Suppression of pancreatic cancer cell invasion by a cyclooxygenase-2-specific inhibitor

• Published in: Clinical & experimental metastasis 2003-01, Vol.20 (7), p.577-584
• Main Authors: Okami, Jiro, Nakamori, Shoji, Hiraoka, Nobuaki, Tsujie, Masanori, Hayashi, Nobuyasu, Yamamoto, Hirofumi, Fujiwara, Yoshiyuki, Nagano, Hiroaki, Dono, Keizo, Umeshita, Koji, Sakon, Masato, Monden, Morito
• Format: Article
• Language: English
• Subjects: Benzenesulfonates - pharmacology; Cell Adhesion - drug effects; Cell Division - drug effects; Cell Movement - drug effects; Cell Survival - drug effects; Cyclooxygenase 2; Cyclooxygenase 2 Inhibitors; Cyclooxygenase Inhibitors - pharmacology; Drug Evaluation; Humans; Isoenzymes - antagonists & inhibitors; Isoenzymes - physiology; Matrix Metalloproteinases - pharmacology; Membrane Proteins; Neoplasm Invasiveness - prevention & control; Oxazoles - pharmacology; Pancreatic cancer; Pancreatic Neoplasms - drug therapy; Pancreatic Neoplasms - enzymology; Pancreatic Neoplasms - pathology; Prostaglandin-Endoperoxide Synthases - physiology; Tumor Cells, Cultured
• ISSN: 0262-0898; 1573-7276
• DOI: 10.1023/a:1027319903359

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.