Downregulation of TRAF2 Mediates NIK-Induced Pancreatic Cancer Cell Proliferation and TumorigenicityReportar como inadecuado




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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.



Autor: Heike Döppler, Geou-Yarh Liou, Peter Storz

Fuente: http://plos.srce.hr/



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