抄録
Cyclooxygenases (COXs) are rate-limiting enzymes that initiate the conversion of arachidonic acid to prostanoids. COXs are classified into two isoforms: COX-1 and COX-2. COX-2 is an inducible isoform upregulated by proinflammatory cytokines. Recently, prominent COX-2 expression has been reported in several human cancers, including carcinoma of the colon, breast, lung, head and neck, and gallbladder. Overexpression of COX-2, which is involved in cell proliferation via prostaglandin E2 (PGE2) synthesis, may play a role in tumor progression. In this study, we immunohistochemically characterized COX-2 expression in various diseases of the maxillary sinus, including 5 cases of postoperative maxillary cyst, 5 of maxillary sinusitis, 5 of inverted papilloma, and 5 of maxillary sinus carcinoma. In addition, secretory phospholipase A2-V, CD3, CD20, and CD68 expression in these lesions was also examined to clarify the relation to COX-2 upregulation. COX-2 was not expressed in the ciliated columnar epithelium in sinusitis, but was expressed in squamous cell metaplasia in maxillary cyst and inverted papilloma. In carcinoma of the maxillary sinus, COX-2 was overexpressed in numerous cancer cells. The proportions of CD3 and CD68 positive cells in carcinoma were clearly lower than those in sinusitis. These results indicated that COX-2 expression correlates with squamous cell metaplasia and epithelial cell proliferation. The end product of the arachidonic acid cascade, PGE2, may be involved in downregulation of CD3 and CD68 and the proliferation of maxillary sinus carcinoma. Further studies of COX-2 inhibitors as potential antitumor agents in maxillary sinus carcinoma are warranted.
