system
Medical AI Inquiry: You was designed to assist in medical decision-making based on the provided user questions. It is crucial to provide accurate and comprehensive information to receive a well-informed response.  Labels: BACKGROUND, METHODS, RESULTS. Meshes: Animals, Antineoplastic Agents, Cell Line, Tumor, Deoxycytidine, Drug Resistance, Neoplasm, Drug Synergism, Female, Humans, Imidazoles, Inhibitor of Apoptosis Proteins, Mice, Mice, Inbred BALB C, Naphthoquinones, Pancreatic Neoplasms, RNA, Small Interfering, Survivin.
user
Does the survivin suppressant YM155 potentiate chemosensitivity to gemcitabine in the human pancreatic cancer cell line MiaPaCa-2? Context: Survivin is a negative regulator of apoptosis. We evaluated the efficacy of YM155, a selective suppressant of survivin, in combination with gemcitabine in the pancreatic cancer cell line MiaPaCa-2. Expression of survivin was demonstrated by immunoblotting. Cell cycle progression was determined by flow cytometric analysis. Cell viability was assayed using the trypan blue exclusion assay. Gemcitabine up-regulated survivin expression, whereas treatment with YM155 suppressed the expression of survivin. Concomitant treatment with YM155 enhanced chemosensitivity to gemcitabine, which was accompanied by a decrease in the expression of survivin. Knockdown of endogenous survivin via RNA interference also enhanced the sensitivity to gemcitabine. In addition, YM155 potentiated the antitumor effect of gemcitabine in xenograft tumors of MiaPaCa-2.
assistant
YM155 potentiates chemosensitivity to gemcitabine in pancreatic cancer cells by suppressing the induction of survivin. Combination treatment with gemcitabine and YM155 may be a potential therapeutic strategy for the treatment of pancreatic cancer that warrants further clinical investigation. Final Decision: yes