Evidence map›Paper›PMID 26990535›Full record

ArticleBlood cancer journal2016

miR-203 and miR-221 regulate SOCS1 and SOCS3 in essential thrombocythemia.

A Navarro, S Pairet, A Álvarez-Larrán, A Pons, G Ferrer, R Longarón, C Fernández-Rodríguez, L Camacho, M Monzó, C Besses and 1 more

Open access · goldAbstract read
In one paragraph

Article in Blood cancer journal, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
2.4field-weighted citation impact, top 12% 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

20 citing papers in PubMed, 30 citations in OpenAlex.

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  17. miRNA in Macrophage Development and Function.Antioxidants & redox signaling · 2016
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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 2 institutions in 1 country.

A NavarroMolecular Oncology and Embryology Laboratory, Human Anatomy Unit, School of Medicine, University of Barcelona, IDIBAPS, Barcelona, Spain.
S PairetDepartment of Pathology, Hospital del Mar, IDIBAPS, Barcelona, Spain.
A Álvarez-LarránGrup de Recerca Clínica Aplicada en Neoplàsies Hematològiques, IMIM (Hospital del Mar Medical Research Institute), IDIBAPS, Barcelona, Spain.
A PonsGrup de Recerca Clínica Aplicada en Neoplàsies Hematològiques, IMIM (Hospital del Mar Medical Research Institute), IDIBAPS, Barcelona, Spain.
G FerrerInstitute of Hematology and Oncology, Hospital Clinic, IDIBAPS, Barcelona, Spain.
R LongarónDepartment of Pathology, Hospital del Mar, IDIBAPS, Barcelona, Spain.
C Fernández-RodríguezGrup de Recerca Clínica Aplicada en Neoplàsies Hematològiques, IMIM (Hospital del Mar Medical Research Institute), IDIBAPS, Barcelona, Spain.
L CamachoGrup de Recerca Clínica Aplicada en Neoplàsies Hematològiques, IMIM (Hospital del Mar Medical Research Institute), IDIBAPS, Barcelona, Spain.
M MonzóMolecular Oncology and Embryology Laboratory, Human Anatomy Unit, School of Medicine, University of Barcelona, IDIBAPS, Barcelona, Spain.
C BessesGrup de Recerca Clínica Aplicada en Neoplàsies Hematològiques, IMIM (Hospital del Mar Medical Research Institute), IDIBAPS, Barcelona, Spain.
B BellosilloDepartment of Pathology, Hospital del Mar, IDIBAPS, Barcelona, Spain.
Hospital Del Mar · ESConsorci Institut D'Investigacions Biomediques August Pi I Sunyer · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The biological basis of essential thrombocythemia (ET) patients lacking known mutations is still unknown. MicroRNAs (miRNA) regulate hematopoietic differentiation and are deregulated in several hematopoietic malignancies. However, miRNA expression in ET patients has been poorly explored. We performed miRNA profiling in platelets from 19 ET patients and 10 healthy controls. Hierarchical cluster analysis showed two well-separated clusters between patients and controls, indicating that ET platelets had a characteristic 70-miRNA signature (P<0.0001), 68 of which were downregulated. According to the mutational status, three differentially expressed miRNAs, miR-15a (P=0.045), miR-150 (P=0.001) and miR-519a (P=0.036), were identified. A 40-miRNA signature was identified characterizing JAK2V617F-positive ET patients. Eight genes, whose interaction with the miRNAs could activate the JAK/STAT pathway were identified. An inverse correlation was observed between miRNAs expression and their target genes for SOCS1 and miR-221, SOCS3 and miR-221, SOCS3 and miR-203, and PTPN11 and miR-23a. All three miRNAs were upregulated in JAK2V617F-negative ET patients. SOCS1 and SOCS3 were validated as targets of miR-221 and miR-203, respectively. In summary, our study shows that platelets from JAK2V617F-negative ET patients harbor a specific miRNA signature that can participate in the modulation of the JAK/STAT pathway through regulation of key genes as SOCS1 and SOCS3.

Indexed as

Gene Expression RegulationCluster AnalysisFemaleGene Expression ProfilingGenes, ReporterHumansJanus Kinase 2MaleMicroRNAsReproducibility of ResultsRNA InterferenceSignal TransductionSTAT Transcription FactorsSuppressor of Cytokine Signaling 1 ProteinSuppressor of Cytokine Signaling 3 ProteinSuppressor of Cytokine Signaling ProteinsJanus Kinase 2MicroRNAsMIR221, humanMIRN203 microRNA, humanSOCS1 protein, humanSOCS3 protein, humanSTAT Transcription FactorsSuppressor of Cytokine Signaling 1 ProteinSuppressor of Cytokine Signaling 3 ProteinSuppressor of Cytokine Signaling Proteins

Identifiers

PMID26990535
PMCPMC4817095
OpenAlexW2299959072

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.