Evidence map›Paper›PMID 23695020›Full record

ArticleBritish journal of cancer2013

Proto-oncogenic isoform A2 of eukaryotic translation elongation factor eEF1 is a target of miR-663 and miR-744.

A Vislovukh, G Kratassiouk, E Porto, N Gralievska, C Beldiman, G Pinna, A El'skaya, A Harel-Bellan, B Negrutskii, I Groisman

Open access · hybridAbstract read
In one paragraph

Article in British journal of cancer, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.

0numbers the graph read from it
0cells of the map it votes in
53citing papers in PubMed
4.2field-weighted citation impact, top 6% 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

53 citing papers in PubMed, 103 citations in OpenAlex.

  1. Review
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  3. EEF1A2 identified as a hub gene associated with the severity of metabolic dysfunction-associated steatotic liver disease.Mammalian genome : official journal of the International Mammalian Genome Society · 2025
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  19. Exosomal MiR-744 Inhibits Proliferation and Sorafenib Chemoresistance in Hepatocellular Carcinoma by Targeting PAX2.Medical science monitor : international medical journal of experimental and clinical research · 2019
    Article
  20. Inflammatory pathways are central to posterior cerebrovascular artery remodelling prior to the onset of congenital hypertension.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2019
    Article
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

10 authors at 6 institutions in 2 countries.

A VislovukhState Key Laboratory on Molecular and Cell biology, Institute of Molecular Biology and Genetics, National Academy of Sciences of Ukraine, Kiev 03680, Ukraine.
G Kratassiouk
E Porto
N Gralievska
C Beldiman
G Pinna
A El'skaya
A Harel-Bellan
B Negrutskii
I Groisman
Génétique Quantitative et Évolution Le Moulon · FRInstitute of Molecular Biology and Genetics · UAUniversité Paris-Sud · FRCentre de Génétique Moléculaire · FRCentre National de la Recherche Scientifique · FRNational Academy of Sciences of Ukraine · UA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundEukaryotic translation elongation factor 1A2 (eEF1A2) is a known proto-oncogene. We proposed that stimulation of the eEF1A2 expression in cancer tissues is caused by the loss of miRNA-mediated control.

methodsImpact of miRNAs on eEF1A2 at the mRNA and protein levels was examined by qPCR and western blot, respectively. Dual-luciferase assay was applied to examine the influence of miRNAs on 3'-UTR of EEF1A2. To detect miRNA-binding sites, mutations into the 3'-UTR of EEF1A2 mRNA were introduced by the overlap extension PCR.

resultsmiR-663 and miR-744 inhibited the expression of luciferase gene attached to the 3'-UTR of EEF1A2 up to 20% and 50%, respectively. In MCF7 cells, overexpression of miR-663 and miR-744 reduced the EEF1A2 mRNA level by 30% and 50%. Analogous effects were also observed at the eEF1A2 protein level. In resveratrol-treated MCF7 cells the upregulation of mir-663 and mir-744 was accompanied by downregulation of EEF1A2 mRNA. Both miRNAs were able to inhibit the proliferation of MCF7 cells.

conclusionmiR-663 and miR-744 mediate inhibition of the proto-oncogene eEF1A2 expression that results in retardation of the MCF7 cancer cells proliferation. Antitumour effect of resveratrol may include stimulation of the miR-663 and miR-744 expression.

Indexed as

Breast NeoplasmsCell Growth ProcessesCell MovementDown-RegulationFemaleHumansMCF-7 CellsMicroRNAsPeptide Elongation Factor 1Proto-Oncogene MasResveratrolRNA, MessengerStilbenesTransfectionEEF1A2 protein, humanMAS1 protein, humanMicroRNAsMIRN663 microRNA, humanMIRN744 microRNA, humanPeptide Elongation Factor 1Proto-Oncogene MasResveratrolRNA, MessengerStilbenes

Identifiers

PMID23695020
PMCPMC3681015
OpenAlexW2035014104

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
Read underepoch 390

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.