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| 001 | 143815 | ||
| 005 | 20240229112609.0 | ||
| 024 | 7 | _ | |a 10.1002/ijc.32312 |2 doi |
| 024 | 7 | _ | |a pmid:30945750 |2 pmid |
| 024 | 7 | _ | |a 0020-7136 |2 ISSN |
| 024 | 7 | _ | |a 1097-0215 |2 ISSN |
| 024 | 7 | _ | |a altmetric:59057949 |2 altmetric |
| 037 | _ | _ | |a DKFZ-2019-01377 |
| 041 | _ | _ | |a eng |
| 082 | _ | _ | |a 610 |
| 100 | 1 | _ | |a Kyuno, Daisuke |b 0 |
| 245 | _ | _ | |a Claudin7-dependent exosome-promoted reprogramming of nonmetastasizing tumor cells. |
| 260 | _ | _ | |a Bognor Regis |c 2019 |b Wiley-Liss |
| 336 | 7 | _ | |a article |2 DRIVER |
| 336 | 7 | _ | |a Output Types/Journal article |2 DataCite |
| 336 | 7 | _ | |a Journal Article |b journal |m journal |0 PUB:(DE-HGF)16 |s 1567670221_28320 |2 PUB:(DE-HGF) |
| 336 | 7 | _ | |a ARTICLE |2 BibTeX |
| 336 | 7 | _ | |a JOURNAL_ARTICLE |2 ORCID |
| 336 | 7 | _ | |a Journal Article |0 0 |2 EndNote |
| 520 | _ | _ | |a 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. |
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| 700 | 1 | _ | |a Zhao, Kun |b 1 |
| 700 | 1 | _ | |a Schnölzer, Martina |0 P:(DE-He78)38b33779833838a98c2a241ce465fb07 |b 2 |u dkfz |
| 700 | 1 | _ | |a Provaznik, Jan |b 3 |
| 700 | 1 | _ | |a Hackert, Thilo |b 4 |
| 700 | 1 | _ | |a Zöller, Margot |b 5 |
| 773 | _ | _ | |a 10.1002/ijc.32312 |g p. ijc.32312 |0 PERI:(DE-600)1474822-8 |n 8 |p 2182-2200 |t International journal of cancer |v 145 |y 2019 |x 1097-0215 |
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| 910 | 1 | _ | |a Deutsches Krebsforschungszentrum |0 I:(DE-588b)2036810-0 |k DKFZ |b 2 |6 P:(DE-He78)38b33779833838a98c2a241ce465fb07 |
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| 914 | 1 | _ | |y 2019 |
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