RAC3 OVEREXPRESSION INDUCES A TUMOR INICIATING CELL PHENOTYPE

LAURA PANELO; FELIPE MARTÍN JAWORSKI; MARÍA FERNANDA RUBIO; M. CECILIA LIRA; FRANCISCO ROSA; ELBA VAZQUEZ; MÓNICA A. COSTAS

Mar del Plata, Buenos Aires

Congreso; LXI REUNIÓN ANUAL DE LA SOCIEDAD ARGENTINA DE INVESTIGACIÓN CLÍNICA; 2016

SOCIEDAD ARGENTINA DE INVESTIGACIÓN CLÍNICA

RAC3 is a nuclear receptor coactivator whose expression isalmost undetectable in differentiated cells, but it is overexpressedin several tumor types and required to maintain pluripotency instem cells. We have previously demonstrated that RAC3 overexpressionincreases proliferation, apoptosis resistance and theinvasive capacity of different tumor cell lines. We investigated ifRAC3 overexpression in non-tumoral cells could be inducing aCSC-like phenotype. Non-tumoral HEK293 cells were transfectedwith a RAC3 expression vector (RAC3) or the empty vector (EV)and, then, different CSC parameters were analyzed. We found asignificant increase in CD44 protein levels in RAC3 compared withEV (p