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目的:研究抗癌药物米托蒽醌诱导乳腺癌细胞系MCF-7耐药过程中,聚ADP-核糖聚合-1(poly ADP-ribosepolymerase-1,PARP-1)的表达变化,探讨MCF-7耐药细胞株中多药耐药的形成机制。方法:分别设米托蒽醌6个不同浓度实验组(0.005、0.01、0.02、0.04、0.08、0.16μmol/L),先以0.005μmol/L的米托蒽醌持续作用MCF-7细胞30d后,改用下一个剂量0.01μmol/L继续作用30d,依次按由低到高的浓度顺序进行,诱导产生耐药细胞。并设未用米托蒽醌处理的MCF-7为对照组。采用实时荧光定量RT-PCR和蛋白免疫印迹杂交分别检测米托蒽醌各浓度组细胞中PARP-1mRNA和蛋白的表达水平。结果:与对照组相比,随着米托蒽醌浓度的增加,PARP-1表达水平呈增高趋势,并且有剂量-反应效应,其中0.02、0.04和0.08μmol/L等3个浓度组的表达量显著高于对照组(P<0.05)。结论:米托蒽醌持续染毒可诱导MCF-7细胞中PARP-1的表达,其表达参与了肿瘤多药耐药的形成。
Objective: To investigate the expression of poly ADP-ribose polymerase-1 (PARP-1) in the mitoxantrone-induced breast cancer cell line MCF-7, Multidrug resistance in drug-resistant cell lines. Methods: Six mitoxantrone-treated groups (0.005,0.01,0.02,0.04,0.08,0.16μmol / L) were treated with mitoxantrone (0.005μmol / L) for 30 days. , Switch to the next dose of 0.01μmol / L to continue the role of 30d, followed by the concentration of low to high order, induced drug-resistant cells. MCF-7, which was not treated with mitoxantrone, was set as the control group. Real-time fluorescent quantitative RT-PCR and Western blotting were used to detect the expression of PARP-1 mRNA and protein in mitoxantrone group. Results: Compared with the control group, PARP-1 expression increased with the increase of mitoxantrone concentration, and there was a dose-response effect, of which 0.02, 0.04 and 0.08μmol / L were the three concentrations The amount was significantly higher than the control group (P <0.05). CONCLUSION: Mitoxantrone can induce the expression of PARP-1 in MCF-7 cells and its expression is involved in the formation of multidrug resistance in MCF-7 cells.