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Carcinogenesis, Vol 18, 795-799, Copyright © 1997 by Oxford University Press

ARTICLES

Benzo[a]pyrene up-regulates cyclooxygenase-2 gene expression in oral epithelial cells

DJ Kelley, JR Mestre, K Subbaramaiah, PG Sacks, SP Schantz, T Tanabe, H Inoue, JT Ramonetti and AJ Dannenberg
Head and Neck Service, Department of Surgery, Memorial Sloan Kettering Cancer Center, New York, NY 10021, USA.

Cyclooxygenase may be important in the pathogenesis of smoking-related cancer because it activates carcinogens and catalyzes prostaglandin biosynthesis. We determined the effects of benzo[a]pyrene (B[a]P), a polycyclic aromatic hydrocarbon in tobacco smoke, on cyclooxygenase-2 (Cox-2) mRNA, protein and synthesis of prostaglandin E2 (PGE2) in normal and transformed oral epithelial cells. Treatment with B[a]P caused a dose-dependent increase in production of PGE2, with a maximal increase of approximately 100%. Enhanced synthesis of PGE2 was associated with increased amounts of Cox-2 protein. B[a]P also caused a two-fold increase in Cox-2 mRNA in both normal and transformed cells. Transient transfections with a Cox-2 promoter construct showed that B[a]P-mediated induction of Cox-2 mRNA reflected increased transcription. Levels of Cox-1 were unaffected by B[a]P. B[e]P did not affect the synthesis of PGE2 or amounts of Cox-2. These data are important because B[a]P-mediated induction of Cox-2 may predispose to carcinogenesis by enhancing the production of mutagens and the synthesis of prostaglandins.
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