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Claudin-7 promotes the epithelial: mesenchymal transition in human colorectal cancer
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| Veröffentlicht in: | OncoTarget 6(2015), 4, Seite 2046-2063 |
|---|---|
| Personen und Körperschaften: | , , , , , |
| Titel: | Claudin-7 promotes the epithelial: mesenchymal transition in human colorectal cancer/ Rahel Philip, Sarah Heiler, Wei Mu, Markus W. Büchler, Margot Zöller and Florian Thuma |
| Format: | E-Book-Kapitel |
| Sprache: | Englisch |
| veröffentlicht: |
2015
|
| Gesamtaufnahme: |
: OncoTarget, 6(2015), 4, Seite 2046-2063
, volume:6 |
| Quelle: | Verbunddaten SWB Lizenzfreie Online-Ressourcen |
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| 520 | |a In colorectal cancer (CoCa) EpCAM is frequently associated with claudin-7. There is evidence that tumor-promoting EpCAM activities are modulated by the association with claudin-7. To support this hypothesis, claudin-7 was knocked-down (kd) in HT29 and SW948 cells., HT29-cld7kd and SW948-cld7kd cells display decreased anchorage-independent growth and the capacity for holoclone-, respectively, sphere-formation is reduced. Tumor growth is delayed and cld7kd cells poorly metastasize. In line with this, migratory and invasive potential of cld7kd clones is strongly impaired, migration being inhibited by anti-CD49c, but not anti-EpCAM, although motility is reduced in EpCAM siRNA-treated cells. This is due to claudin-7 recruiting EpCAM in glycolipid-enriched membrane fractions towards claudin-7-associated TACE and presenilin2, which cleave EpCAM. The cleaved intracellular domain, EpIC, promotes epithelial-mesenchymal transition (EMT)-associated transcription factor expression, which together with fibronectin and vimentin are reduced in claudin-7kd cells. But, uptake of HT29wt and SW948wt exosomes by the claudin-7kd lines sufficed for transcription factor upregulation and for restoring motility., Thus, claudin-7 contributes to motility and invasion and is required for recruiting EpCAM towards TACE/presenilin2. EpIC generation further supports motility by promoting a shift towards EMT. Notably, EMT features of cld7-competent metastatic CoCa cells can be transferred via exosomes to poorly metastatic cells. | ||
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| author | Philip, Rahel, Heiler, Sarah, Mu, Wei, Büchler, Markus W., Zöller, Margot, Thuma, Florian |
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| contents | In colorectal cancer (CoCa) EpCAM is frequently associated with claudin-7. There is evidence that tumor-promoting EpCAM activities are modulated by the association with claudin-7. To support this hypothesis, claudin-7 was knocked-down (kd) in HT29 and SW948 cells., HT29-cld7kd and SW948-cld7kd cells display decreased anchorage-independent growth and the capacity for holoclone-, respectively, sphere-formation is reduced. Tumor growth is delayed and cld7kd cells poorly metastasize. In line with this, migratory and invasive potential of cld7kd clones is strongly impaired, migration being inhibited by anti-CD49c, but not anti-EpCAM, although motility is reduced in EpCAM siRNA-treated cells. This is due to claudin-7 recruiting EpCAM in glycolipid-enriched membrane fractions towards claudin-7-associated TACE and presenilin2, which cleave EpCAM. The cleaved intracellular domain, EpIC, promotes epithelial-mesenchymal transition (EMT)-associated transcription factor expression, which together with fibronectin and vimentin are reduced in claudin-7kd cells. But, uptake of HT29wt and SW948wt exosomes by the claudin-7kd lines sufficed for transcription factor upregulation and for restoring motility., Thus, claudin-7 contributes to motility and invasion and is required for recruiting EpCAM towards TACE/presenilin2. EpIC generation further supports motility by promoting a shift towards EMT. Notably, EMT features of cld7-competent metastatic CoCa cells can be transferred via exosomes to poorly metastatic cells. |
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| spelling | Philip, Rahel VerfasserIn (DE-588)1136808248 (DE-627)893606812 (DE-576)490858899 aut, Claudin-7 promotes the epithelial mesenchymal transition in human colorectal cancer Rahel Philip, Sarah Heiler, Wei Mu, Markus W. Büchler, Margot Zöller and Florian Thuma, 2015, 18, Text txt rdacontent, Computermedien c rdamedia, Online-Ressource cr rdacarrier, Published online December 03, 2014, Gesehen am 14.07.2017, In colorectal cancer (CoCa) EpCAM is frequently associated with claudin-7. There is evidence that tumor-promoting EpCAM activities are modulated by the association with claudin-7. To support this hypothesis, claudin-7 was knocked-down (kd) in HT29 and SW948 cells., HT29-cld7kd and SW948-cld7kd cells display decreased anchorage-independent growth and the capacity for holoclone-, respectively, sphere-formation is reduced. Tumor growth is delayed and cld7kd cells poorly metastasize. In line with this, migratory and invasive potential of cld7kd clones is strongly impaired, migration being inhibited by anti-CD49c, but not anti-EpCAM, although motility is reduced in EpCAM siRNA-treated cells. This is due to claudin-7 recruiting EpCAM in glycolipid-enriched membrane fractions towards claudin-7-associated TACE and presenilin2, which cleave EpCAM. The cleaved intracellular domain, EpIC, promotes epithelial-mesenchymal transition (EMT)-associated transcription factor expression, which together with fibronectin and vimentin are reduced in claudin-7kd cells. But, uptake of HT29wt and SW948wt exosomes by the claudin-7kd lines sufficed for transcription factor upregulation and for restoring motility., Thus, claudin-7 contributes to motility and invasion and is required for recruiting EpCAM towards TACE/presenilin2. EpIC generation further supports motility by promoting a shift towards EMT. Notably, EMT features of cld7-competent metastatic CoCa cells can be transferred via exosomes to poorly metastatic cells., Heiler, Sarah VerfasserIn (DE-588)1076379494 (DE-627)834815982 (DE-576)445266783 aut, Mu, Wei VerfasserIn (DE-588)1076380204 (DE-627)83481756X (DE-576)44526845X aut, Büchler, Markus W. 1955- VerfasserIn (DE-588)120893339 (DE-627)080952526 (DE-576)292434146 aut, Zöller, Margot 1943- VerfasserIn (DE-588)1071580337 (DE-627)826058647 (DE-576)433167572 aut, Thuma, Florian 1980- VerfasserIn (DE-588)1016373058 (DE-627)705515214 (DE-576)34837884X aut, Enthalten in OncoTarget [S.l.] : Impact Journals LLC, 2010 6(2015), 4, Seite 2046-2063 Online-Ressource (DE-627)63035975X (DE-600)2560162-3 (DE-576)325343764 1949-2553 nnns, volume:6 year:2015 number:4 pages:2046-2063 extent:18, http://dx.doi.org/undefined Verlag Resolving-System kostenfrei Volltext, http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4385835/ Verlag kostenfrei Volltext, http://dx.doi.org/undefined LFER, LFER 2017-08-09T00:00:00Z |
| spellingShingle | Philip, Rahel, Heiler, Sarah, Mu, Wei, Büchler, Markus W., Zöller, Margot, Thuma, Florian, Claudin-7 promotes the epithelial: mesenchymal transition in human colorectal cancer, In colorectal cancer (CoCa) EpCAM is frequently associated with claudin-7. There is evidence that tumor-promoting EpCAM activities are modulated by the association with claudin-7. To support this hypothesis, claudin-7 was knocked-down (kd) in HT29 and SW948 cells., HT29-cld7kd and SW948-cld7kd cells display decreased anchorage-independent growth and the capacity for holoclone-, respectively, sphere-formation is reduced. Tumor growth is delayed and cld7kd cells poorly metastasize. In line with this, migratory and invasive potential of cld7kd clones is strongly impaired, migration being inhibited by anti-CD49c, but not anti-EpCAM, although motility is reduced in EpCAM siRNA-treated cells. This is due to claudin-7 recruiting EpCAM in glycolipid-enriched membrane fractions towards claudin-7-associated TACE and presenilin2, which cleave EpCAM. The cleaved intracellular domain, EpIC, promotes epithelial-mesenchymal transition (EMT)-associated transcription factor expression, which together with fibronectin and vimentin are reduced in claudin-7kd cells. But, uptake of HT29wt and SW948wt exosomes by the claudin-7kd lines sufficed for transcription factor upregulation and for restoring motility., Thus, claudin-7 contributes to motility and invasion and is required for recruiting EpCAM towards TACE/presenilin2. EpIC generation further supports motility by promoting a shift towards EMT. Notably, EMT features of cld7-competent metastatic CoCa cells can be transferred via exosomes to poorly metastatic cells. |
| swb_id_str | 490860028 |
| title | Claudin-7 promotes the epithelial: mesenchymal transition in human colorectal cancer |
| title_auth | Claudin-7 promotes the epithelial mesenchymal transition in human colorectal cancer |
| title_full | Claudin-7 promotes the epithelial mesenchymal transition in human colorectal cancer Rahel Philip, Sarah Heiler, Wei Mu, Markus W. Büchler, Margot Zöller and Florian Thuma |
| title_fullStr | Claudin-7 promotes the epithelial mesenchymal transition in human colorectal cancer Rahel Philip, Sarah Heiler, Wei Mu, Markus W. Büchler, Margot Zöller and Florian Thuma |
| title_full_unstemmed | Claudin-7 promotes the epithelial mesenchymal transition in human colorectal cancer Rahel Philip, Sarah Heiler, Wei Mu, Markus W. Büchler, Margot Zöller and Florian Thuma |
| title_in_hierarchy | Claudin-7 promotes the epithelial: mesenchymal transition in human colorectal cancer / Rahel Philip, Sarah Heiler, Wei Mu, Markus W. Büchler, Margot Zöller and Florian Thuma, |
| title_short | Claudin-7 promotes the epithelial |
| title_sort | claudin 7 promotes the epithelial mesenchymal transition in human colorectal cancer |
| title_sub | mesenchymal transition in human colorectal cancer |
| url | http://dx.doi.org/undefined, http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4385835/ |