RAC3 overexpression induces a tumor initiating cell phenotype

PANELO, LAURA; LIRA, C; COSTAS, MÓNICA; JAWORSKI, FELIPE MARTÍN; ROSA, F; RUBIO, F; VAZQUEZ, ELBA SUSANA

MEDICINA (BUENOS AIRES)

MEDICINA (BUENOS AIRES)

Lugar: Buenos Aires; Año: 2016

0025-7680

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. We investigated if RAC3 overexpression in non-tumoral cells could induce a CSC like phenotype. Non-tumoral HEK293 cells were transfected with a RAC3 expression vector (RAC3) or the empty vector (EV) and, then, different CSC parameters were analyzed. We found CD44 protein levels significant increased in RAC3 respect to EV cells (p