NF-κB promotes epithelial-mesenchynmal transition, migration and invasion of pancreatic carcinoma cells

被引：197

作者：

Maier, Harald J. ^{[1
]}

Schmidt-Strassburger, Uta ^{[1
]}

Huber, Margit A. ^{[2
,3
]}

Wiedemann, Eva M. ^{[3
]}

Beug, Hartmut ^{[3
]}

Wirth, Thomas ^{[1
]}

机构：

[1] Univ Ulm, Inst Physiol Chem, D-89081 Ulm, Germany

[2] Univ Ulm, Dept Dermatol & Allerg Dis, D-89081 Ulm, Germany

[3] Res Inst Mol Pathol, A-1030 Vienna, Austria

来源：

CANCER LETTERS | 2010年 / 295卷 / 02期

关键词：

NF-kappa B; Epithelial-mesenchymal transition; Pancreatic adenocarcinoma; Tumour progression; Cell migration; Cell invasion; GROWTH-FACTOR; SNAIL TRANSCRIPTION; GENE-EXPRESSION; TUMOR-GROWTH; ACTIVATION; CANCER; ALPHA; BETA; INFLAMMATION; ADENOCARCINOMA;

D O I：

10.1016/j.canlet.2010.03.003

中图分类号：

R73 [肿瘤学];

学科分类号：

100214 ;

摘要：

The transcription factor NF-kappa B is constitutively active in pancreatic adenocarcinoma. Here we explore the contribution of NF-kappa B to the malignant phenotype of pancreatic cancer cells in addition to its anti-apoptotic role. Block of NF-kappa B signalling by non-destructible ham rendered cells resistant to TGF-beta-induced epithelial-mesenchymal transition (EMT). In contrast, NF-kappa B 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-kappa B inhibition or activation, respectively. (C) 2010 Elsevier Ireland Ltd. All rights reserved.

引用

页码：214 / 228

页数：15

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