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pubmed-article:20350779pubmed:abstractTextThe 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.lld:pubmed
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pubmed-article:20350779pubmed:copyrightInfo2010 Elsevier Ireland Ltd. All rights reserved.lld:pubmed
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pubmed-article:20350779pubmed:articleTitleNF-kappaB promotes epithelial-mesenchymal transition, migration and invasion of pancreatic carcinoma cells.lld:pubmed
pubmed-article:20350779pubmed:affiliationInstitute of Physiological Chemistry, University of Ulm, Germany.lld:pubmed
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