S100P Promotes Pancreatic Cancer Growth, Survival, and Invasion

摘要: Purpose: In the current study, we examined functional significance and mechanism of action S100P in pancreatic cancer cells. Experimental Design: levels were increased Panc-1 cells, which do not express S100P, by transfection with an cDNA reduced BxPC3 high small interfering RNA gene silencing. Effects these manipulations on cell proliferation, resistance to apoptotic insults, migration, invasion estimated vitro using standard assays. The influences tumor growth vivo studied xenograft mouse models. To identify mechanisms involved responses, coimmunoprecipitation studies conducted receptor for advanced glycation end products (RAGE) effects inhibiting RAGE antagonistic peptide analyzed. Results: correlated rates survival, both models . , tumors mice s.c.-implanted cells decreased after orthotopic implantation BxPC-3 A direct interaction between was indicated molecules from antagonist inhibited this also biological Conclusions: These data suggest that plays a major role aggressiveness is likely mediated its ability activate RAGE. Thus, interference may provide novel approach treatment cancer.