Critical role of NF-κB in pancreatic cancer

Lakshmi Prabhu _, Rasika Mundade, Murray Korc, Patrick J. Loehrer and Tao Lu

PDF  |  HTML  |  How to cite

Oncotarget. 2014; 5:10969-10975. https://doi.org/10.18632/oncotarget.2624

Metrics: PDF 3134 views  |   HTML 3181 views  |   ?  


Lakshmi Prabhu1, Rasika Mundade1, Murray Korc2,3, Patrick J. Loehrer4, Tao Lu1,3,5

1Department of Pharmacology and Toxicology, Indiana University School of Medicine, Indianapolis, IN, USA

2Department of Medicine, Indiana University School of Medicine, Indianapolis, IN, USA

3Department of Biochemistry and Molecular Biology, Indiana University School of Medicine, Indianapolis, IN, USA

4Division of Hematology and Oncology, Indiana Cancer Pavilion, Indianapolis, IN, USA

5Department of Medical and Molecular Genetics, Indiana University School of Medicine, Indianapolis, IN, USA

Correspondence to:

Tao Lu, e-mail: [email protected]

Keywords: NF-κB, pancreatic cancer

Received: August 26, 2014     Accepted: October 23, 2014     Published: December 19, 2014


Pancreatic ductal adenocarcinoma (PDAC) is one of the deadliest cancers, and in spite of intense efforts there are limited therapeutic options for patients with PDAC. PDACs harbor a high frequency of Kras mutations and other driver mutations that lead to altered signaling pathways and contribute to therapeutic resistance. Importantly, constitutive activation of nuclear factor κB (NF-κB) is frequently observed in PDAC. An increasing body of evidence suggests that both classical and non-classical NF-κB pathways play a crucial role in PDAC development and progression. In this review, we update the most recent advances regarding different aspects of NF-κB involvement in PDAC development and progression, emphasizing its potential as a therapeutic target and the need to discover pathway-specific cytosolic NF-κB regulators which could be used to design novel therapeutic strategies for PDAC.

Creative Commons License All site content, except where otherwise noted, is licensed under a Creative Commons Attribution 3.0 License.
PII: 2624