MicroRNA-2355-5p regulates γ-globin expression in human erythroid cells by inhibiting KLF6
MicroRNA-2355-5p regulates γ-globin expression in human erythroid cells by inhibiting KLF6
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MicroRNA-2355-5p 通过抑制 KLF6 调节人红细胞中的 γ-珠蛋白表达
DOI：
10.1111/bjh.17134
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发表时间：
2020-12-24
影响因子：
6.5
通讯作者：
Xu, Xiangmin
中科院分区：
文献类型：
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作者：
Cheng, Yi;Shang, Xuan;Xu, Xiangmin
kruppel样因子（KLFs）是一个高度保守的转录因子家族。我们分析了klf的表达谱数据，发现KLF6是一种新的红细胞生成的潜在调节因子。敲低KLF6的表达可显著提高红细胞系HUDEP-2和造血祖细胞（CD34(+)）中γ -珠蛋白mRNA和蛋白水平。我们发现，在HUDEP-2和CD34（+）细胞中，microRNA (miR)-2355-5p的过表达通过抑制KLF6的表达与γ -珠蛋白合成增加相关。我们发现miR-2355-5p和KLF6之间的相互作用影响γ -珠蛋白的表达，可能为β -地中海贫血患者的临床管理提供更多信息。
Kruppel-like factors (KLFs) are a highly conserved family of transcription factors. We analysed expression profile data of KLFs and identified KLF6 as a new potential regulator of erythropoiesis. Knocking down the expression of KLF6 significantly raised gamma-globin mRNA and protein levels in the erythroid cell line HUDEP-2 and haematopoietic progenitor (CD34(+)) cells. We found that overexpression of microRNA (miR)-2355-5p in HUDEP-2 and CD34(+) cells correlated with increased gamma-globin synthesis by suppressing expression of KLF6. Our discovery that the interaction between miR-2355-5p and KLF6 affects the expression of gamma-globin may provide more information for the clinical management of beta-thalassaemia patients.