Journal
MOLECULAR ONCOLOGY
Volume 8, Issue 8, Pages 1626-1639Publisher
ELSEVIER SCI LTD
DOI: 10.1016/j.molonc.2014.06.013
Keywords
Prostaglandin E-2; EP4 receptor; Tumor promotion; Skin tumors; Murine skin
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Funding
- National Institutes of Health [CA100140, P30 CA16672-30]
- DHHS/NCI Cancer Center Support Grant (CCSG)
- CPRIT Core Facility Support Grant [RP120348]
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To determine whether the EP4 receptor for prostaglandin E-2 (PGE(2)) contributes to the tumor promoting activity of PGs in murine skin, EP4 over-expressing mice (BK5.EP4) were generated and subjected carcinogenesis protocols. An initiation/promotion protocol resulted in 25-fold more squamous cell carcinomas (SCCs) in the BK5.EP4 mice than wild type (WT) mice. An increase in SCCs also occurred following treatment with initiator alone or UV irradiation. The initiator dimethylbenz[a]anthracene caused cytotoxicity in BK5.EP4, but not WT mice, characterized by sloughing of the interfollicular epidermis, regeneration and subsequent SCC development. A comparison of transcriptomes between BK5.EP4 and WT mice treated with PGE(2) showed a significant upregulation of a number of genes known to be associated with tumor development, supporting a pro-tumorigenic role for the EP4 receptor. (C) 2014 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved.
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