Exposure to long-term evolution radiofrequency electromagnetic fields decreases neuroblastoma cell proliferation via Akt/mTOR-mediated cellular senescence. Issue 20 (18th October 2021)

• Record Type: Journal Article
• Authors: Kim, Ju Hwan; Jeon, Sangbong; Choi, Hyung-Do; Lee, Jae-Hun; Bae, Jun-Sang; Kim, Nam; Kim, Hyung-Gun; Kim, Kyu-Bong; Kim, Hak Rim
• Is Part Of: Journal of toxicology and environmental health. Volume 84:Issue 20(2021)
• Page Start: 846
• Page End: 857
• Publication Date: 2021-10-18
• Subjects: RF-EMF -- cell proliferation -- cell cycle -- Akt -- mTOR -- pRb; Toxicology -- Periodicals; Environmental health -- Periodicals; 615.90205
• DOI: 10.1080/15287394.2021.1944944
• Languages: English
• ISSNs: 1528-7394

Abstract

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.