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Verfasst von:Große Steffen, Thomas [VerfasserIn]   i
 Giese, Thomas [VerfasserIn]   i
 Giese, Nathalia [VerfasserIn]   i
 Longerich, Thomas [VerfasserIn]   i
 Schirmacher, Peter [VerfasserIn]   i
 Hänsch, Gertrud Maria [VerfasserIn]   i
 Gaida, Matthias [VerfasserIn]   i
Titel:Epithelial-to-mesenchymal transition in pancreatic ductal adenocarcinoma and pancreatic tumor cell lines
Titelzusatz:the role of neutrophils and neutrophil-derived elastase
Verf.angabe:Thomas Große-Steffen, Thomas Giese, Nathalia Giese, Thomas Longerich, Peter Schirmacher, G. Maria Hänsch, Matthias M. Gaida
Fussnoten:Gesehen am 11.06.2018
Titel Quelle:Enthalten in: Clinical & developmental immunology
Jahr Quelle:2012
Band/Heft Quelle:(2012)Artikel-Nummer ID 720768, 12 Seiten
ISSN Quelle:1740-2530
Abstract:Pancreatic ductal adenocarcinoma (PDAC) is frequently associated with fibrosis and a prominent inflammatory infiltrate in the desmoplastic stroma. Moreover, in PDAC, an epithelial-to-mesenchymal transition (EMT) is observed. To explore a possible connection between the infiltrating cells, particularly the polymorphonuclear neutrophils (PMN) and the tumor cell transition, biopsies of patients with PDAC () were analysed with regard to PMN infiltration and nuclear expression of β-catenin and of ZEB1, well-established indicators of EMT. In biopsies with a dense PMN infiltrate, a nuclear accumulation of β-catenin and of ZEB1 was observed. To address the question whether PMN could induce EMT, they were isolated from healthy donors and were cocultivated with pancreatic tumor cells grown as monolayers. Rapid dyshesion of the tumor cells was seen, most likely due to an elastase-mediated degradation of E-cadherin. In parallel, the transcription factor TWIST was upregulated, β-catenin translocated into the nucleus, ZEB1 appeared in the nucleus, and keratins were downregulated. EMT was also induced when the tumor cells were grown under conditions preventing attachment to the culture plates. Here, also in the absence of elastase, E-cadherin was downmodulated. PMN as well as prevention of adhesion induced EMT also in liver cancer cell line. In conclusion, PMN via elastase induce EMT in vitro, most likely due to the loss of cell-to-cell contact. Because in pancreatic cancers the transition to a mesenchymal phenotype coincides with the PMN infiltrate, a contribution of the inflammatory response to the induction of EMT and—by implication—to tumor progression is possible.
DOI:doi:10.1155/2012/720768
URL:Bitte beachten Sie: Dies ist ein Bibliographieeintrag. Ein Volltextzugriff für Mitglieder der Universität besteht hier nur, falls für die entsprechende Zeitschrift/den entsprechenden Sammelband ein Abonnement besteht oder es sich um einen OpenAccess-Titel handelt.

Kostenfrei: Verlag: http://dx.doi.org/10.1155/2012/720768
 Kostenfrei: Verlag: https://www.hindawi.com/journals/jir/2012/720768/
 DOI: https://doi.org/10.1155/2012/720768
Datenträger:Online-Ressource
Sprache:eng
K10plus-PPN:1576229157
Verknüpfungen:→ Zeitschrift

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