NDLI: Activation of Toll-Like Receptor 4 Is Required for the Synergistic Induction of Dual Oxidase 2 and Dual Oxidase A2 by Interferon-γ and Lipopolysaccharide in Human Pancreatic Cancer Cell $Lines^{§}$

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Activation of Toll-Like Receptor 4 Is Required for the Synergistic Induction of Dual Oxidase 2 and Dual Oxidase A2 by Interferon-γ and Lipopolysaccharide in Human Pancreatic Cancer Cell $Lines^{§}$

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Activation of Toll-Like Receptor 4 Is Required for the Synergistic Induction of Dual Oxidase 2 and Dual Oxidase A2 by Interferon-γ and Lipopolysaccharide in Human Pancreatic Cancer Cell $Lines^{§}$

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Haines, Diana C. Wu, Yongzhong Liu, Han Hollingshead, Melinda Butcher, Donna Meitzler, Jennifer L. Roy, Krishnendu Lu, Jiamo Juhasz, Agnes Jiang, Guojian Doroshow, James H. Antony, Smitha
Description	Country affiliation: United States Author Affiliation: Wu Y ( Laboratory of Molecular Pharmacology, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA.)
Abstract	Pancreatitis is associated with release of proinflammatory cytokines and reactive oxygen species and plays an important role in the development of pancreatic cancer. We recently demonstrated that dual oxidase (Duox)2, an NADPH oxidase essential for reactive oxygen species-related, gastrointestinal host defense, is regulated by IFN-Î³-mediated Stat1 binding to the Duox2 promoter in pancreatic tumor lines. Because LPS enhances the development and invasiveness of pancreatic cancer in vivo following TLR4-related activation of NF-κB, we examined whether LPS, alone or combined with IFN-Î³, regulated Duox2. We found that upregulation of TLR4 by IFN-Î³ in BxPC-3 and CFPAC-1 pancreatic cancer cells was augmented by LPS, resulting in activation of NF-κB, accumulation of NF-κB (p65) in the nucleus, and increased binding of p65 to the Duox2 promoter. TLR4 silencing with small interfering RNAs, as well as two independent NF-κB inhibitors, attenuated LPS- and IFN-Î³-mediated Duox2 upregulation in BxPC-3 cells. Induction of Duox2 expression by IFN-Î³ and LPS may result from IFN-Î³-related activation of Stat1 acting in concert with NF-κB-related upregulation of Duox2. Sustained extracellular accumulation of H(2)O(2) generated by exposure to both LPS and IFN-Î³ was responsible for an â ¼50% decrease in BxPC-3 cell proliferation associated with a G(1) cell cycle block, apoptosis, and DNA damage. We also demonstrated upregulation of Duox expression in vivo in pancreatic cancer xenografts and in patients with chronic pancreatitis. These results suggest that inflammatory cytokines can interact to produce a Duox-dependent pro-oxidant milieu that could increase the pathologic potential of pancreatic inflammation and pancreatic cancer cells.
ISSN	00221767
e-ISSN	15506606
DOI	10.4049/jimmunol.1201725
Journal	The Journal of Immunology
Issue Number	4
Volume Number	190
Language	English
Publisher	The American Association of Immunologists
Publisher Date	2013-02-15
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Interferon-gamma Physiology Lipopolysaccharides Membrane Proteins Biosynthesis Nadph Oxidase Pancreatic Neoplasms Immunology Metabolism Toll-like Receptor 4 Animals Cell Line, Tumor Chronic Disease Mice Mice, Nude Neoplasm Transplantation Enzymology Pancreatitis Random Allocation Reactive Oxygen Species Signal Transduction Tumor Cells, Cultured Research Support, N.i.h., Extramural Discipline Immunology
Content Type	Text
Resource Type	Article
Subject	Immunology and Allergy Immunology

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Activation of Toll-Like Receptor 4 Is Required for the Synergistic Induction of Dual Oxidase 2 and Dual Oxidase A2 by Interferon-γ and Lipopolysaccharide in Human Pancreatic Cancer Cell Lines§

NADPH oxidase 4 modulates hepatic responses to lipopolysaccharide mediated by Toll-like receptor-4

Mice Plasmacytoid Dendritic Cells Were Activated by Lipopolysaccharides Through Toll-Like Receptor 4/Myeloid Differentiation Factor 2

Physical contact between lipopolysaccharide and toll-like receptor 4 revealed by genetic complementation.

Up-regulation and Sustained Activation of Stat1 Are Essential for Interferon-γ (IFN-γ)-induced Dual Oxidase 2 (Duox2) and Dual Oxidase A2 (DuoxA2) Expression in Human Pancreatic Cancer Cell Lines*

Up-regulation and Sustained Activation of Stat1 Are Essential for Interferon-γ (IFN-γ)-induced Dual Oxidase 2 (Duox2) and Dual Oxidase A2 (DuoxA2) Expression in Human Pancreatic Cancer Cell Lines

Phospholipase Cγ-2 and Intracellular Calcium Are Required for Lipopolysaccharide-induced Toll-like Receptor 4 (TLR4) Endocytosis and Interferon Regulatory Factor 3 (IRF3) Activation

CD14 knockdown reduces lipopolysaccharide-induced cell viability and expression of inflammation-associated genes in gastric cancer cells in vitro and in nude mouse xenografts.

Lipopolysaccharide inhibition of glucose production through the Toll-like receptor-4, myeloid differentiation factor 88, and nuclear factor kappa b pathway.

Activation of Toll-Like Receptor 4 Is Required for the Synergistic Induction of Dual Oxidase 2 and Dual Oxidase A2 by Interferon-γ and Lipopolysaccharide in Human Pancreatic Cancer Cell $Lines^{§}$

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