期刊
INTERNATIONAL JOURNAL OF HEMATOLOGY
卷 106, 期 6, 页码 811-819出版社
SPRINGER JAPAN KK
DOI: 10.1007/s12185-017-2314-1
关键词
miR-1; miR-133; EVI1; AML
类别
资金
- Japan Society for the Promotion of Science
- Japan Leukemia Research Fund
- Research Program on Hepatitis from Japan Agency for Medical Research and Development, AMED
- Grants-in-Aid for Scientific Research [15K06838, 17H04212] Funding Source: KAKEN
miR-1 and miR-133 are clustered on the same chromosomal loci and are transcribed together as a single transcript that is positively regulated by ecotropic virus integration site-1 (EVI1). Previously, we described how miR-133 has anti-tumorigenic potential through repression of EVI1 expression. It has also been reported that miR-1 is oncogenic in the case of acute myeloid leukemia (AML). Here, we show that expression of miR-1 and miR-133, which have distinct functions, is differentially regulated between AML cell lines. Interestingly, the expression of miR-1 and EVI1, which binds to the promoter of the miR-1/miR-133 cluster, is correlative. The expression levels of TDP-43, an RNA-binding protein that has been reported to increase the expression, but inhibits the activity, of miR-1, were not correlated with expression levels of miR-1 in AML cells. Taken together, our observations raise the possibility that the balance of polycistronic miRNAs is regulated post-transcriptionally in a hierarchical manner possibly involving EVI1, suggesting that the deregulation of this balance may play some role in AML cells with high EVI1 expression.
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