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Int J Hematol ; 106(6): 811-819, 2017 Dec.
Article in English | MEDLINE | ID: mdl-28831750

ABSTRACT

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.


Subject(s)
Gene Expression Regulation, Leukemic , Leukemia, Myeloid, Acute/metabolism , MicroRNAs/biosynthesis , Multigene Family , RNA, Neoplasm/biosynthesis , DNA-Binding Proteins/biosynthesis , DNA-Binding Proteins/genetics , HL-60 Cells , Humans , Leukemia, Myeloid, Acute/genetics , MDS1 and EVI1 Complex Locus Protein/biosynthesis , MDS1 and EVI1 Complex Locus Protein/genetics , MicroRNAs/genetics , Neoplasm Proteins/biosynthesis , Neoplasm Proteins/genetics , RNA, Neoplasm/genetics , THP-1 Cells , U937 Cells
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