Differential β₂-adrenergic receptor expression defines the phenotype of non-tumorigenic and malignant human breast cell lines.
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.
Instituto de Biología y Medicina Experimental-CONICET, Vuelta de Obligado 2490, C1428ADN, CABA, Argentina.
Lucía
L
Gargiulo
Instituto de Biología y Medicina Experimental-CONICET, Vuelta de Obligado 2490, C1428ADN, CABA, Argentina. Laboratorio de Farmacología de Receptores, Departamento de Farmacología, Facultad de Farmacia y Bioquímica, Universidad de Buenos Aires, Junin 956 (1113) CABA, Argentina.
Sabrina
S
Copsel
Instituto de Biología y Medicina Experimental-CONICET, Vuelta de Obligado 2490, C1428ADN, CABA, Argentina.
Ezequiel M
EM
Rivero
Institut 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.
Céline
C
Galés
Institut 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.
Jean-Michel
JM
Sénard
Instituto de Biología y Medicina Experimental-CONICET, Vuelta de Obligado 2490, C1428ADN, CABA, Argentina.
Isabel A
IA
Lüthy
Laboratorio de Farmacología de Receptores, Departamento de Farmacología, Facultad de Farmacia y Bioquímica, Universidad de Buenos Aires, Junin 956 (1113) CABA, Argentina.
Carlos
C
Davio
Instituto de Biología y Medicina Experimental-CONICET, Vuelta de Obligado 2490, C1428ADN, CABA, Argentina.
Ariana
A
Bruzzone
D058666:Adrenergic beta-2 Receptor Agonists / Q000494:pharmacology; D001943:Breast Neoplasms / Q000378:metabolism* / Q000473:pathology*; D002448:Cell Adhesion / Q000187:drug effects / Q000502:physiology; D002460:Cell Line; D045744:Cell Line, Tumor; D049109:Cell Proliferation / Q000502:physiology; D020927:Dexmedetomidine / Q000494:pharmacology; D018450:Disease Progression; D004837:Epinephrine / Q000494:pharmacology; D005260:Female; D055785:Gene Knockdown Techniques; D006801:Humans; D007545:Isoproterenol / Q000494:pharmacology; D061986:MCF-7 Cells; D010641:Phenotype; D018343:Receptors, Adrenergic, beta-2 / Q000096:biosynthesis* / Q000235:genetics; D015398:Signal Transduction; D014162:Transfection
D058666:Adrenergic beta-2 Receptor Agonists; D018343:Receptors, Adrenergic, beta-2; D020927:Dexmedetomidine; D007545:Isoproterenol; D004837:Epinephrine