Department of Hematology, Nanjing First Affiliated Hospital of Nanjing Medical University, Nanjing, Jiangsu, China (mainland).
Med Sci Monit. 2018 Sep 24;24:6735-6741. doi: 10.12659/MSM.910325.
BACKGROUND This study aimed to investigate the effect of deferoxamine (DFO) on leukemia in vitro, and to explore the underlying molecular mechanism. MATERIAL AND METHODS K562 leukemia cells were treated with various concentrations of DFO (10, 50, and 100 µmol/l) with or without 10 µmol/l ferric chloride for 12 h. Then, total cellular iron was detected. CCK-8 kit and flow cytometry were used for cell viability and apoptosis detection. In addition, expression of apoptosis-related genes was determined by Western blotting and qRT-PCR, respectively. RESULTS The results suggested that DFO significantly inhibited K562 cell viability and induced cell apoptosis in a dose-dependent manner. We also found that the protein and mRNA levels of Bax, p53, and Fas dose-dependently increased in DFO-treated K562 cells, while the level of Bcl-2 markedly decreased in a dose-dependent manner. Moreover, the findings showed that ferric chloride eliminated these effects on K562 cells caused by DFO treatment. CONCLUSIONS Our results indicate that DFO plays a protective role in leukemia via inhibiting leukemia cell viability and inducing cell apoptosis by the regulation of apoptosis-related genes expression.
本研究旨在探讨去铁胺（DFO）对体外白血病的影响，并探讨其潜在的分子机制。
用不同浓度的 DFO（10、50 和 100µmol/l）处理 K562 白血病细胞，并用或不用 10µmol/l 氯化铁处理 12 小时。然后，检测总细胞铁含量。CCK-8 试剂盒和流式细胞术用于检测细胞活力和细胞凋亡。此外，通过 Western blot 和 qRT-PCR 分别检测凋亡相关基因的表达。
结果表明，DFO 可显著抑制 K562 细胞活力，并呈剂量依赖性诱导细胞凋亡。我们还发现，DFO 处理的 K562 细胞中 Bax、p53 和 Fas 的蛋白和 mRNA 水平呈剂量依赖性增加，而 Bcl-2 水平则呈剂量依赖性显著降低。此外，研究结果表明，氯化铁消除了 DFO 处理对 K562 细胞产生的这些影响。
我们的结果表明，DFO 通过调节凋亡相关基因的表达抑制白血病细胞活力并诱导细胞凋亡，从而在白血病中发挥保护作用。
