Evidence map›Paper›PMID 26637059›Full record

ArticleCell cycle (Georgetown, Tex.)2016

Overexpression of miR-26b-5p regulates the cell cycle by targeting CCND2 in GC-2 cells under exposure to extremely low frequency electromagnetic fields.

Yong Liu, Wen-Bin Liu, Kai-Jun Liu, Lin Ao, Jia Cao, Julia Li Zhong, Jin-Yi Liu

Open access · bronzeAbstract read
In one paragraph

Article in Cell cycle (Georgetown, Tex.), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
4.1field-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

23 citing papers in PubMed, 33 citations in OpenAlex.

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  17. Transcriptional changes in the hypothalamus, pituitary, and mammary gland underlying decreased lactation performance in mice under heat stress.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2019
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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

7 authors at 2 institutions in 1 country.

Yong Liua College of Bioengineering, Chongqing University , Chongqing , China.
Wen-Bin Liub Institute of Toxicology, College of Preventive Medicine, Third Military Medical University , Chongqing , China.
Kai-Jun Liub Institute of Toxicology, College of Preventive Medicine, Third Military Medical University , Chongqing , China.
Lin Aob Institute of Toxicology, College of Preventive Medicine, Third Military Medical University , Chongqing , China.
Jia Caob Institute of Toxicology, College of Preventive Medicine, Third Military Medical University , Chongqing , China.
Julia Li Zhonga College of Bioengineering, Chongqing University , Chongqing , China.
Jin-Yi Liub Institute of Toxicology, College of Preventive Medicine, Third Military Medical University , Chongqing , China.
Army Medical University · CNChongqing University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The increasing prevalence of extremely low frequency electromagnetic fields (ELF-EMFs) exposure has raised considerable public concern regarding the potential hazardous effects of ELF-EMFs on male reproductive function. Increasing evidence indicates that miRNAs are necessary for spermatogenesis and male fertility. However, the regulation of miRNA expression and the roles of miRNAs in response to ELF-EMFs remain unclear. In our study, mouse spermatocyte-derived GC-2 cells were intermittently exposed to a 50 Hz ELF-EMF for 72 h (5 min on/10 min off) at magnetic field intensities of 1 mT, 2 mT and 3 mT. MiR-26b-5p was differentially expressed in response to different magnetic field intensities of ELF-EMFs. The host gene CTDSP1 showed an unmethylation status in GC-2 cells at different magnetic field intensities of ELF-EMF exposure. MiR-26b-5p had no significant, obvious influence on the cell viability, apoptosis or cell cycle of GC-2 cells. However, the overexpression of miR-26b-5p significantly decreased the percentage of G0/G1 phase cells and slightly increased the percentage of S phase cells compared to the sham group that was exposed to a 50 Hz ELF-EMF. Computational algorithms identified Cyclin D2 (CCND2) as a direct target of miR-26b-5p. MiR-26b-5p and a 50 Hz ELF-EMF altered the expression of CCND2 at both the mRNA and protein levels. Overexpressed miR-26b-5p in GC-2 cells can change the mRNA expression of CCND2 following 50 Hz ELF-EMF at 3 mT. These findings demonstrate that miR-26b-5p could serve as a potential biomarker following 50 Hz ELF-EMF exposure, and miR-26b-5p-CCND2-mediated cell cycle regulation might play a pivotal role in the biological effects of ELF-EMFs.

Indexed as

3' Untranslated RegionsAnimalsBase SequenceBlotting, WesternCell LineCell SurvivalCyclin D2Electromagnetic FieldsG1 Phase Cell Cycle CheckpointsMiceMicroRNAsOligonucleotides, AntisensePhosphoprotein PhosphatasesReal-Time Polymerase Chain ReactionSequence Alignment3' Untranslated RegionsCcnd2 protein, mouseCyclin D2MicroRNAsMirn26 microRNA, mouseOligonucleotides, AntisensePhosphoprotein PhosphatasesCCND2cell cycleextremely low frequency electromagnetic fieldsmiR-26b-5preproductive toxicity

Identifiers

PMID26637059
PMCPMC4943694
OpenAlexW2191577401

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.