cancer cells reduced their
                      invasive potential and their ability to form invadopodia.
                      Whereas TKS5 is known to be a major component, we could
                      identify MYLK as a novel player in invadopodia formation. In
                      summary, TKS5 and MYLK represent two mediators of invasive
                      behavior of cancer cells that are regulated by the
                      ZEB1/miR-200 feedback loop.},
      keywords     = {Actins (NLM Chemicals) / Adaptor Proteins, Vesicular
                      Transport (NLM Chemicals) / CDH1 protein, human (NLM
                      Chemicals) / Cadherins (NLM Chemicals) / Calcium-Binding
                      Proteins (NLM Chemicals) / Homeodomain Proteins (NLM
                      Chemicals) / MIRN200 microRNA, human (NLM Chemicals) /
                      MicroRNAs (NLM Chemicals) / SH3PXD2A protein, human (NLM
                      Chemicals) / Transcription Factors (NLM Chemicals) / ZEB1
                      protein, human (NLM Chemicals) / Zinc Finger E-box-Binding
                      Homeobox 1 (NLM Chemicals) / MYLK protein, human (NLM
                      Chemicals) / Myosin-Light-Chain Kinase (NLM Chemicals)},
      cin          = {A190},
      ddc          = {610},
      cid          = {I:(DE-He78)A190-20160331},
      pnm          = {311 - Signalling pathways, cell and tumor biology
                      (POF3-311)},
      pid          = {G:(DE-HGF)POF3-311},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:26334100},
      pmc          = {pmc:PMC4694975},
      doi          = {10.18632/oncotarget.4807},
      url          = {https://inrepo02.dkfz.de/record/127584},
}