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@ARTICLE{Kyuno:143815,
      author       = {D. Kyuno and K. Zhao and M. Schnölzer$^*$ and J. Provaznik
                      and T. Hackert and M. Zöller},
      title        = {{C}laudin7-dependent exosome-promoted reprogramming of
                      nonmetastasizing tumor cells.},
      journal      = {International journal of cancer},
      volume       = {145},
      number       = {8},
      issn         = {1097-0215},
      address      = {Bognor Regis},
      publisher    = {Wiley-Liss},
      reportid     = {DKFZ-2019-01377},
      pages        = {2182-2200},
      year         = {2019},
      abstract     = {Claudin7 (cld7) is a cancer-initiating cell (CIC) marker in
                      gastrointestinal tumors, a cld7-knockdown (kd) being
                      accompanied by loss of tumor progression. Tumor exosomes
                      (TEX) restoring CIC activities, we explored the contribution
                      of cld7. This became particularly interesting, as tight
                      junction (TJ)- and glycolipid-enriched membrane domain
                      (GEM)-derived cld7 is recruited into distinct TEX. TEXs were
                      derived from CIC or cld7kd cells of a rat pancreatic and a
                      human colon cancer line. TEX derived from pancreatic cancer
                      cld7kd cells rescued with palmitoylation site-deficient cld7
                      (cld7mP) allowed selectively evaluating the contribution of
                      GEM-derived TEX, only palmitoylated cld7 being integrated
                      into GEM. Cld7 CIC-TEX promoted tumor cell dissemination and
                      metastatic growth without a major impact on proliferation,
                      apoptosis resistance and epithelial-mesenchymal transition.
                      Instead, migration, invasion and (lymph)angiogenesis were
                      strongly supported, only migration being selectively
                      fostered by GEM-derived cld7 TEX. CIC-TEX coculture of
                      cld7kd cells uncovered significant changes in the cld7kd
                      cell protein and miRNA profiles. However, changes did not
                      correspond to the CIC-TEX profile, CIC-TEX rather initiating
                      integrin, protease and RTK, particularly lymphangiogenic
                      receptor activation. CIC-TEX preferentially rescuing
                      cld7kd-associated defects in signal transduction was backed
                      up by an RTK inhibitor neutralizing the impact of CIC-TEX on
                      tumor progression. In conclusion, cld7 contributes to
                      selective steps of the metastatic cascade. Defects of cld7kd
                      and cld7mP cells in migration, invasion and
                      (lymph)angiogenesis are effaced by CIC-TEX that act by
                      signaling cascade activation. Accordingly, RTK inhibitors
                      are an efficient therapeutic defeating CIC-TEX.},
      cin          = {B100},
      ddc          = {610},
      cid          = {I:(DE-He78)B100-20160331},
      pnm          = {312 - Functional and structural genomics (POF3-312)},
      pid          = {G:(DE-HGF)POF3-312},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:30945750},
      doi          = {10.1002/ijc.32312},
      url          = {https://inrepo02.dkfz.de/record/143815},
}