1. ^*Department of Dermatology, College of Physicians and Surgeons, Columbia University, New York, New York, USA
2. ^†Division of Cancer Prevention, National Cancer Institute, Bethesda, Maryland, USA

Correspondence: Mohammad Athar, Department of Dermatology, Vanderbilt Clinic 15-204, Columbia University College of Physicians and Surgeons, 630 West 168th Street, New York, NY 10032, USA. Email: ma493@columbia.edu

Received 21 December 2004; Revised 4 April 2005; Accepted 8 April 2005.

Abstract

Enhanced prostaglandin production via upregulated cyclooxygenase-2 (COX-2) expression is a likely contributing factor in ultraviolet B (UVB)-induced non-melanoma skin cancer (NMSC), which consists primarily of squamous cell carcinoma (SCC) and basal cell carcinoma (BCC). The four E prostanoid (EP) receptors, designated EP₁ through EP₄, are known to bind prostaglandin E₂ (PGE₂), the major prostaglandin present in the skin. We used murine models of UVB-induced SCC and BCC, as well as human NMSC from sun-exposed sites, to investigate the expression of EP receptors during UVB-induced tumorigenesis. We observed that UVB-induced murine SCC are associated with markedly altered expression patterns of the EP receptors when compared with non-irradiated skin. In contrast, expression of all EP receptors was largely absent in UVB-induced murine BCC. We also observed expression of all four EP receptors in human SCC, with altered expression of their mRNA levels as compared with adjacent tumor-free skin. Consistent with our murine studies, no EP receptor expression was detected in human BCC, and their mRNA expression levels showed no change from the adjacent non-tumor-bearing skin. These data suggest that altered EP receptor expression may play a differential role in the development of UVB-induced SCC and BCC in murine and human skin.