基础医学与临床 ›› 2019, Vol. 39 ›› Issue (9): 1259-1264.

• 研究论文 • 上一篇    下一篇

miR-150通过调节c-Myb抑制人慢性髓系白血病细胞系K562增殖

陈连香1,曹丽霞2   

  1. 1. 内蒙古医科大学附属医院血液内科
    2. 内蒙古医科大学附属医院
  • 收稿日期:2018-10-10 修回日期:2018-12-21 出版日期:2019-09-05 发布日期:2019-09-06
  • 通讯作者: 曹丽霞 E-mail:caolilixiaoxia@sina.com

miR-150 inhibits cell proliferation through regulating c-Myb in human chronic myeloid leukemia cell line K562

Lian-xiang Chen1,Lixia Cao   

  • Received:2018-10-10 Revised:2018-12-21 Online:2019-09-05 Published:2019-09-06
  • Contact: Lixia Cao E-mail:caolilixiaoxia@sina.com

摘要: 目的 探讨miR-150在人慢性髓系白血病细胞系K562中的功能和作用机制。方法 以临床收集的慢性髓系白血病人、和正常人外周血中的单个核细胞为实验材料,实时定量 PCR检测miR-150和c-Myb mRNA的表达水平;使用miR-150模拟物转染K562细胞;通过CCK-8法检测K562细胞增殖;通过流式细胞计量术检测K562细胞周期;荧光素酶报告基因实验结合Western blot检测miR-150对其下游靶基因c-Myb的调控作用。结果 慢性髓系白血病病人与正常人相比,miR-150表达降低,而c-Myb表达升高。过量表达miR-150可以抑制K562细胞的增殖(p<0.05);同时,阻滞K562细胞周期的运行。miR-150可以下调靶基因c-Myb的表达。结论 miR-150在慢性髓系白血病中表达下调,其作用机制是通过抑制癌基因c-Myb的表达抑制白血病细胞的增殖。

关键词: 微小RNA, c-Myb, K562, 细胞周期

Abstract: Objective To investigate the function and mechanism of miR-150 in human chronic myeloid leukemia cell line K562. Methods clinic CML patients and normal controls were collected. The peripheral blood mononuclear cells from above CML and controls were isolated. Quantitative RT-PCR analysis was used to determine the expression level of miR-150 and c-Myb mRNA; miR-150 mimic and negative control were transfected into K562 cells, respectively. CCK-8 analysis was performed to examine K562 cell proliferation. FACS analysis was used to detect cell cycle. Dual-luciferase assay and Western blot were used to detect the influence of miR-150 on target gene c-Myb. Results when compared to the normal control, the miR-150 level was down-regulated in CML patients, whereas c-Myb expression was up-regulated in CML. Overexpression of miR-150 inhibits K562 cell proliferation and cell cycle progression. miR-150 could reduce c-Myb expression in K562 cells. Conclusions miR-150 is down-regulated in CML, and it can reduce K562 cell growth by repressing the expression of oncogene c-Myb.

Key words: miRNA, c-Myb, K562, cell cycle

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