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

• DOI: 10.1038/srep19204
• Publication Date: 2016-01-12T10:38:49Z
• Authors: 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
• Keywords: 0301 basic medicine; Gene Expression Regulation, Leukemic; Gene Expression Profiling; Models, Biological; Article; MDS1 and EVI1 Complex Locus Protein; 3. Good health; DNA-Binding Proteins; Leukemia, Myeloid, Acute; Mice; MicroRNAs; 03 medical and health sciences; Cell Line, Tumor; Proto-Oncogenes; Animals; Humans; RNA Interference; RNA, Messenger; 3' Untranslated Regions; Transcription Factors

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