Exposure to long-term evolution radiofrequency electromagnetic fields decreases neuroblastoma cell proliferation via Akt/mTOR-mediated cellular senescence.
← Research streamExposure to 1760 MHz LTE RF-EMF at 4 W/kg SAR for 4 hr/day for 4 days significantly decreased SH-SY5Y cell growth rate and proliferation and delayed the cell cycle in G0/G1. The authors report no marked change in γH2AX and no activation of apoptosis, while ob…
Study snapshot
Abstract
The aim of this study was to examine the potential effects of long-term evolution (LTE) radiofrequency electromagnetic fields (RF-EMF) on cell proliferation using SH-SY5Y neuronal cells. The growth rate and proliferation of SH-SY5Y cells were significantly decreased upon exposure to 1760 MHz RF-EMF at 4 W/kg specific absorption rate (SAR) for 4 hr/day for 4 days. Cell cycle analysis indicated that the cell cycle was delayed in the G0/G1 phase after RF-EMF exposure. However, DNA damage or apoptosis was not involved in the reduced cellular proliferation following RF-EMF exposure because the expression levels of histone H2A.X at Ser139 (γH2AX) were not markedly altered and the apoptotic pathway was not activated. However, SH-SY5Y cells exposed to RF-EMF exhibited a significant elevation in Akt and mTOR phosphorylation levels. In addition, the total amount of p53 and phosphorylated-p53 was significantly increased. Data suggested that Akt/mTOR-mediated cellular senescence led to p53 activation via stimulation of the mTOR pathway in SH-SY5Y cells. The transcriptional activation of p53 led to a rise in expression of cyclin-dependent kinase (CDK) inhibitors p21 and p27. Further, subsequent inhibition of CDK2 and CDK4 produced a fall in phosphorylated retinoblastoma (pRb at Ser807/811), which decreased cell proliferation. Taken together, these data suggest that exposure to RF-EMF might induce Akt/mTOR-mediated cellular senescence, which may delay the cell cycle without triggering DNA damage in SH-SY5Y neuroblastoma cells.
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.
Main findings
Exposure to 1760 MHz LTE RF-EMF at 4 W/kg SAR for 4 hr/day for 4 days significantly decreased SH-SY5Y cell growth rate and proliferation and delayed the cell cycle in G0/G1. The authors report no marked change in γH2AX and no activation of apoptosis, while observing increased Akt/mTOR phosphorylation and increased p53 (total and phosphorylated) with downstream increases in p21/p27 and reduced pRb phosphorylation, consistent with Akt/mTOR-mediated cellular senescence.
Outcomes measured
- Cell growth rate
- Cell proliferation
- Cell cycle distribution (G0/G1 delay)
- DNA damage marker γH2AX (H2A.X Ser139)
- Apoptosis pathway activation
- Akt phosphorylation
- mTOR phosphorylation
- p53 total and phosphorylated p53
- p21 and p27 expression
- CDK2 and CDK4 inhibition
- pRb phosphorylation (Ser807/811)
- Cellular senescence (Akt/mTOR-mediated)
View raw extracted JSON
{
"study_type": "in_vitro",
"exposure": {
"band": "RF",
"source": "LTE",
"frequency_mhz": 1760,
"sar_wkg": 4,
"duration": "4 hr/day for 4 days"
},
"population": "SH-SY5Y neuroblastoma (neuronal) cells",
"sample_size": null,
"outcomes": [
"Cell growth rate",
"Cell proliferation",
"Cell cycle distribution (G0/G1 delay)",
"DNA damage marker γH2AX (H2A.X Ser139)",
"Apoptosis pathway activation",
"Akt phosphorylation",
"mTOR phosphorylation",
"p53 total and phosphorylated p53",
"p21 and p27 expression",
"CDK2 and CDK4 inhibition",
"pRb phosphorylation (Ser807/811)",
"Cellular senescence (Akt/mTOR-mediated)"
],
"main_findings": "Exposure to 1760 MHz LTE RF-EMF at 4 W/kg SAR for 4 hr/day for 4 days significantly decreased SH-SY5Y cell growth rate and proliferation and delayed the cell cycle in G0/G1. The authors report no marked change in γH2AX and no activation of apoptosis, while observing increased Akt/mTOR phosphorylation and increased p53 (total and phosphorylated) with downstream increases in p21/p27 and reduced pRb phosphorylation, consistent with Akt/mTOR-mediated cellular senescence.",
"effect_direction": "harm",
"limitations": [],
"evidence_strength": "low",
"confidence": 0.74,
"peer_reviewed_likely": "yes",
"keywords": [
"LTE",
"RF-EMF",
"1760 MHz",
"specific absorption rate",
"SAR 4 W/kg",
"SH-SY5Y",
"neuroblastoma",
"cell proliferation",
"cell cycle",
"G0/G1",
"Akt",
"mTOR",
"p53",
"p21",
"p27",
"cellular senescence",
"γH2AX",
"apoptosis"
],
"suggested_hubs": []
}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: 10.1080/15287394.2021.1944944
PubMed: 34196262
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