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Updated: Jan 31, 2026

An Orthotopic Resectional Mouse Model of Pancreatic Cancer
Published on: September 24, 2020
Advancement of NF-κB Signaling Pathway: A Novel Target in Pancreatic Cancer
Kartick C Pramanik1, Monish Ram Makena2, Kuntal Bhowmick3
1Department of Basic Sciences, Kentucky College of Osteopathic Medicine, University of Pikeville, Pikeville, KY 41501, USA. kartickpramanik@upike.edu.
Abstract:
Pancreatic ductal adenocarcinoma (PDAC) is one of the deadliest cancers and is the third highest among cancer related deaths. Despite modest success with therapy such as gemcitabine, pancreatic cancer incidence remains virtually unchanged in the past 25 years. Among the several driver mutations for PDAC, Kras mutation contributes a central role for its development, progression and therapeutic resistance. In addition, inflammation is implicated in the development of most human cancer, including pancreatic cancer. Nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) is recognized as a key mediator of inflammation and has been frequently observed to be upregulated in PDAC. Several lines of evidence suggest that NF-κB pathways play a crucial role in PDAC development, progression and resistance. In this review, we focused on emphasizing the recent advancements in the involvement of NF-κB in PADC's progression and resistance. We also highlighted the interaction of NF-κB with other signaling pathways. Lastly, we also aim to discuss how NF-κB could be an excellent target for PDAC prevention or therapy. This review could provide insight into the development of novel therapeutic strategies by considering NF-κB as a target to prevent or treat PDAC.
Insights
Nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) is crucial in pancreatic cancer progression and resistance. Targeting NF-κB offers a promising strategy for developing novel pancreatic ductal adenocarcinoma (PDAC) therapies.
Area of Science:
- Oncology
- Molecular Biology
- Cancer Research
Background:
- Pancreatic ductal adenocarcinoma (PDAC) is a leading cause of cancer death with limited therapeutic options.
- Kras mutations and inflammation are key drivers in PDAC development and progression.
- Nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) is a central mediator of inflammation and is upregulated in PDAC.
Purpose of the Study:
- To review recent advancements in understanding NF-κB's role in PDAC progression and therapeutic resistance.
- To highlight the interactions between NF-κB and other signaling pathways in PDAC.
- To explore the potential of targeting NF-κB for PDAC prevention and treatment.
Main Methods:
- Literature review of recent scientific publications.
- Analysis of signaling pathways involved in PDAC.
- Synthesis of information on NF-κB's role in cancer development and resistance.
Main Results:
- NF-κB signaling is significantly involved in PDAC development, progression, and resistance to therapies.
- NF-κB interacts with multiple signaling pathways, influencing PDAC's complex biology.
- Evidence suggests NF-κB is a viable therapeutic target for PDAC.
Conclusions:
- Targeting NF-κB pathways presents a promising avenue for novel therapeutic strategies against PDAC.
- Understanding NF-κB's role can lead to improved prevention and treatment of pancreatic cancer.
- Further research into NF-κB modulation could significantly impact PDAC patient outcomes.
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