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• W2049226990 startingPage "e53676" @default.
• W2049226990 abstract "Background Increased levels of NF-κB are hallmarks of pancreatic ductal adenocarcinoma (PDAC) and both classical and alternative NF-κB activation pathways have been implicated. Methodology/Principal Findings Here we show that activation of the alternative pathway is a source for the high basal NF-κB activity in PDAC cell lines. Increased activity of the p52/RelB NF-κB complex is mediated through stabilization and activation of NF-κB-inducing kinase (NIK). We identify proteasomal downregulation of TNF receptor-associated factor 2 (TRAF2) as a mechanism by which levels of active NIK are increased in PDAC cell lines. Such upregulation of NIK expression and activity levels relays to increased proliferation and anchorage-independent growth, but not migration or survival of PDAC cells. Conclusions/Significance Rapid growth is one characteristic of pancreatic cancer. Our data indicates that the TRAF2/NIK/NF-κB2 pathway regulates PDAC cell tumorigenicity and could be a valuable target for therapy of this cancer." @default.
• W2049226990 created "2016-06-24" @default.
• W2049226990 creator A5019543378 @default.
• W2049226990 creator A5062388236 @default.
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• W2049226990 date "2013-01-03" @default.
• W2049226990 modified "2023-10-05" @default.
• W2049226990 title "Downregulation of TRAF2 Mediates NIK-Induced Pancreatic Cancer Cell Proliferation and Tumorigenicity" @default.
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• W2049226990 doi "https://doi.org/10.1371/journal.pone.0053676" @default.
• W2049226990 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/3536768" @default.
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