1. ¹Department of Pathology, The Ohio State University, Columbus, Ohio, USA
2. ²Department of Surgery, Loyola University Medical Center, Burn & Shock Trauma Institute, Maywood, Illinois, USA
3. ³Department of Veterinary Biosciences, The Ohio State University, Columbus, Ohio, USA
4. ⁴ONO Pharmaceutical Company Ltd, Osaka, Japan

Correspondence: Dr Tatiana M. Oberyszyn, The Ohio State University, 1645 Neil Avenue, 129 Hamilton Hall, Columbus, OH 43210, USA. E-mail: oberyszyn.1@osu.edu

Received 13 May 2005; Revised 23 August 2005; Accepted 2 September 2005.

Abstract

Chronic exposure to UV light, the primary cause of skin cancer, results in the induction of high levels of cyclooxygenase-2 (COX-2) expression in the skin. The involvement of COX-2 in the carcinogenesis process is mediated by its enzymatic product, prostaglandin E₂ (PGE₂). PGE₂ has been shown to have a variety of activities that can contribute to tumor development and growth. The effects of PGE₂ on different cell types are mediated by four E prostanoid (EP) receptors, EP₁–EP₄. While recent studies have demonstrated the importance of EP₁ in the development of colon and breast cancer, the extent of EP₁ involvement in the cutaneous photocarcinogenesis process is unknown. This study found that topical treatment with celecoxib or the specific EP₁ antagonist ONO-8713 decreased acute UVB-induced inflammation in the skin and significantly reduced the number of tumors per mouse following 25 weeks of UVB exposure and topical treatment. This study suggests that drugs designed to block EP₁ may have the potential to be used as anti-inflammatory and/or chemopreventive agents that reduce the risk of skin cancer development.