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@ARTICLE{Niland:142097,
      author       = {S. Niland and D. Komljenovic$^*$ and J. Macas and T. Bracht
                      and T. Bäuerle$^*$ and S. Liebner and J. A. Eble},
      title        = {{R}hodocetin-αβ selectively breaks the endothelial
                      barrier of the tumor vasculature in {HT}1080 fibrosarcoma
                      and {A}431 epidermoid carcinoma tumor models.},
      journal      = {OncoTarget},
      volume       = {9},
      number       = {32},
      issn         = {1949-2553},
      address      = {[S.l.]},
      publisher    = {Impact Journals LLC},
      reportid     = {DKFZ-2018-02327},
      pages        = {22406- 22422},
      year         = {2018},
      abstract     = {The tumor vasculature differs from normal blood vessels in
                      morphology, composition and stability. Here, we describe a
                      novel tumor vessel-disrupting mechanism. In an HT1080/mouse
                      xenograft tumor model rhodocetin-αβ was highly effective
                      in disrupting the tumor endothelial barrier.
                      Mechanistically, rhodocetin-αβ triggered MET signaling via
                      neuropilin-1. As both neuropilin-1 and MET were only
                      lumen-exposed in a subset of abnormal tumor vessels, but not
                      in normal vessels, the prime target of rhodocetin-αβ were
                      these abnormal tumor vessels. Consequently, cells lining
                      such tumor vessels became increasingly motile which
                      compromised the vessel wall tightness. After this initial
                      leakage, rhodocetin-αβ could leave the bloodstream and
                      reach the as yet inaccessible neuropilin-1 on the
                      basolateral side of endothelial cells and thus disrupt
                      nearby vessels. Due to the specific neuropilin-1/MET
                      co-distribution on cells lining such abnormal tumor vessels
                      in contrast to normal endothelial cells, rhodocetin-αβ
                      formed the necessary trimeric signaling complex of
                      rhodocetin-αβ-MET-neuropilin-1 only in these abnormal
                      tumor vessels. This selective attack of tumor vessels,
                      sparing endothelial cell-lined vessels of normal tissues,
                      suggests that the neuropilin-1-MET signaling axis may be a
                      promising drugable target for anti-tumor therapy, and that
                      rhodocetin-αβ may serve as a lead structure to develop
                      novel anti-tumor drugs that target such vessels.},
      cin          = {E020},
      ddc          = {610},
      cid          = {I:(DE-He78)E020-20160331},
      pnm          = {315 - Imaging and radiooncology (POF3-315)},
      pid          = {G:(DE-HGF)POF3-315},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:29854288},
      pmc          = {pmc:PMC5976474},
      doi          = {10.18632/oncotarget.25032},
      url          = {https://inrepo02.dkfz.de/record/142097},
}