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@ARTICLE{CohenDvashi:126276,
      author       = {H. Cohen-Dvashi and N. Ben-Chetrit and R. Russell and S.
                      Carvalho and M. Lauriola and S. Nisani and M. Mancini and N.
                      Nataraj and M. Kedmi and L. Roth and W. Köstler and A.
                      Zeisel and A. Yitzhaky and J. Zylberg and G. Tarcic and R.
                      Eilam and Y. Wigelman and R. Will$^*$ and S. Lavi and Z.
                      Porat and S. Wiemann$^*$ and S. Ricardo and F. Schmitt and
                      C. Caldas and Y. Yarden},
      title        = {{N}avigator-3, a modulator of cell migration, may act as a
                      suppressor of breast cancer progression.},
      journal      = {EMBO molecular medicine},
      volume       = {7},
      number       = {3},
      issn         = {1757-4684},
      address      = {Weinheim},
      publisher    = {Wiley-VCH},
      reportid     = {DKFZ-2017-02391},
      pages        = {299 - 314},
      year         = {2015},
      abstract     = {Dissemination of primary tumor cells depends on migratory
                      and invasive attributes. Here, we identify Navigator-3
                      (NAV3), a gene frequently mutated or deleted in human
                      tumors, as a regulator of epithelial migration and invasion.
                      Following induction by growth factors, NAV3 localizes to the
                      plus ends of microtubules and enhances their polarized
                      growth. Accordingly, NAV3 depletion trimmed microtubule
                      growth, prolonged growth factor signaling, prevented
                      apoptosis and enhanced random cell migration. Mathematical
                      modeling suggested that NAV3-depleted cells acquire an
                      advantage in terms of the way they explore their
                      environment. In animal models, silencing NAV3 increased
                      metastasis, whereas ectopic expression of the wild-type
                      form, unlike expression of two, relatively unstable
                      oncogenic mutants from human tumors, inhibited metastasis.
                      Congruently, analyses of > 2,500 breast and lung cancer
                      patients associated low NAV3 with shorter survival. We
                      propose that NAV3 inhibits breast cancer progression by
                      regulating microtubule dynamics, biasing directionally
                      persistent rather than random migration, and inhibiting
                      locomotion of initiated cells.},
      keywords     = {Membrane Proteins (NLM Chemicals) / NAV3 protein, human
                      (NLM Chemicals) / Nerve Tissue Proteins (NLM Chemicals)},
      cin          = {B050 / W110},
      ddc          = {610},
      cid          = {I:(DE-He78)B050-20160331 / I:(DE-He78)W110-20160331},
      pnm          = {312 - Functional and structural genomics (POF3-312)},
      pid          = {G:(DE-HGF)POF3-312},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:25678558},
      pmc          = {pmc:PMC4364947},
      doi          = {10.15252/emmm.201404134},
      url          = {https://inrepo02.dkfz.de/record/126276},
}