Adrenergic effects on human breast cell proliferation, adhesion and migration

GARGIULO L; COPSEL S; RIVERO E; GALES C; SENARD JM; DAVIO C; PARIS H; LÜTHY IA; BRUZZONE A

Buenos Aires

Jornada; Primer Encuentro Rioplatense de Biología; 2012

Sociedad Argentina de Biología

ADRENERGIC EFFECTS ON HUMAN BREAST CELL PROLIFERATION, ADHESION AND MIGRATION. Gargiulo L, Copsel S, Rivero EM, Galés C, Senard JM, Davio C, Paris H, Luthy IA and Bruzzone A. IByME-CONICET/Cát. Farmacología de Receptores FFyB-UBA/INSERM-Francia. Beta-adrenergic receptors (B-AR) were described in tumor and non tumor breast cell lines. The aim of this work was to study the effect of the endogenous catecholamine epinephrine (Epi), the Beta-agonist isoproterenol (Iso) and the alpha2-agonist (Dex) on cell proliferation (measured by thymidine incorporation and cell count), cell adhesion and migration (transwell assays) on non tumor human breast cell lines MCF-10A and HBL-100 and MCF-7 and MDA-MB-231 tumor cell lines. Epi decreased cell proliferation, increased cell adhesion and reduced migration on non tumor cells. Similar results were obtained when the cells were incubated with Iso, suggesting the role of B-AR as a mediator of stress response in non tumor cells. In MCF-7, Epi increased cell proliferation and migration. Similar results were observed with Dex. Adhesion on tumor cells was not modified by either Epi or Dex. MCF-10A and MCF-7 cells were transfected in order to overexpress the B-AR or knock-down the receptor expression using siRNAs. In both cell lines, receptor over-expression caused a decrease in cell proliferation and an increase of basal cell adhesion. Knock-down of B-RA caused an augment on cell proliferation and a decrease on basal cell adhesion. These results describe the role of AR as mediators of stress response in human tumor and non tumor breast cells.