International Journal of Hematology

, Volume 106, Issue 6, pp 811–819 | Cite as

Imbalanced expression of polycistronic miRNA in acute myeloid leukemia

  • Ryutaro Kotaki
  • Hiroshi Higuchi
  • Daisuke Ogiya
  • Yasuhiro Katahira
  • Natsumi Kurosaki
  • Naoko Yukihira
  • Jun Ogata
  • Haruna Yamamoto
  • Syakira Mohamad Alba
  • Azran Azhim
  • Tatsuo Kitajima
  • Shigeaki Inoue
  • Kazuhiro Morishita
  • Koh Ono
  • Ryo Koyama-Nasu
  • Ai Kotani
Original Article
  • 363 Downloads

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.

Keywords

miR-1 miR-133 EVI1 AML 

Notes

Acknowledgements

We thank all our lab members for helpful discussions and continuous encouragement, and the entire staff of the Education and Research Support Center at Tokai University for technical assistance. This work was supported by the Japan Society for the Promotion of Science, Japan Leukemia Research Fund and the Research Program on Hepatitis from Japan Agency for Medical Research and Development, AMED.

Compliance with ethical standards

Conflict of interest

No financial interests/relationships with financial interests relating to the topic of this article have been declared.

Supplementary material

12185_2017_2314_MOESM1_ESM.pptx (59 kb)
Supplementary material 1 (PPTX 58 kb)

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Copyright information

© The Japanese Society of Hematology 2017

Authors and Affiliations

  • Ryutaro Kotaki
    • 1
  • Hiroshi Higuchi
    • 1
  • Daisuke Ogiya
    • 2
  • Yasuhiro Katahira
    • 1
  • Natsumi Kurosaki
    • 1
  • Naoko Yukihira
    • 1
  • Jun Ogata
    • 1
  • Haruna Yamamoto
    • 1
  • Syakira Mohamad Alba
    • 3
  • Azran Azhim
    • 4
  • Tatsuo Kitajima
    • 3
  • Shigeaki Inoue
    • 5
  • Kazuhiro Morishita
    • 6
  • Koh Ono
    • 7
  • Ryo Koyama-Nasu
    • 1
  • Ai Kotani
    • 1
    • 2
  1. 1.Division of Hematological Malignancy, Institute of Medical SciencesTokai UniversityIseharaJapan
  2. 2.Department of Hematology and OncologyTokai University School of MedicineIseharaJapan
  3. 3.Department of Electronic Systems Engineering, Malaysia-Japan International Institute of TechnologyUniversity of Technology MalaysiaKuala LumpurMalaysia
  4. 4.Department of Biotechnology, Kulliyyah of ScienceInternational Islamic University MalaysiaKuantanMalaysia
  5. 5.Department of Emergency and Critical Care MedicineTokai University School of MedicineIseharaJapan
  6. 6.Department of Medical Sciences, Faculty of MedicineUniversity of MiyazakiMiyazakiJapan
  7. 7.Department of Cardiovascular Medicine, Graduate School of MedicineKyoto UniversityKyotoJapan

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