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Carcinogenesis Advance Access published online on August 19, 2005
Carcinogenesis, doi:10.1093/carcin/bgi213
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© The Author 2005. Published by Oxford University Press. All rights reserved. For permissions, please email: journals.permissions@oupjournals.org
Received April 14, 2005
Revised July 21, 2005
Accepted August 12, 2005

CARCINOGENESIS

Potentiation of tumor formation by topical administration of 15-deoxy-{Delta}12,14-prostaglandin J2 in a model of skin carcinogenesis

Olga Millán 1 {dagger}, Daniel Rico 1 {dagger}, Héctor Peinado 2, Natasha Zarich 3, Konstantinos Stamatakis 4, Dolores Pérez-Sala 4, José M. Rojas 3, Amparo Cano 2, and Lisardo Boscá 1*

1 Instituto de Bioquímica, CSIC-UCM. 28040 Madrid, Spain; Centro Nacional de Investigaciones Cardiovasculares. 28029 Madrid, Spain
2 Instituto de Investigaciones Biomédicas, CSIC. 28029 Madrid, Spain
3 Unidad de Biología Celular. Centro Nacional de Microbiología. Instituto de Salud Carlos III. 28220 Majadahonda, Madrid, Spain
4 Departamento de Estructura y Función de Proteínas. Centro de Investigaciones Biológicas, CSIC. 28040 Madrid, Spain

* To whom correspondence should be addressed.
Lisardo Boscá, E-mail: lbosca{at}cnic.es


  Abstract

The effect of prostaglandins on the development of papillomas has been investigated in mice receiving PGE2 or the cyclopentenone 15-deoxy-{Delta}12,14-PGJ2 (15dPGJ2) topically, and using the 7,12-dimethylbenz[a]anthracene (DMBA)-induced tetradecanoylphorbol acetate (TPA)-promoted model of skin carcinogenesis. The presence of 15dPGJ2 during DMBA and TPA treatment inhibited apoptosis and increased the rate, number, size and vascularization of the papillomas, some of them progressing into carcinomas. Moreover, skin sections from mice treated for one week with DMBA and 15dPGJ2 showed a very reduced rate of apoptotic cells, and an enhanced expression of VEGF, when compared with animals receiving DMBA, with or without PGE2. Analysis of molecular events in the MCA3D keratinocyte cell line showed that 15dPGJ2 activated Ras and improved cell viability by inhibiting DMBA-dependent apoptosis. In addition to this, cell adhesion was impaired in MCA3D keratinocytes co-treated with 15dPGJ2 and DMBA, at the time that expression of cyclooxygenase 2 was observed under these conditions. These effects mediated by 15dPGJ2 might contribute to understand the role of cyclooxygenase 2 metabolites in carcinogenesis, leading to an increase of cell viability after mutagenic injury and therefore, in the progression of tumors.

{dagger} OM and DR contributed equally to this work


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