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Objective:To investigate the proteasome inhibitor MG132-induced apoptosis pathway in HL-60 cells and the role of allogeneic mixed lymphocyte reaction. Methods:Cell apoptosis was analyzed by flow cytometry.The expressions of p21 protein,p27 protein and p53 protein in HL-60 cells treated with MG132 were measured by Western blot.The proliferation of,peripheral blood mononuclear cells(PBMNCs) after treatment with 75 Gy irradiated HL-60 cells treated with MG132 was measured with CCK-8. Results:High-dose MG132 induced apoptosis in HL-60 cells.No significant change was observed in MG132-induced apoptosis after inhibiting caspase-8 and caspase-9 pathway.The expressions of p21 protein and p27 protein increased in MG132-induced apoptosis.HL-60 cells treated with low-dose MG132 improved the proliferation of PBMNCs from healthy volunteers. Conclusion:High-dose MG132 induced apoptosis and directly killed HL-60 cells.MG132 induced apoptosis in a caspase-8- and caspase-9-independent pathway.p21 protein and p27 protein were involved in MG132-induced apoptosis in HL-60 cells.HL-60 cells treated with Low-dose MG132 improved the effect of promoting the proliferation of PBMNCs from healthy volunteers.
Objective: To investigate the proteasome inhibitor MG132-induced apoptosis pathway in HL-60 cells and the role of allogeneic mixed lymphocyte reaction. Methods: Cell apoptosis was analyzed by flow cytometry. The expressions of p21 protein, p27 protein and p53 protein in HL- 60 cells treated with MG132 were measured by Western blot. The proliferation of, peripheral blood mononuclear cells (PBMNCs) after treatment with 75 Gy irradiated HL-60 cells treated with MG132 was measured with CCK-8. in HL-60 cells. Significant change was observed in MG132-induced apoptosis after inhibiting caspase-8 and caspase-9 pathway. The expressions of p21 protein and p27 protein increased in MG132-induced apoptosis. HL-60 cells treated with low- dose MG132 improved the proliferation of PBMNCs from healthy volunteers. Conclusion: High-dose MG132 induced apoptosis and directly killed HL-60 cells. MG132 induced apoptosis in a caspase-8- and caspase-9-independent pathway. p21 prote in and p27 protein were involved in MG132-induced apoptosis in HL-60 cells. HL-60 cells treated with Low-dose MG132 improved the effect of promoting the proliferation of PBMNCs from healthy volunteers.