Abstract
Pancreatic cancer is characterized by invasive and metastatic potential. In this study, effects of the COX-2 inhibitor JTE-522 on cell viability, invasion, and invasion-related cellular properties were determined. JTE-522 (10 microM) induced a 75-90% reduction in invasion, compared to cells treated with a vehicle only, in the COX-2-expressing cells. In contrast, this inhibitor caused no significant reduction in cells lacking COX-2. Determinants of cell invasion, such as cell motility, adhesion to the extracellular matrix, and gelatinolytic activity of metalloproteinase, were also modulated in COX-2-positive pancreatic cancer cells. Thus, COX-2-specific inhibitors may be a useful anti-invasive therapeutic option in pancreatic cancer.
Publication types
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Evaluation Study
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Research Support, Non-U.S. Gov't
MeSH terms
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Benzenesulfonates / pharmacology*
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Cell Adhesion / drug effects
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Cell Division / drug effects
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Cell Movement / drug effects
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Cell Survival / drug effects
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Cyclooxygenase 2
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Cyclooxygenase 2 Inhibitors
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Cyclooxygenase Inhibitors / pharmacology*
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Drug Evaluation
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Humans
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Isoenzymes / antagonists & inhibitors
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Isoenzymes / physiology*
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Matrix Metalloproteinases / pharmacology
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Membrane Proteins
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Neoplasm Invasiveness / prevention & control*
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Oxazoles / pharmacology*
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Pancreatic Neoplasms / drug therapy
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Pancreatic Neoplasms / enzymology*
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Pancreatic Neoplasms / pathology
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Prostaglandin-Endoperoxide Synthases / physiology*
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Tumor Cells, Cultured
Substances
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4-(4-cyclohexyl-2-methyloxazol-5-yl)-2-fluorobenzenesulfonamide
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Benzenesulfonates
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Cyclooxygenase 2 Inhibitors
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Cyclooxygenase Inhibitors
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Isoenzymes
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Membrane Proteins
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Oxazoles
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Cyclooxygenase 2
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PTGS2 protein, human
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Prostaglandin-Endoperoxide Synthases
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Matrix Metalloproteinases