Affiliations 

  • 1 Division of Hematological Malignancy, Institute of Medical Sciences, Tokai University, 143 Shimokasuya, Isehara, Kanagawa, 259-1193, Japan
  • 2 Department of Hematology and Oncology, Tokai University School of Medicine, Isehara, Kanagawa, 259-1193, Japan
  • 3 Department of Electronic Systems Engineering, Malaysia-Japan International Institute of Technology, University of Technology Malaysia, 54100, Kuala Lumpur, Malaysia
  • 4 Department of Biotechnology, Kulliyyah of Science, International Islamic University Malaysia, 25200, Kuantan, Malaysia
  • 5 Department of Emergency and Critical Care Medicine, Tokai University School of Medicine, Isehara, Kanagawa, 259-1193, Japan
  • 6 Department of Medical Sciences, Faculty of Medicine, University of Miyazaki, Miyazaki, Japan
  • 7 Department of Cardiovascular Medicine, Graduate School of Medicine, Kyoto University, Kyoto, Japan
  • 8 Division of Hematological Malignancy, Institute of Medical Sciences, Tokai University, 143 Shimokasuya, Isehara, Kanagawa, 259-1193, Japan. ryonasu@tokai.ac.jp
  • 9 Division of Hematological Malignancy, Institute of Medical Sciences, Tokai University, 143 Shimokasuya, Isehara, Kanagawa, 259-1193, Japan. aikotani@k-lab.jp
Int J Hematol, 2017 Dec;106(6):811-819.
PMID: 28831750 DOI: 10.1007/s12185-017-2314-1

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.

* Title and MeSH Headings from MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.