Evidence map›Paper›PMID 26754824›Full record

ArticleScientific reports2016

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 and 4 more

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.7field-weighted citation impact, top 15% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

18 citing papers in PubMed, 32 citations in OpenAlex.

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  14. The role of zinc and its compounds in leukemia.Journal of biological inorganic chemistry : JBIC : a publication of the Society of Biological Inorganic Chemistry · 2018
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

14 authors at 8 institutions in 1 country.

Haruna YamamotoDepartment of Hematological Malignancy, Institute of Medical Science, Tokai University, 143 Shimokasuya, Isehara, Kanagawa 259-1193 Japan.
Jun LuDepartment of Intractable Diseases, Institute of National Center for Global Health and Medicine, 1-21-1 Toyama, Shinjuku-ku, Tokyo 162-8655 Japan.
Shigeyoshi ObaDepartment of Nephrology and Endocrinology, the University of Tokyo Hospital, 7-3-1 Hongo, Bunkyo-ku, Tokyo 113-8655 Japan.
Toyotaka KawamataDepartment of Hematology/ Oncology, Institute of Medical Science, University of Tokyo, 4-6-1 Shirokanedai, Minato-ku, Tokyo 108-8639 Japan.
Akihide YoshimiDepartment of Hematology and Oncology, Graduate School of Medicine, the University of Tokyo, 4-6-1 Shirokanedai, Minato-ku, Tokyo 108-8639 Japan.
Natsumi KurosakiDepartment of Hematological Malignancy, Institute of Medical Science, Tokai University, 143 Shimokasuya, Isehara, Kanagawa 259-1193 Japan.
Kazuaki YokoyamaDepartment of Hematology/ Oncology, Institute of Medical Science, University of Tokyo, 4-6-1 Shirokanedai, Minato-ku, Tokyo 108-8639 Japan.
Hiromichi MatsushitaDepartment of Hematology / Oncology, School of Medicine, Tokai University, 143 Shimokasuya, Isehara, Kanagawa 259-1193 Japan.
Mineo KurokawaDepartment of Hematology and Oncology, Graduate School of Medicine, the University of Tokyo, 4-6-1 Shirokanedai, Minato-ku, Tokyo 108-8639 Japan.
Arinobu TojoDepartment of Hematology/ Oncology, Institute of Medical Science, University of Tokyo, 4-6-1 Shirokanedai, Minato-ku, Tokyo 108-8639 Japan.
Kiyoshi AndoDepartment of Hematology / Oncology, School of Medicine, Tokai University, 143 Shimokasuya, Isehara, Kanagawa 259-1193 Japan.
Kazuhiro MorishitaDepartment of Medical Science, Faculty of Medicine, University of Miyazaki, 5200 Kiyotakecho Kihara, Miyazaki-city, Miyazaki 889-1692 Japan.
Koko KatagiriDepartment of Biosciences, School of Science, Kitasato University 1-15-1, Kitasato, Minami-ku, Sagamihara, Knagawa 252-0373 Japan.
Ai KotaniDepartment of Hematological Malignancy, Institute of Medical Science, Tokai University, 143 Shimokasuya, Isehara, Kanagawa 259-1193 Japan.
Tokai University · JPTokyo University of Science · JPThe University of Tokyo · JPJapan Science and Technology Agency · JPKitasato University · JPNational Center for Global Health and Medicine · JPUniversity of Miyazaki · JPUniversity of Tokyo Hospital · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

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.

Indexed as

Gene Expression Regulation, Leukemic3' Untranslated RegionsAnimalsCell Line, TumorDNA-Binding ProteinsGene Expression ProfilingHumansLeukemia, Myeloid, AcuteMDS1 and EVI1 Complex Locus ProteinMiceMicroRNAsModels, BiologicalProto-OncogenesRNA InterferenceRNA, MessengerTranscription Factors3' Untranslated RegionsDNA-Binding ProteinsMDS1 and EVI1 Complex Locus ProteinMECOM protein, humanMicroRNAsMIRN133 microRNA, humanRNA, MessengerTranscription Factors

Identifiers

PMID26754824
PMCPMC4709720
OpenAlexW2414172708

What OpenQuestion holds

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.