IMBECU   20882
INSTITUTO DE MEDICINA Y BIOLOGIA EXPERIMENTAL DE CUYO
Unidad Ejecutora - UE
congresos y reuniones científicas
Título:
ESTRADIOL REGULATES BREAST CANCER CELL MOVEMENT VIA Src/FAK/ Paxillin
Autor/es:
SHORTREDE JE; NEIRA FJ; JAHN GA; FLAMINI MI; FANELLI MA ; SANCHEZ AM
Reunión:
Congreso; XXXI Reunión Anual de la Sociedad de Biología de Cuyo,; 2013
Resumen:
Breast cancer is the major cause of cancer-related death in women. Estrogens stimulate the growth of hormone-dependent breast cancer by increasing cellular proliferation. The ability of cells to migrate in tissue is essential to the metastatic process. 17-beta-estradiol (E2) activates several signaling pathways that control different process like cell mobility. These actions are driven by actin remodeling and are stabilized by the development of adhesion sites to extracellular matrix (ECM). Paxillin is a scaffold protein that localizes to the intracellular surface of sites of cell adhesion to the ECM. Paxillin phosphorylation facilitate the functional integration of many focal adhesion proteins like Src and FAK kinase, leading to the recruitment of numerous regulatory and structural proteins that together control the dynamic changes in cell adhesion and cytoskeletal reorganization that are necessary for cell mobility. We studied the rapid actions of physiological concentration of E2 on Src, FAK and Paxillin activation, through the estrogens receptors, and they implicance on cell morphology and cellular movement in MCF-7 (ER+) breast cancer cells. We show that E2 regulates actin remodeling and cell movement in MCF-7 cells via activation by phosphorylation of Src, FAK and Paxillin. Our findings provide a molecular mechanism by which estrogens exert this action in breast cancer cells