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TNF-α-induced IL-32 expression in esophageal cancer: cross talk JNK/Akt signaling pathways

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Jack M. Neuzillet, Cailin Traynor, Grace Hullmann, Gabriel Tyritzis, John Shimizu¹∗

 
 
 Abstract

Esophageal cancer is the seventh leading cause of cancer death in males in USA, Interleukin (IL)-32 is a recently identified proinflammatory cytokine that is one of the IL-18 inducible genes, and plays an important role in autoimmune and inflammatory diseases. IL-32 is recently described in esophageal cancer pathway via induction of nuclear factor NF-κB activation. We investigated the expression of IL-32 by TNF-α in esophageal cancer. Human esophageal cancer cells were cultured in the presence or absence of TNF-α to analyze the expression of IL-32 by quantitative RT-PCR and enzyme-linked immunosorbent assay. Further, activation of Akt and JNK signaling pathways were investigated by Western blot. TNF-α induced enhanced IL-32 release in human esophageal cancer cells. These data suggest that activation of Akt and JNK pathways regulated TNF-α-induced IL-32 expression in human esophageal cancer. We concluded that TNF-α/IL-32 pathway may be a potential marker and may be therapeutic target for esophageal cancer.

Keywords: Esophageal cancer; IL-32; TNF-α; Akt and JNK pathways; NF-κB activation

 

Copyright © 2016 by The American Society for BioMedicine and BM-Publisher, Inc.

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DOI: 10.18081/ajbm/2333-5106-013-12/73-85

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Case Report
American Journal of BioMedicine Volume 1, Issue 2, pages 73-85
Received July 22, 2013; accepted November 03, 2013; published December 11, 2013

How to cite this article
Neuzillet JM, Traynor C, Hullmann G, Tyritzis G, Shimizu J. TNF-α-induced IL-32 expression in esophageal cancer: cross talk JNK/Akt signaling pathways. American Journal of BioMedicine 2013;1(2):73-85.

Article outline
1. Abstract
2. Keywords
3. Introduction
4. Materials and Methods
6. Discussion
7. Acknowledgements
8. References

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