MiR-133 regulates Evi1 expression in AML cells as a potential therapeutic target

Haruna Yamamoto, Jun Lu, Shigeyoshi Oba, Toyotaka Kawamata, Akihide Yoshimi, Natsumi Kurosaki, Kazuaki Yokoyama, Hiromichi Matsushita, Mineo Kurokawa, Arinobu Tojo, Kiyoshi Ando, Kazuhiro Morishita, Koko Katagiri, Ai Kotani

Research output: Contribution to journalArticlepeer-review

19 Citations (Scopus)

Abstract

The Ecotropic viral integration site 1 (Evi1) is a zinc finger transcription factor, which is located on chromosome 3q26, over-expression in some acute myeloid leukemia (AML) and myelodysplastic syndrome (MDS). Elevated Evi1 expression in AML is associated with unfavorable prognosis. Therefore, Evi1 is one of the strong candidate in molecular target therapy for the leukemia. MicroRNAs (miRNAs) are small non-coding RNAs, vital to many cell functions that negatively regulate gene expression by translation or inducing sequence-specific degradation of target mRNAs. As a novel biologics, miRNAs is a promising therapeutic target due to its low toxicity and low cost. We screened miRNAs which down-regulate Evi1. miR-133 was identified to directly bind to Evi1 to regulate it. miR-133 increases drug sensitivity specifically in Evi1 expressing leukemic cells, but not in Evi1-non-expressing cells The results suggest that miR-133 can be promising therapeutic target for the Evi1 dysregulated poor prognostic leukemia.

Original languageEnglish
Article number19204
JournalScientific reports
Volume6
DOIs
Publication statusPublished - 2016 Jan 12
Externally publishedYes

ASJC Scopus subject areas

  • General

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