ANGIOTENSIN II INDUCE EMT THROUGH AKT ACTIVATION. ANGIOTENSIN 1-7 INHIBIT ANGIOTENSINA II INDUCED TUMORIGENIC FEATURES IN BREAST CANCER CELLS.

NADIA CAMBADOS; SUBERBORDES, MELISA DEL VALLLE; CAROLINA P. SCHERE LEVY; THOMAS WALTHER

Ciudad de Buenos Aires

Congreso; Sociedad Argentina de Investigación Clínica; 2016

SAIC

Angiotensin II (AngII), the main effector peptide of the Renin Angiotensin System, has been implicated in multiple aspects of cancer progression. Angiotensin (1-7) [Ang (1-7)], is a biologically active heptapeptide, generated predominantly from AngII that counterbalances AngII actions in different pathophysiological settings. The porpoise of this study was to analyse the impact of Ang-(1-7) on AngII-induced pro-tumorigenic features on normal mammary epithelial cells and breast cancer cells. We found that AngII promoted EMT on normal mammary epithelial cell NMuMG, epithelial markers such as E-cadherin were inhibited (Agni vs C, p