期刊
GENE
卷 620, 期 -, 页码 1-9出版社
ELSEVIER SCIENCE BV
DOI: 10.1016/j.gene.2017.04.002
关键词
microRNA-125b; AML; Monocytic differentiation; Fes; PU.1; MCSFR
资金
- National Major Special Program of New Drug Research and Development [2013ZX09301303-005]
- Priority Academic Program Development (PAPD) of Jiangsu Higher Education Institutions
- Qing Lan Project
- National Natural Science Foundation of China [81372331]
- Fundamental Research Funds for the Central Universities [2015ZD004]
MicroRNA-125b (miR-125b) has been reported to be upregulated in several kinds of leukemia, suggesting that miR-125b plays a role in Leukemia development. In this study, it was shown that miR-125b expression level decreased in response to 1 alpha 25-dihydroxy-vitamin D3 (1,25D(3)) in a dose- and time-dependent manner and miR125b blocked 1,25D(3)-induced monocytic differentiation of U937 cells. In addition, miR-125b decreased mRNA expression of myelomonocytic differentiation markers, including CD11c, CD18 and CD64 and arrested the cell cycle at the S phase in U937 and HL60 cells. Fes was identified as a novel direct target of miR-125b and miR-125b could also reduce the expression levels of PU.1 and macrophage colony-stimulating factor receptor (MCSFR). Furthermore, Fes was found to be involved in monocytic differentiation via upregulation of PU.1 and MCSFR and Fes siRNA could also inhibit 1,25D(3)-induced monocytic differentiation of U937 and HL60 cells and decrease mRNA expression of CD11c, CD18 and CD64. Importantly, the inhibition of Fes siRNA on 1,25D(3)-induced monocytic differentiation could be rescued by transfection with miR-125b inhibitor. Our data highlights an important role of miR-125b in AML progression, implying the potential application of miR-125b in AML therapy.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据