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2-甲氧基雌二醇逆转K562/AO2细胞耐药及其机制的初步研究[J]. 肿瘤防治研究, 2011, 38(11): 1257-1259. DOI: 10.3971/j.issn.1000-8578.2011.11.010
引用本文: 2-甲氧基雌二醇逆转K562/AO2细胞耐药及其机制的初步研究[J]. 肿瘤防治研究, 2011, 38(11): 1257-1259. DOI: 10.3971/j.issn.1000-8578.2011.11.010
Mechanism of 2-methoxyestradiol Reversing Multidrug Resistance of K562/AO2 Cells[J]. Cancer Research on Prevention and Treatment, 2011, 38(11): 1257-1259. DOI: 10.3971/j.issn.1000-8578.2011.11.010
Citation: Mechanism of 2-methoxyestradiol Reversing Multidrug Resistance of K562/AO2 Cells[J]. Cancer Research on Prevention and Treatment, 2011, 38(11): 1257-1259. DOI: 10.3971/j.issn.1000-8578.2011.11.010

2-甲氧基雌二醇逆转K562/AO2细胞耐药及其机制的初步研究

Mechanism of 2-methoxyestradiol Reversing Multidrug Resistance of K562/AO2 Cells

  • 摘要: 目的研究2-甲氧基雌二醇(2-ME)对K562/AO2细胞耐药性逆转作用及其可能机制。方法利用不同浓度的2-ME作用于K562及K562/AO2细胞,MTT法检测细胞对阿霉素的耐药性,计算耐药倍数及逆转倍数;利用AnnexinV /PI双染色法检测K562/AO2细胞的凋亡效应。结果与K562细胞相比,K562/AO2细胞的耐药倍数为50倍;2-ME可显著降低阿霉素对K562/AO2细胞的IC50,逆转倍数为5.9倍。AnnexinV /PI双染色法检测显示,1、4、16 μmol/L的2-ME处理K562/AO2细胞后细胞凋亡率分别为10.32%、21.56% 和16.45%, 而对照组凋亡率仅为6.68%。结论2-ME能够逆转K562/AO2阿霉素耐药,其机制可能与诱导K562/AO2细胞凋亡有关。

     

    Abstract: ObjectiveTo investigate the possible mechanism of 2-methoxyestradiol reversing multidrug resistance of K562/AO2 cells. MethodsThe inhibitory effects of 2-methoxyestradiol on the proliferation of K562 and K562/AO2 cells were observed by MTT assay. Annexin V-FITC /PI staining was used to detect apoptosis. ResultsThe resistance of K562/AO2 cells to ADR was 50 folds compared with K562 cells. The IC50 of ADR was evidently reduced by 2-methoxyestradiol. The reversal folds of 2-methoxyestradiol for K562/AO2 cells were 5.9. The result of Annexin-V /PI staining showed that rates of the apoptotic cells were 10.32%,21.56% and 16.45% respectively, which were remarkably higher than that of control (6.68% ) . Conclusion 2-methoxyestradiol has reverse effect on K562/AO2 cells,its possible mechanism might be related with apoptosis of K562/AO2 cells.

     

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