Evidence map›Paper›PMID 36652154›Full record

ArticleMolecular biology reports2023

Impact of silencing eEF2K expression on the malignant properties of chordoma.

Esra Aydemir, Emre Can Tüysüz, Ömer Faruk Bayrak, Didem Tecimel, Ayşen Aslı Hızlı-Deniz, Fikrettin Şahin

Abstract read
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In one paragraph

Article in Molecular biology reports, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
0.3field-weighted citation impact, top 41% 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

1 citing paper in PubMed, 1 citations in OpenAlex.

  1. 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

6 authors at 3 institutions in 2 countries.

Esra AydemirDepartment of Biomedical Engineering, Faculty of Engineering and Natural Sciences, Biruni University, 10. Yil Cad, Protokol Yolu, No: 45 Topkapı, 34010, Istanbul, Turkey. eaydemir@biruni.edu.tr.ORCID http://orcid.org/0000-0002-6965-2838
Emre Can TüysüzDepartment of Genetics and Bioengineering, Faculty of Engineering, Yeditepe University, Istanbul, Turkey.ORCID http://orcid.org/0000-0002-2264-0303
Ömer Faruk BayrakDepartment of Medical Genetics, Yeditepe University Medical School and Yeditepe University Hospital, Istanbul, Turkey.ORCID http://orcid.org/0000-0001-7562-6604
Didem TecimelDepartment of Genetics and Bioengineering, Faculty of Engineering, Yeditepe University, Istanbul, Turkey.ORCID http://orcid.org/0000-0002-0776-1238
Ayşen Aslı Hızlı-DenizDepartment of Genetics and Bioengineering, Faculty of Engineering, Yeditepe University, Istanbul, Turkey.ORCID http://orcid.org/0000-0003-0490-7737
Fikrettin ŞahinDepartment of Genetics and Bioengineering, Faculty of Engineering, Yeditepe University, Istanbul, Turkey.ORCID http://orcid.org/0000-0003-1503-5567
Yeditepe University · TRBiruni University · TRYeditepe University Hospital · TR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundEukaryotic elongation factor 2 kinase (eukaryotic elongation factor 2 kinase, eEF2K) is a calcium calmodulin dependent protein kinase that keeps the highest energy consuming cellular process of protein synthesis under check through negative regulation. eEF2K pauses global protein synthesis rates at the translational elongation step by phosphorylating its only kown substrate elongation factor 2 (eEF2), a unique translocase activity in ekaryotic cells enabling the polypeptide chain elongation. Therefore, eEF2K is thought to preserve cellular energy pools particularly upon acute development of cellular stress conditions such as nutrient deprivation, hypoxia, or infections. Recently, high expression of this enzyme has been associated with poor prognosis in an array of solid tumor types. Therefore, in a growing number of studies tremendous effort is being directed to the development of treatment methods aiming to suppress eEF2K as a novel therapeutic approach in the fight against cancer.

methodsIn our study, we aimed to investigate the changes in the tumorigenicity of chordoma cells in presence of gene silencing for eEF2K. Taking a transient gene silencing approach using siRNA particles, eEF2K gene expression was suppressed in chordoma cells.

resultsSilencing eEF2K expression was associated with a slight increase in cellular proliferation and a decrease in death rates. Furthermore, no alteration in the sensitivity of chordoma cells to chemotherapy was detected in response to the decrease in eEF2K expression which intriguingly promoted suppression of cell migratory and invasion related properties.

conclusionOur findings indicate that the loss of eEF2K expression in chordoma cell lines results in the reduction of metastatic capacity.

Indexed as

ChordomaElongation Factor 2 KinaseCell LineHumansPhosphorylationSignal TransductionEEF2K protein, humanElongation Factor 2 KinaseChordomaeEF2KMigrationsiRNAs

Identifiers

PMID36652154
OpenAlexW4317212046

What Socratic 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 Socratic graph.