Rosigitazone induces mature differen tiation of HL-60 leukemia cells with mediation of PPARγ activailon
AIM: To study the role of peroxisome proliferator-activated receptory ( PPARγ ) in HL-60 promyeloid leukemia cells' differentiation. METHODS: Cationic lipid transfection reagent lipofectamine 2000 was used to transfect plasmids into HL-60 cells. The experiments were subdivided into 4 groups, including simple HL-60 cells culture, pIRES2-EGFP empty plasmid transfection, 10 μmol/L rosiglitazone intervention, and 10 μmol/ L rosiglitazone combined with phPPARγ -IRES2-EGFP transfec-tion. The GFP expression was observed under fluorescence microscope. The transfection efficiency of HL-60 cells and the expression of granulocyte and monocyte specific markers of CD11b and CD14 in transfected HL-60 cells were analyzed by flow cytometry. RESULTS: GFP expression was observed in the phPPARγ-IRES2-EGFP transfected HL-60 cells with the transfection efficiency of 55%. PPARγ ligand rosiglitazone alone and in combination with phPPARγ-IRES2-EGFP transfection synergistically up-regulated CD11b and CD14 expression of HL-60 cells compared with pIRES2-EGRP transfected or non-transfected HL-60 cells (P < 0.05). No significant difference was observed in CD11 b and CD14 expression rate between pIRES2-EGFP transfected and non-transfected HL-60) cells (P > 0.05 ). CONCLUSION: Rosiglitazone induces mature differentiation of HL-60 cells toward granulocytes and monocytes via PPARγ activation, suggesting that rosiglitazone may offer a new therapeutic approach to the treatment of leukemia.
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