Article
Authorship
GARGIULO L
;
COPSEL SABRINA
;
RIVERO EM
;
GALES C
;
SENARD JM
;
LUTHY I
;
DAVIO, CARLOS ALBERTO
;
BRUZZONE ARIANA
Date
2014
Publishing House and Editing Place
impact journal
Magazine
ONCOTARGET,
vol. 20
(pp. 10058-10069)
- ISSN 1949-2553
impact journal
impact journal
ISSN
1949-2553
Summary
Information provided by the agent in
SIGEVA
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 MDAMB- 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...
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 MDAMB- 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.
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Key Words
human breast cancer cellsnon-tumorigenic breast cellsadrenergic receptorsepinephrine