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首页> 外文期刊>Cellular Physiology and Biochemistry >MiR-27a Promotes Hemin-Induced Erythroid Differentiation of K562 Cells by Targeting CDC25B
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MiR-27a Promotes Hemin-Induced Erythroid Differentiation of K562 Cells by Targeting CDC25B

机译：MiR-27a通过靶向CDC25B促进血红素诱导的K562细胞类红细胞分化

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Background/Aims MicroRNAs (miRNAs) play a crucial role in erythropoiesis. MiR-23a～27a～24-2 clusters have been proven to take part in erythropoiesis via some proteins. CDC25B (cell division control Cdc2 phosphostase B) is also the target of mir-27a; whether it regulates erythropoiesis and its mechanism are unknown. Methods To evaluate the potential role of miR-27a during erythroid differentiation, we performed miR-27a gain- and loss-of-function experiments on hemin-induced K562 cells. We detected miR-27a expression after hemin stimulation at different time points. At the same time, the γ-globin gene also was measured via real-time PCR. According to the results of the chips, we screened the target protein of miR-27a through a dual-luciferase reporter assay and identified it via Western blot analyses. To evaluate the function of CDC25B, benzidine staining and flow cytometry were employed to detect the cell differentiation and cell cycle. Results We found that miR-27a promotes hemin-induced erythroid differentiation of human K562 cells by targeting cell division cycle 25 B (CDC25B). Overexpression of miR-27a promotes the differentiation of hemin-induced K562 cells, as demonstrated by γ-globin overexpression. The inhibition of miR-27a expression suppresses erythroid differentiation, thus leading to a reduction in the γ-globin gene. CDC25B was identified as a new target of miR-27a during erythroid differentiation. Overexpression of miR-27a led to decreased CDC25B expression after hemin treatment, and CDC25B was up-regulated when miR-27a expression was inhibited. Moreover, the inhibition of CDC25B affected erythroid differentiation, as assessed by γ-globin expression. Conclusion This study is the first report of the interaction between miR-27a and CDC25B, and it improves the understanding of miRNA functions during erythroid differentiation.
机译：背景/目的MicroRNA（miRNA）在红细胞生成中起关键作用。已经证明，MiR-23a〜27a〜24-2团簇通过某些蛋白质参与红细胞生成。 CDC25B（细胞分裂控制Cdc2磷酸酶B）也是mir-27a的靶标;是否调节红细胞生成及其机制尚不清楚。方法为了评估miR-27a在红系分化过程中的潜在作用，我们对血红素诱导的K562细胞进行了miR-27a功能获得和丧失实验。我们在不同时间点的血红素刺激后检测到miR-27a表达。同时，还通过实时PCR测量了γ-珠蛋白基因。根据芯片的结果，我们通过双重荧光素酶报告基因分析筛选了miR-27a的目标蛋白，并通过Western印迹分析对其进行了鉴定。为了评估CDC25B的功能，使用联苯胺染色和流式细胞仪检测细胞分化和细胞周期。结果我们发现miR-27a通过靶向细胞分裂周期25 B（CDC25B）促进血红素诱导的人K562细胞红系分化。 miR-27a的过表达促进了血红素诱导的K562细胞的分化，这由γ-珠蛋白的过表达证明。对miR-27a表达的抑制会抑制类红细胞分化，从而导致γ-珠蛋白基因的减少。 CDC25B被确定为红系分化期间miR-27a的新靶标。血红素处理后，miR-27a的过度表达导致CDC25B表达下降，而miR-27a的表达受到抑制，则CDC25B上调。此外，对CDC25B的抑制会影响红系分化，如通过γ-珠蛋白表达所评估的。结论这项研究是miR-27a与CDC25B相互作用的首次报道，它增进了对红系分化过程中miRNA功能的了解。

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