Overexpression of Cyclooxygenase-2 in Nasopharyngeal Carcinoma and Association With Epidermal Growth Factor Receptor Expression

Open Access
Publisher Website
Google Scholar
Abstract
Cyclooxygenase (COX), a key enzyme in the synthesis of prostaglandins, exists in 2 isoforms: COX-1 and COX-2. COX-1 is expressed constitutively in most tissues and is responsible for the production of prostaglandins that mediates normal physiologic functions. COX-2, in contrast, is undetectable in most normal tissues and is induced by inflammatory cytokines, tumor promoters, and growth factors.1 COX-2 appears to have an important role in carcinogenesis. COX-2 overexpression has been detected in various malignancies,2 and inhibition of tumor growth, metastases, and angiogenesis by selective COX-2 inhibitors has been shown in vitro and in animal models.3 The mechanisms that underlie the tumorigenic effect of COX-2 include inhibition of apoptosis, increase of metastatic potential, and tumor angiogenesis via up-regulation of vascular endothelial growth factor (VEGF).3,4