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目的:研究K562/AS2细胞株对三氧化二砷(ATO)耐药的机制。方法:采用MTT法检测细胞毒性。细胞表面P-糖蛋白(P-gp)、细胞内柔红霉素(DNR)浓度采用流式细胞术检测。DNA聚合酶、拓扑异构酶Ⅱ(TopoⅡ)、多药耐药基因1(mdr1)、多药耐药相关蛋白1(MRP1)以及肺耐药相关蛋白基因(lrp)表达水平的检测采用RT-PCR法。结果:K562和K562/AS2细胞表面P-gp任意荧光强度、K562/AS2细胞内DNR浓度均无显著差异(P>0.05)。K562/AS2细胞株MRP1和TopoⅡ表达明显高于K562细胞(P<0.05),DNA多聚酶,mdr1和lrp表达与敏感细胞株K562细胞相同(P>0.05)。结论:ATO耐药细胞K562/AS2高表达MRP1,并产生低倍数的多药耐药。K562/AS2细胞TopoⅡ基因表达增高,其意义有待进一步阐明。
Objective: To study the mechanism of K562 / AS2 cell line resistance to arsenic trioxide (ATO). Methods: MTT assay cytotoxicity. Cell surface P-glycoprotein (P-gp), intracellular daunorubicin (DNR) concentration using flow cytometry. The expression of DNA polymerase, TopoⅡ, mdr1, MRP1 and lrp were detected by RT- PCR method. Results: There was no significant difference in any P-gp fluorescence intensity between K562 and K562 / AS2 cells and K562 / AS2 intracellular DNR concentration (P> 0.05). The expression of MRP1 and TopoⅡ in K562 / AS2 cell line was significantly higher than that in K562 cell line (P <0.05). The expression of DNA polymerase, mdr1 and lrp was the same as that in K562 cell line (P> 0.05). CONCLUSION: MRP1 is highly expressed in K562 / AS2 cells resistant to ATO and produces low-fold multidrug resistance. Topo Ⅱ gene expression increased in K562 / AS2 cells, and its significance needs to be further elucidated.