Evidence map›Paper›PMID 28831750›Full record

ArticleInternational journal of hematology2017

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 and 6 more

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Article in International journal of hematology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
–field-weighted citation impact
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

3 citing papers in PubMed.

  1. Review
  2. Article
  3. Review
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

16 authors.

Ryutaro KotakiDivision of Hematological Malignancy, Institute of Medical Sciences, Tokai University, 143 Shimokasuya, Isehara, Kanagawa, 259-1193, Japan.
Hiroshi HiguchiDivision of Hematological Malignancy, Institute of Medical Sciences, Tokai University, 143 Shimokasuya, Isehara, Kanagawa, 259-1193, Japan.
Daisuke OgiyaDepartment of Hematology and Oncology, Tokai University School of Medicine, Isehara, Kanagawa, 259-1193, Japan.
Yasuhiro KatahiraDivision of Hematological Malignancy, Institute of Medical Sciences, Tokai University, 143 Shimokasuya, Isehara, Kanagawa, 259-1193, Japan.
Natsumi KurosakiDivision of Hematological Malignancy, Institute of Medical Sciences, Tokai University, 143 Shimokasuya, Isehara, Kanagawa, 259-1193, Japan.
Naoko YukihiraDivision of Hematological Malignancy, Institute of Medical Sciences, Tokai University, 143 Shimokasuya, Isehara, Kanagawa, 259-1193, Japan.
Jun OgataDivision of Hematological Malignancy, Institute of Medical Sciences, Tokai University, 143 Shimokasuya, Isehara, Kanagawa, 259-1193, Japan.
Haruna YamamotoDivision of Hematological Malignancy, Institute of Medical Sciences, Tokai University, 143 Shimokasuya, Isehara, Kanagawa, 259-1193, Japan.
Syakira Mohamad AlbaDepartment of Electronic Systems Engineering, Malaysia-Japan International Institute of Technology, University of Technology Malaysia, 54100, Kuala Lumpur, Malaysia.
Azran AzhimDepartment of Biotechnology, Kulliyyah of Science, International Islamic University Malaysia, 25200, Kuantan, Malaysia.
Tatsuo KitajimaDepartment of Electronic Systems Engineering, Malaysia-Japan International Institute of Technology, University of Technology Malaysia, 54100, Kuala Lumpur, Malaysia.
Shigeaki InoueDepartment of Emergency and Critical Care Medicine, Tokai University School of Medicine, Isehara, Kanagawa, 259-1193, Japan.
Kazuhiro MorishitaDepartment of Medical Sciences, Faculty of Medicine, University of Miyazaki, Miyazaki, Japan.
Koh OnoDepartment of Cardiovascular Medicine, Graduate School of Medicine, Kyoto University, Kyoto, Japan.
Ryo Koyama-NasuDivision of Hematological Malignancy, Institute of Medical Sciences, Tokai University, 143 Shimokasuya, Isehara, Kanagawa, 259-1193, Japan. ryonasu@tokai.ac.jp.
Ai KotaniDivision of Hematological Malignancy, Institute of Medical Sciences, Tokai University, 143 Shimokasuya, Isehara, Kanagawa, 259-1193, Japan. aikotani@k-lab.jp.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

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.

Indexed as

Gene Expression Regulation, LeukemicMultigene FamilyDNA-Binding ProteinsHL-60 CellsHumansLeukemia, Myeloid, AcuteMDS1 and EVI1 Complex Locus ProteinMicroRNAsNeoplasm ProteinsRNA, NeoplasmTHP-1 CellsU937 CellsDNA-Binding ProteinsMDS1 and EVI1 Complex Locus ProteinMECOM protein, humanMicroRNAsMIRN133 microRNA, humanMIRN1 microRNA, humanNeoplasm ProteinsRNA, NeoplasmTARDBP protein, humanAMLEVI1miR-1miR-133

Identifiers

PMID28831750

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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.