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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: Anti-Inflammatory Agents, Non-Steroidal, Apoptosis, Blotting, Western, Caspase 3, Caspases, Cytoskeletal Proteins, Dose-Response Relationship, Drug, HL-60 Cells, Humans, Indomethacin, Proto-Oncogene Proteins c-myb, Signal Transduction, Time Factors, Trans-Activators, beta Catenin.
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Is [ Indomethacin-induced HL-60 cell apoptosis associated with inhibition of beta-catenin/c-myc signal transduction pathway ]? Context: To investigate the effects of indomethacin on HL-60 cell proliferation and apoptosis, and elucidate partly the molecular mechanism about the anti-leukemia effect of indomethacin by studying beta-catenin signal transduction pathway. HL-60 cells were treated with indomethacin at different concentrations (0, 25, 50, 100, 200, 400 micro mol/L). Cells viability and proliferation were determined by Trypan blue staining and cell counting respectively. DNA ladder pattern and cell morphology were used to identify cell apoptosis. The expression and cleavage of caspase-3, beta-catenin, c-myc were detected by Western blot techniques. Indomethacin could significantly inhibit HL-60 cells proliferation and induce cells apoptosis with a time and dose dependent manner. An up-regulating expression and cleavage of caspase-3 were observed. Indomethacin could inhibit beta-catenin expression and induce its degradation, c-myc protein exhibited a down-regulation with a concentration dependent manner.
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Indomethacin could inhibit HL-60 cell proliferation and induce cells apoptosis. Anti-leukemia effect of indomethacin was associated with the inhibition of "beta-catenin --> c-myc" signal pathway. Final Decision: yes