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Cancer Lett ; 295(2): 214-28, 2010 Sep 28.
Article in English | MEDLINE | ID: mdl-20350779

ABSTRACT

The transcription factor NF-kappaB is constitutively active in pancreatic adenocarcinoma. Here we explore the contribution of NF-kappaB to the malignant phenotype of pancreatic cancer cells in addition to its anti-apoptotic role. Block of NF-kappaB signalling by non-destructible IkappaBalpha rendered cells resistant to TGF-beta-induced epithelial-mesenchymal transition (EMT). In contrast, NF-kappaB activation by TNF-alpha or expression of constitutively active IKK2 induced an EMT-phenotype with up-regulation of vimentin and ZEB1, and down-regulation of E-cadherin. EMT could also be induced in cells with defective TGF-beta signalling. Functional assays demonstrated reduced or strongly enhanced migration and invasion upon NF-kappaB inhibition or activation, respectively.


Subject(s)
Epithelial Cells/pathology , Mesoderm/pathology , NF-kappa B/physiology , Pancreatic Neoplasms/pathology , Cell Line, Tumor , Cell Movement , Extracellular Signal-Regulated MAP Kinases/physiology , Homeodomain Proteins/physiology , Humans , MAP Kinase Signaling System , Matrix Metalloproteinases/physiology , Mitogen-Activated Protein Kinase Kinases/physiology , Neoplasm Invasiveness , Transcription Factors/physiology , Transforming Growth Factor beta/pharmacology , Tumor Necrosis Factor-alpha/pharmacology , Zinc Finger E-box-Binding Homeobox 1
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