Role of Survivin in modulating autophagy in response to U0126, a MAPK inhibitor, in pancreatic tumor cells

MARIÁNGELES DÍAZ; SILVINA LAURA LOMPARDÍA; DANIELA L. PAPADEMETRIO; CINTIA Y. MIHALEZ; MATIAS PIBUEL; MARTIN LEVERMANN; ELIDA ALVAREZ; SUSANA N. COSTANTINO; TOMÁS LOMBARDO

Ciudad de Buenos Aires

Conferencia; Buenos Aires Research Conference on Autophagy. Molecular Mechanisms in Biology and Diseases; 2017

Pancreaticcancer is one of the most difficult neoplastic pathologies 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. For that, we propose to study the relationship between autophagy, a mechanism 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 level in MIAPaCa-2WT cells (p0.05). In addition, we observed a decreased of LC3-IIB levels in MIAPaCa-2surv-/- vs MIAPaCa-2WT by western blot (p