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目的:探讨SU11248对人髓系白血病细胞株HL-60的效应及其对HL-60细胞表达P27KIP1和cyclin G蛋白改变的影响。方法:应用MTT法检测SU11248对HL-60细胞增殖能力的影响;采用Western blot检测SU11248干预HL-60细胞前后P27KIP1和cyclin G蛋白表达水平的变化及其相关性。结果:不同浓度(0.5、1.0、2.0、4.0、8.0mg/L)SU11248作用HL-60细胞24h、48h、72h、96h后,SU11248可抑制HL-60细胞增殖,抑制作用呈现剂量和时间依赖性,半数抑制浓度(IC50)约为2.0mg/L。2.0mg/LSU11248作用HL-60细胞72h时抑制率达到最高。2.0mg/LSU11248作用HL-60细胞后cyclin G蛋白表达呈时间依赖性降低,而P27KIP1蛋白表达呈时间依赖性升高。两蛋白各时间组的改变与对照组相比差异均有统计学意义(P<0.05)。结论:SU11248具有抑制HL-60细胞增殖的生物效应,在HL-60细胞及SU11248干预HL-60细胞过程中,P27KIP1基因可能对cyclin G基因及细胞周期发挥负性调控作用。SU11248通过上P27KIP1、下调cyclin G而干扰细胞周期可能是其发挥抑制肿瘤细胞分裂的环节之一。
AIM: To investigate the effect of SU11248 on human myeloid leukemia cell line HL-60 and its effect on the expression of P27KIP1 and cyclin G in HL-60 cells. Methods: The effect of SU11248 on the proliferation of HL-60 cells was detected by MTT assay. The expressions of P27KIP1 and cyclin G protein in HL-60 cells were detected by Western blot. Results: SU11248 could inhibit the proliferation of HL-60 cells in a dose-and time-dependent manner at 24h, 48h, 72h, 96h after treated with SU11248 at different concentrations (0.5,1.0,2.0,4.0 and 8.0 mg / L) , Half inhibitory concentration (IC50) of about 2.0mg / L. HL-60 cells treated with 2.0mg / LSU11248 had the highest inhibitory rate at 72h. The protein expression of cyclin G in HL-60 cells treated with 2.0mg / LSU11248 decreased in a time-dependent manner, while the expression of P27KIP1 protein increased in a time-dependent manner. The changes of the two proteins in each time group were significantly different from those in the control group (P <0.05). Conclusion: SU11248 can inhibit the proliferation of HL-60 cells in a biological manner. The expression of P27KIP1 may play a negative regulatory role in cyclin G gene and cell cycle in HL-60 cells and SU11248 cells. SU11248 through the P27KIP1, down-cyclin G and interfere with the cell cycle may be one of its parts to inhibit tumor cell division.