Evidence map›Paper›PMID 26174629›Full record

ArticleLeukemia2016

Aberrant expression of miR-9/9* in myeloid progenitors inhibits neutrophil differentiation by post-transcriptional regulation of ERG.

K Nowek, S M Sun, L Bullinger, E M J Bindels, C Exalto, M K Dijkstra, K van Lom, H Döhner, S J Erkeland, B Löwenberg and 1 more

Abstract read
PubMed Publisher
In one paragraph

Article in Leukemia, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.7field-weighted citation impact, top 16% 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

17 citing papers in PubMed, 25 citations in OpenAlex.

  1. Article
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  5. Effects of hsa-miR-9-3p and hsa-miR-9-5p on Topoisomerase IIThe Journal of pharmacology and experimental therapeutics · 2023
    Article
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  9. Peripheral Circulating Exosome-Mediated Delivery of miR-155 as a Novel Mechanism for Acute Lung Inflammation.Molecular therapy : the journal of the American Society of Gene Therapy · 2019
    Article
  10. Review
  11. Article
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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

11 authors at 3 institutions in 2 countries.

K NowekDepartment of Hematology, Erasmus University Medical Center Cancer Institute, Rotterdam, The Netherlands.
S M SunDepartment of Hematology, Erasmus University Medical Center Cancer Institute, Rotterdam, The Netherlands.
L BullingerDepartment of Internal Medicine III, University of Ulm, Ulm, Germany.
E M J BindelsDepartment of Hematology, Erasmus University Medical Center Cancer Institute, Rotterdam, The Netherlands.
C ExaltoDepartment of Hematology, Erasmus University Medical Center Cancer Institute, Rotterdam, The Netherlands.
M K DijkstraDepartment of Hematology, Erasmus University Medical Center Cancer Institute, Rotterdam, The Netherlands.
K van LomDepartment of Hematology, Erasmus University Medical Center Cancer Institute, Rotterdam, The Netherlands.
H DöhnerDepartment of Internal Medicine III, University of Ulm, Ulm, Germany.
S J ErkelandDepartment of Hematology, Erasmus University Medical Center Cancer Institute, Rotterdam, The Netherlands.
B LöwenbergDepartment of Hematology, Erasmus University Medical Center Cancer Institute, Rotterdam, The Netherlands.
M Jongen-LavrencicDepartment of Hematology, Erasmus University Medical Center Cancer Institute, Rotterdam, The Netherlands.
Erasmus MC · NLErasmus MC Cancer Institute · NLUniversität Ulm · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Aberrant post-transcriptional regulation by microRNAs (miRNAs) has been shown to be involved in the pathogenesis of acute myeloid leukemia (AML). In a previous study, we performed a large functional screen using a retroviral barcoded miRNA expression library. Here, we report that overexpression of miR-9/9* in myeloid 32D cell line (32D-miR-9/9*) had profound impact on granulocyte colony-stimulating factor-induced differentiation. Further in vitro studies showed that enforced expression of miR-9/9* blocked normal neutrophil development in 32D and in primary murine lineage-negative bone marrow cells. We examined the expression of miR-9/9* in a cohort of 647 primary human AMLs. In most cases, miR-9 and miR-9* were significantly upregulated and their expression levels varied according to AML subtype, with the highest expression in MLL-related leukemias harboring 11q23 abnormalities and the lowest expression in AML cases with t(8;21) and biallelic mutations in CEBPA. Gene expression profiling of AMLs with high expression of miR-9/9* and 32D-miR-9/9* identified ETS-related gene (Erg) as the only common potential target. Upregulation of ERG in 32D cells rescued miR-9/9*-induced block in neutrophil differentiation. Taken together, this study demonstrates that miR-9/9* are aberrantly expressed in most of AML cases and interfere with normal neutrophil differentiation by downregulation of ERG.

Indexed as

AnimalsCell DifferentiationGene Expression Regulation, LeukemicHumansLeukemia, Myeloid, AcuteMiceMice, Inbred C57BLMicroRNAsMyeloid Progenitor CellsNeutrophilsTrans-ActivatorsTranscriptional Regulator ERGERG protein, humanMicroRNAsMIRN92 microRNA, humanTrans-ActivatorsTranscriptional Regulator ERG

Identifiers

PMID26174629
OpenAlexW1888444219

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.