Navigation überspringen
Universitätsbibliothek Heidelberg
Status: Bibliographieeintrag

Verfügbarkeit
Standort: ---
Exemplare: ---
heiBIB
 Online-Ressource
Verfasst von:Abiatari, Ivane [VerfasserIn]   i
 Esposito, Irene [VerfasserIn]   i
 Oliveira, Tiago De [VerfasserIn]   i
 Felix, Klaus M. [VerfasserIn]   i
 Xin, Hong [VerfasserIn]   i
 Penzel, Roland [VerfasserIn]   i
 Giese, Thomas [VerfasserIn]   i
 Friess, Helmut [VerfasserIn]   i
 Kleeff, Jörg [VerfasserIn]   i
Titel:Moesin-dependent cytoskeleton remodelling is associated with an anaplastic phenotype of pancreatic cancer
Verf.angabe:Ivane Abiatari, Irene Esposito, Tiago De Oliveira, Klaus Felix, Hong Xin, Roland Penzel, Thomas Giese, Helmut Friess, Jörg Kleeff
E-Jahr:2010
Jahr:14 June 2010
Umfang:14 S.
Fussnoten:Gesehen am 15.11.2022
Titel Quelle:Enthalten in: Journal of cellular and molecular medicine
Ort Quelle:Hoboken, NJ : Wiley-Blackwell, 2000
Jahr Quelle:2010
Band/Heft Quelle:14(2010), 5, Seite 1166-1179
ISSN Quelle:1582-4934
Abstract:Cell motility is controlled by the dynamic cytoskeleton and its related proteins, such as members of the ezrin/radixin/moesin (ERM) family, which act as signalling molecules inducing cytoskeleton remodelling. Although ERM proteins have been identified as important factors in various malignancies, functional redundancy between these proteins has hindered the dissection of their individual contribution. The aim of the present study was to analyse the functional role of moesin in pancreatic malignancies. Cancer cells of different malignant lesions of human and transgenic mice pancreata were evaluated by immunohistochemistry. For functional analysis, cell growth, adhesion and invasion assays were carried out after transient and stable knock-down of moesin expression in pancreatic cancer cells. In vivo tumourigenicity was determined using orthotopic and metastatic mouse tumour models. We now show that moesin knock-down increases migration, invasion and metastasis and influences extracellular matrix organization of pancreatic cancer. Moesin-regulated migratory activities of pancreatic cancer cells were in part promoted through cellular translocation of β-catenin, and re-distribution and organization of the cytoskeleton. Analysis of human and different transgenic mouse pancreatic cancers demonstrated that moesin is a phenotypic marker for anaplastic carcinoma, suggesting that this ERM protein plays a specific role in pancreatic carcinogenesis.
DOI:doi:10.1111/j.1582-4934.2009.00772.x
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.

Volltext ; Verlag: https://doi.org/10.1111/j.1582-4934.2009.00772.x
 Volltext: https://onlinelibrary.wiley.com/doi/abs/10.1111/j.1582-4934.2009.00772.x
 DOI: https://doi.org/10.1111/j.1582-4934.2009.00772.x
Datenträger:Online-Ressource
Sprache:eng
Sach-SW:anaplastic cancer
 cytoskeleton
 extracellular matrix
 moesin
 pancreatic ductal adenocarcinoma
 β-catenin
K10plus-PPN:1822508479
Verknüpfungen:→ Zeitschrift

Permanenter Link auf diesen Titel (bookmarkfähig):  https://katalog.ub.uni-heidelberg.de/titel/68985541   QR-Code
zum Seitenanfang