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Artículo

Classical membrane progesterone receptors in murine mammary carcinomas: agonistic effects of progestins and RU-486 mediating rapid non-genomic effects.

Bottino, Maria CeciliaIcon ; Cerliani, Juan PabloIcon ; Rojas, Paola AndreaIcon ; Giulianelli, Sebastian JesusIcon ; Soldati, Rocío; Mondillo, CarolinaIcon ; Gorostiaga, Maria AliciaIcon ; Pignataro, Omar PedroIcon ; Calvo, Juan CarlosIcon ; Gutkind, Silvio J.; Amornphimoltham, Panomwat; Molinolo, Alfredo A.; Luthy, Isabel AliciaIcon ; Lanari, Claudia Lee MalvinaIcon
Fecha de publicación: 04/2010
Editorial: Springer
Revista: Breast Cancer Research And Treatment
ISSN: 0167-6806
e-ISSN: 1573-7217
Idioma: Inglés
Tipo de recurso: Artículo publicado
Clasificación temática:
Patología; Oncología

Resumen

In this article, we demonstrate the expression of functional progesterone binding sites at the cell membrane in murine mammary carcinomas that are stimulated by progestins and inhibited by antiprogestins. Using confocal immunofluorescence, ligand binding and cell compartment-specific western blots, we were able to identify the presence of the classical progesterone receptors. Medroxyprogesterone acetate (MPA) and RU-486 (1 × 10(-11) and 1 × 10(-8) M) behaved as agonists activating extracellular signal-regulated kinases (ERKs) and progestin-regulated proteins, except for Cyclin D1 and Tissue factor which failed to increase with 1 × 10(-8) M RU-486, an experimental condition that allows PR to bind DNA. These results predicted a full agonist effect at low concentrations of RU-486. Accordingly, at concentrations lower than 1 × 10(-11) M, RU-486 increased cell proliferation in vitro. This effect was abolished by incubation with the ERK kinase inhibitor PD 98059 or by OH-tamoxifen. In vivo, at a daily dose of 1.2 μg/kg body weight RU-486 increased tumor growth, whereas at 12 mg/kg induces tumor regression. Our results indicate that low concentrations of MPA and RU-486 induce similar agonistic non-genomic effects, whereas RU-486 at higher concentrations may inhibit cell proliferation by genomic-induced effects. This suggests that RU-486 should be therapeutically administered at doses high enough to guarantee its genomic inhibitory effect.
Palabras clave: Membrane Progesterone Receptors , Mammary Carcinomas , Progesterone Receptor Isoforms , Membrane-Initiated Steroid Signaling , Antiprogestins , Breast Cancer Treatment , Non-Genomic Effects , Progestins
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info:eu-repo/semantics/openAccess Excepto donde se diga explícitamente, este item se publica bajo la siguiente descripción: Creative Commons Attribution-NonCommercial-ShareAlike 2.5 Unported (CC BY-NC-SA 2.5)
Identificadores
URI: http://hdl.handle.net/11336/14295
URL: https://link.springer.com/article/10.1007/s10549-010-0971-3
URL: http://dx.doi.org/10.1007/s10549-010-0971-3
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Articulos(IBYME)
Articulos de INST.DE BIOLOGIA Y MEDICINA EXPERIMENTAL (I)
Citación
Bottino, Maria Cecilia; Cerliani, Juan Pablo; Rojas, Paola Andrea; Giulianelli, Sebastian Jesus; Soldati, Rocío; et al.; Classical membrane progesterone receptors in murine mammary carcinomas: agonistic effects of progestins and RU-486 mediating rapid non-genomic effects.; Springer; Breast Cancer Research And Treatment; 126; 3; 4-2010; 621-636
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