ROLE OF SURVIVIN IN MODULATING AUTOPH- AGY IN RESPONSE TO U0126, A MAPK INHIBITOR, IN PANCREATIC TUMOR CELLS

MARIÁNGELES DIAZ; SILVINA LAURA LOMPARDÍA; DANIELA LAURA PAPADEMETRIO; MARTÍN LEVERMANN; CINTIA YAMILA MIHALEZ; SUSANA COSTANTINO; DANIELA L. PAPADEMETRIO; VICTOEIA CAVALIERE; TANIA C. SIMUNOVICH; SUSANA N. COSTANTINO; TOMÁS LOMBARDO; MARÍA I. COLOMBO; GUILLERMO BLANCO; CLAUDIO M. FADER AND ELIDA ALVAREZ.; MATÍAS PIBUEL; ELIDA ALVAREZ

Mar del Plata, Buenos Ares

Congreso; LXI Reunión Científica Anual de la Sociedad Argentina de Investigación Clínica (SAIC). LXIV Reunión Anual de la Sociedad Argentina de Inmunología (SAI). XLVIII Reunión Anual de la Sociedad Argentina de Farmacología Experimental (SAFE); 2016

SAIC-SAI-SAFE

Pancreatic cancer is one of the most difficult neoplastic pathol-ogies to treat, with high resistance to both radio and chemotherapy. The lack of an effective protocol makes extremely important any approach to the understanding of these diseases. Because of that, we propose to study the relationship between autophagy, a mecha-nism launched by pancreatic tumors to evade the pro-apoptotic effects of a wide range of compounds, and survivin, one of the IAPs proteins, expressed on an elevated rate in these tumors. We studied the capability of U0126, an inhibitor of the survival pathway MAPK, to modulate autophagy in MIAPaCa-2WT and MIAPaCa-2surv-/-, a derivate cell line knock down for surivivin. First, we demonstrated by western blot that U0126 increased survivin levels in MIAPaCa-2WT cells (p0.05). In addition, we observed decreased levels of LC3-IIB in MIAPaCa-2surv-/- vs MIAPaCa-2WT by western blot (p