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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: BACKGROUND, METHODS, RESULTS. Meshes: Antimetabolites, Antineoplastic, Cell Line, Tumor, Deoxycytidine, Humans, Imidazoles, Pancreatic Neoplasms, Protein-Serine-Threonine Kinases, Quinoxalines, Receptor, Transforming Growth Factor-beta Type I, Receptors, Transforming Growth Factor beta.
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Does transforming growth factor beta receptor I inhibitor sensitize drug-resistant pancreatic cancer cells to gemcitabine? Context: Resistance to gemcitabine is a major obstacle in the treatment of advanced pancreatic cancer. Previous exploration of protein kinase inhibitors demonstrated that blocking transforming growth factor-β (TGFβ) signal enhances the efficacy of gemcitabine in pancreatic cancer cells. We analyzed the cell viability after combinational treatment of TGFβ receptor I (TβRI) inhibitors, SB431542 and SB525334 with gemcitabine in pancreatic cancer cells. In addition, apoptotic cell death and cell migration were measured. Combination with TβRI inhibitors significantly augmented the cytotoxicity of gemcitabine in both parental and gemcitabine resistant pancreatic cancer cells. SB525334 significantly increased apoptotic cell death in gemcitabine-resistant cells. Treatment of SB525334 also affected the AKT signalling pathway, which plays a crucial role in gemcitabine resistance. Migration assay also revealed that blocking TβRI reduces cell migration.
assistant
Chemotherapeutic approaches using SB525334 might enhance the treatment benefit of the gemcitabine-containing regimens in the treatment of pancreatic cancer patients. Final Decision: yes