Differential β2-adrenergic receptor expression defines the phenotype of non-tumorigenic and malignant human breast cell lines
Metrics: PDF 1227 views | HTML 1773 views | ?
Lucía Gargiulo1,*, Sabrina Copsel1,2,*, Ezequiel M. Rivero1, Céline Galés3, Jean-Michel Sénard3, Isabel A. Lüthy1, Carlos Davio2,*, Ariana Bruzzone1,*
1Instituto de Biología y Medicina Experimental-CONICET, Vuelta de Obligado 2490, C1428ADN, CABA, Argentina
2Laboratorio de Farmacología de Receptores, Departamento de Farmacología, Facultad de Farmacia y Bioquímica, Universidad de Buenos Aires, Junin 956 (1113) CABA, Argentina
3Institut des Maladies Métaboliques et Cardiovasculaires, Institut National de la Santé et de la Recherche Médicale, U1048, Université Toulouse III Paul Sabatier, F-31432 Toulouse, France
*These authors contributed equally to this work
Ariana Bruzzone, e-mail: email@example.com
Keywords: human breast cancer cells, non-tumorigenic breast cells, epinephrine, adrenergic receptors.
Received: June 17, 2014 Accepted: September 06, 2014 Published: November 07, 2014
Breast cancer is the most frequent malignancy in women. Several reports demonstrated that adrenergic receptors (ARs) are involved in breast cancer. Here we observed that epinephrine (Epi), an endogenous AR agonist, caused opposite effects in non-tumorigenic (MCF-10A and HBL-100) and tumor cells (MCF-7 and MDA-MB-231). Thus, Epi, in non-tumor breast cells, as well as isoproterenol (β-agonist), in all cell lines, maintained a benign phenotype, decreasing cell proliferation and migration, and stimulating cell adhesion. β-AR expression and cAMP levels were higher in MCF-10A than in MCF-7 cells. β2-AR knock-down caused a significant increase of cell proliferation and migration, and a decrease of cell adhesion both in basal and in Iso-stimulated conditions. Coincidently, β2-AR over-expression induced a significant decrease of cell proliferation and migration, and an increase of cell adhesion. Therefore, β2-AR is implied in cell phenotype and its agonists or antagonists could eventually complement cancer therapy.
All site content, except where otherwise noted, is licensed under a Creative Commons Attribution 3.0 License.