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miR-133 regulates Evi1 expression in AML cells as a potential therapeutic target
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...
Autores principales: | , , , , , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Nature Publishing Group
2016
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4709720/ https://www.ncbi.nlm.nih.gov/pubmed/26754824 http://dx.doi.org/10.1038/srep19204 |
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author | Yamamoto, Haruna Lu, Jun Oba, Shigeyoshi Kawamata, Toyotaka Yoshimi, Akihide Kurosaki, Natsumi Yokoyama, Kazuaki Matsushita, Hiromichi Kurokawa, Mineo Tojo, Arinobu Ando, Kiyoshi Morishita, Kazuhiro Katagiri, Koko Kotani, Ai |
author_facet | Yamamoto, Haruna Lu, Jun Oba, Shigeyoshi Kawamata, Toyotaka Yoshimi, Akihide Kurosaki, Natsumi Yokoyama, Kazuaki Matsushita, Hiromichi Kurokawa, Mineo Tojo, Arinobu Ando, Kiyoshi Morishita, Kazuhiro Katagiri, Koko Kotani, Ai |
author_sort | Yamamoto, Haruna |
collection | PubMed |
description | 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. |
format | Online Article Text |
id | pubmed-4709720 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2016 |
publisher | Nature Publishing Group |
record_format | MEDLINE/PubMed |
spelling | pubmed-47097202016-01-20 miR-133 regulates Evi1 expression in AML cells as a potential therapeutic target Yamamoto, Haruna Lu, Jun Oba, Shigeyoshi Kawamata, Toyotaka Yoshimi, Akihide Kurosaki, Natsumi Yokoyama, Kazuaki Matsushita, Hiromichi Kurokawa, Mineo Tojo, Arinobu Ando, Kiyoshi Morishita, Kazuhiro Katagiri, Koko Kotani, Ai Sci Rep Article 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. Nature Publishing Group 2016-01-12 /pmc/articles/PMC4709720/ /pubmed/26754824 http://dx.doi.org/10.1038/srep19204 Text en Copyright © 2016, Macmillan Publishers Limited http://creativecommons.org/licenses/by/4.0/ This work is licensed under a Creative Commons Attribution 4.0 International License. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/ |
spellingShingle | Article Yamamoto, Haruna Lu, Jun Oba, Shigeyoshi Kawamata, Toyotaka Yoshimi, Akihide Kurosaki, Natsumi Yokoyama, Kazuaki Matsushita, Hiromichi Kurokawa, Mineo Tojo, Arinobu Ando, Kiyoshi Morishita, Kazuhiro Katagiri, Koko Kotani, Ai miR-133 regulates Evi1 expression in AML cells as a potential therapeutic target |
title | miR-133 regulates Evi1 expression in AML cells as a potential therapeutic target |
title_full | miR-133 regulates Evi1 expression in AML cells as a potential therapeutic target |
title_fullStr | miR-133 regulates Evi1 expression in AML cells as a potential therapeutic target |
title_full_unstemmed | miR-133 regulates Evi1 expression in AML cells as a potential therapeutic target |
title_short | miR-133 regulates Evi1 expression in AML cells as a potential therapeutic target |
title_sort | mir-133 regulates evi1 expression in aml cells as a potential therapeutic target |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4709720/ https://www.ncbi.nlm.nih.gov/pubmed/26754824 http://dx.doi.org/10.1038/srep19204 |
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