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

Cell cycle (Georgetown, Tex.) · 2016 · Mixed · Low evidence

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MixedLow evidencePaper 4888

Study snapshot

PublicationCell cycle (Georgetown, Tex.) · 2016

Study typein_vitro

Reported directionMixed

Evidence ratingLow

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.

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AI evidence extraction

Structured fields below were generated from the paper’s abstract and metadata to make the evidence easier to inspect. Automated extraction may be incomplete or incorrect; verify important details against the original paper.

Study typein_vitro

Effect directionmixed

PopulationNot supplied

Sample sizeNot supplied

ExposureELF · 0.05 MHz · 72 h intermittent (5 min on/10 min off)

Evidence strengthLowConfidence: 74% · Peer reviewed: yes

Main findings

Mouse spermatocyte-derived GC-2 cells were intermittently exposed to a 50 Hz ELF-EMF (1, 2, 3 mT) for 72 h. miR-26b-5p was differentially expressed by magnetic field intensity; CTDSP1 showed an unmethylation status under different intensities. miR-26b-5p alone had no significant obvious influence on viability, apoptosis, or cell cycle, but miR-26b-5p overexpression decreased the G0/G1 fraction and slightly increased the S-phase fraction versus a sham group exposed to 50 Hz ELF-EMF; CCND2 was identified as a direct target and miR-26b-5p and 50 Hz ELF-EMF altered CCND2 at mRNA and protein levels, with overexpression changing CCND2 mRNA following 3 mT exposure.

Outcomes measured

miR-26b-5p expression
CTDSP1 methylation status
cell viability
apoptosis
cell cycle phase distribution (G0/G1, S)
CCND2 (Cyclin D2) mRNA expression
CCND2 protein expression

Limitations

In vitro model (GC-2 mouse spermatocyte-derived cells); relevance to in vivo male reproductive outcomes not established in abstract
Sample size and replication details not reported in abstract
Exposure source/setup details beyond frequency, intensity, and intermittency not provided in abstract
Some reported effects depend on miR-26b-5p overexpression rather than ELF-EMF exposure alone

View raw extracted JSON

{
  "study_type": "in_vitro",
  "exposure": {
    "band": "ELF",
    "source": null,
    "frequency_mhz": 0.05,
    "sar_wkg": null,
    "duration": "72 h intermittent (5 min on/10 min off)"
  },
  "population": null,
  "sample_size": null,
  "outcomes": [
    "miR-26b-5p expression",
    "CTDSP1 methylation status",
    "cell viability",
    "apoptosis",
    "cell cycle phase distribution (G0/G1, S)",
    "CCND2 (Cyclin D2) mRNA expression",
    "CCND2 protein expression"
  ],
  "main_findings": "Mouse spermatocyte-derived GC-2 cells were intermittently exposed to a 50 Hz ELF-EMF (1, 2, 3 mT) for 72 h. miR-26b-5p was differentially expressed by magnetic field intensity; CTDSP1 showed an unmethylation status under different intensities. miR-26b-5p alone had no significant obvious influence on viability, apoptosis, or cell cycle, but miR-26b-5p overexpression decreased the G0/G1 fraction and slightly increased the S-phase fraction versus a sham group exposed to 50 Hz ELF-EMF; CCND2 was identified as a direct target and miR-26b-5p and 50 Hz ELF-EMF altered CCND2 at mRNA and protein levels, with overexpression changing CCND2 mRNA following 3 mT exposure.",
  "effect_direction": "mixed",
  "limitations": [
    "In vitro model (GC-2 mouse spermatocyte-derived cells); relevance to in vivo male reproductive outcomes not established in abstract",
    "Sample size and replication details not reported in abstract",
    "Exposure source/setup details beyond frequency, intensity, and intermittency not provided in abstract",
    "Some reported effects depend on miR-26b-5p overexpression rather than ELF-EMF exposure alone"
  ],
  "evidence_strength": "low",
  "confidence": 0.74,
  "peer_reviewed_likely": "yes",
  "keywords": [
    "extremely low frequency electromagnetic fields",
    "ELF-EMF",
    "50 Hz",
    "magnetic field",
    "1 mT",
    "2 mT",
    "3 mT",
    "GC-2 cells",
    "spermatocyte-derived",
    "miR-26b-5p",
    "CTDSP1",
    "methylation",
    "cell cycle",
    "CCND2",
    "Cyclin D2",
    "male reproductive function",
    "biomarker"
  ],
  "suggested_hubs": [
    {
      "slug": "occupational-exposure",
      "weight": 0.25,
      "reason": "Study uses relatively high-intensity 50 Hz magnetic fields (mT range), which can be relevant to occupational ELF exposure contexts."
    }
  ]
}

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AI-extracted fields are generated from the abstract and metadata and may be incomplete or incorrect. This material is for informational purposes and is not medical advice.

Identifiers and source

DOI: 10.1080/15384101.2015.1120924
PubMed: 26637059

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