RAC3 OVEREXPRESSION INDUCES A TUMOR INITIATING CELL PHENOTYPE

MARÍA F. RUBIO; ELBA VÁZQUEZ; JAWORSKI MARTIN FELIPE; FRANCISCO ROSA; LAURA C. PANELO; MARÍA CECILIA LIRA; MÓNICA ALEJANDRA COSTAS

Mar del Plata

Congreso; Reunión conjunta anual de la Sociedad Argentina de Investigación Clínica (SAIC); 2016

Sociedad Argentina de Investigación Clínica (SAIC)

RAC3 is a nuclear receptor coactivator whose expression is almost undetectable in differentiated cells, but it is overexpressed in several tumor types and required to maintain pluripotency in stem cells. We have previously demonstrated that RAC3 overexpression increases proliferation, apoptosis resistance and the invasive capacity of different tumor cell lines. 9e investigated if RAC3 overexpression in non-tumoral cells could be inducing a CSC-like phenotype. Non-tumoral HEK-293 cells were transfected with a RAC3 expression vector (RAC3) or the empty vector (EV) and, then, different CSC parameters were analyzed. We found a significant increase in CSC protein levels in RAC3 compared with EV (p