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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: OBJECTIVE, METHODS, RESULTS. Meshes: Cell Line, Tumor, Cell Survival, Dose-Response Relationship, Drug, Enzyme Inhibitors, Glyceraldehyde-3-Phosphate Dehydrogenases, Glycolysis, Hexokinase, Humans, Intracellular Signaling Peptides and Proteins, Iodoacetates, Mitogen-Activated Protein Kinase 3, Pancreatic Neoplasms, Phosphorylation, Protein-Serine-Threonine Kinases, Proto-Oncogene Proteins c-akt, Pyruvates, Signal Transduction, TOR Serine-Threonine Kinases, ras Proteins.
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Do glycolytic enzyme inhibitors affect pancreatic cancer survival by modulating its signaling and energetics? Context: The importance of glycolysis in cancer cells is well documented. The effects of inhibiting glycolysis using metabolic inhibitors iodoacetate (IAA), an inhibitor of GAPDHase, and 3-bromopyruvate (3BP), an inhibitor of hexokinase-II, on survival and signaling of pancreatic cancer cells (Panc-1) were investigated. Cellular survival was evaluated using the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay. Lactate dehydrogenase (LDH) assay was used to analyze the induced necrosis and protein levels were evaluated using Western blot analysis. The results show that the inhibitors lowered cellular survival and increased cellular necrosis. Mitogenic signaling pathways were affected by 3BP but not by IAA.
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We conclude that there may be a cross-talk between signaling pathways and glycolysis in regulating pancreatic cancer cell survival and signaling. Thus, a combination of agents that inhibit both energy production and cell signaling may provide a novel and effective approach to target pancreatic cancer effectively. Final Decision: yes