Exposure to long-term evolution radiofrequency electromagnetic fields decreases neuroblastoma cell proliferation via Akt/mTOR-mediated cellular senescence

Kim, Woo Jung; Jeon, Sang Bong; Choi, Hyung‐Do; Lee, Jae‐Hun; Bae, Jun-Sang; Kim, Nam; Kim, Hyunggun; Kim, Kyu‐Bong; Kim, Hak Rim

doi:10.1080/15287394.2021.1944944

Cited by 6 publications

(7 citation statements)

References 48 publications

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“…Interestingly, miR34a has been previously reported as a member of the p53 transcriptional network regulating tumour suppression in cancers including oesophageal squamous cancer [37,48]. We also reviewed that RF-EMF in SH-SY5Y cells led to altered Akt/mTOR levels; the activation of p53, p21 and p27 and reduced pRb levels [36]. This study brought into focus how RF-EMF as a treatment modality in various cancers [44] may also induce senescence.…”

Section: Discussionmentioning

confidence: 80%

“…Delving deeper into the mechanisms revealed that Akt/mTOR activation triggered p53 and also led to the activation of p21 and p27, decreasing levels of CDK2 and CDK4. Also, reduced pRb at Ser807/811 and a consequent cell proliferation reduction ensued [36] (Fig. 1).…”

Section: Tablementioning

confidence: 90%

“…As discussed, therapy may trigger senescence as an important step in preventing cancer cell proliferation and malignant progression. Consistently, the effect of long-term radiofrequency electromagnetic fields (RF-EMF) on NB cell lines including SH-SY5Y was investigated, and the results revealed that their growth rate was dramatically reduced following exposure to these waves [36]. RF-EMF treatment, with a dose set at 1760 MHz with 4 W/kg for 4 h per day for 4 days, induced G0/G1 cell cycle delay in SH-SY5Y cells.…”

Section: Tablementioning

confidence: 96%

“…Contrastingly, signalling molecules including Akt/mTOR were altered (e.g. phospho-mTOR was elevated) in addition to increased levels of p53 and phosphorylated p53 [36]. Delving deeper into the mechanisms revealed that Akt/mTOR activation triggered p53 and also led to the activation of p21 and p27, decreasing levels of CDK2 and CDK4.…”

Section: Tablementioning

confidence: 99%

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The Role of lncRNAs and miRNAs in Therapy-Induced Senescence in Neuroblastoma

Jahangiri

Ishola

2022

Curr Mol Bio Rep

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Purpose of Review Neuroblastoma, a paediatric malignancy of the sympathoadrenal lineage with a variable clinical course, is the most prevalent extra-cranial cancer in children. The majority of multi-modal therapeutics utilised for treating neuroblastoma may drive cells towards cell death or cellular senescence. Recent Findings Although cellular senescence has been historically regarded as a permanent state of non-proliferation, new evidence supports the notion that this process may indeed be much more dynamic than previously thought. Further, senescent tumour cells may escape treatment and further promote inflammation and migration through their repertoire of secreted molecules, leading to disease relapse. Summary Given this background, we review here the role of non-coding RNAs inclusive of long non-coding RNAs (lncRNAs) and miRNAs in therapy-induced senescence-related processes in neuroblastoma and discuss how these molecules may be manipulated for therapeutic gain.

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Section: Discussionmentioning

confidence: 80%

Section: Tablementioning

confidence: 90%

Section: Tablementioning

confidence: 96%

Section: Tablementioning

confidence: 99%

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The Role of lncRNAs and miRNAs in Therapy-Induced Senescence in Neuroblastoma

Jahangiri

Ishola

2022

Curr Mol Bio Rep

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“…Several previous studies have observed the effects of RF-EMR on neuronal cells at SAR value of 4 W/kg, showing the confirmed effect of RF-EMR exposure on dendritic development, cell cycle, etc. ( 9 , 44 – 46 ).…”

Section: Discussionmentioning

confidence: 99%

1,800 MHz Radiofrequency Electromagnetic Irradiation Impairs Neurite Outgrowth With a Decrease in Rap1-GTP in Primary Mouse Hippocampal Neurons and Neuro2a Cells

Deng

Chen

et al. 2021

Front. Public Health

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Background: With the global popularity of communication devices such as mobile phones, there are increasing concerns regarding the effect of radiofrequency electromagnetic radiation (RF-EMR) on the brain, one of the most important organs sensitive to RF-EMR exposure at 1,800 MHz. However, the effects of RF-EMR exposure on neuronal cells are unclear. Neurite outgrowth plays a critical role in brain development, therefore, determining the effects of 1,800 MHz RF-EMR exposure on neurite outgrowth is important for exploring its effects on brain development.Objectives: We aimed to investigate the effects of 1,800 MHz RF-EMR exposure for 48 h on neurite outgrowth in neuronal cells and to explore the associated role of the Rap1 signaling pathway.Material and Methods: Primary hippocampal neurons from C57BL/6 mice and Neuro2a cells were exposed to 1,800 MHz RF-EMR at a specific absorption rate (SAR) value of 4 W/kg for 48 h. CCK-8 assays were used to determine the cell viability after 24, 48, and 72 h of irradiation. Neurite outgrowth of primary hippocampal neurons (DIV 2) and Neuro2a cells was observed with a 20 × optical microscope and recognized by ImageJ software. Rap1a and Rap1b gene expressions were detected by real-time quantitative PCR. Rap1, Rap1a, Rap1b, Rap1GAP, and p-MEK1/2 protein expressions were detected by western blot. Rap1-GTP expression was detected by immunoprecipitation. The role of Rap1-GTP was assessed by transfecting a constitutively active mutant plasmid (Rap1-Gly_Val-GFP) into Neuro2a cells.Results: Exposure to 1,800 MHz RF-EMR for 24, 48, and 72 h at 4 W/kg did not influence cell viability. The neurite length, primary and secondary neurite numbers, and branch points of primary mouse hippocampal neurons were significantly impaired by 48-h RF-EMR exposure. The neurite-bearing cell percentage and neurite length of Neuro2a cells were also inhibited by 48-h RF-EMR exposure. Rap1 activity was inhibited by 48-h RF-EMR with no detectable alteration in either gene or protein expression of Rap1. The protein expression of Rap1GAP increased after 48-h RF-EMR exposure, while the expression of p-MEK1/2 protein decreased. Overexpression of constitutively active Rap1 reversed the decrease in Rap1-GTP and the neurite outgrowth impairment in Neuro2a cells induced by 1,800 MHz RF-EMR exposure for 48 h.Conclusion: Rap1 activity and related signaling pathways are involved in the disturbance of neurite outgrowth induced by 48-h 1,800 MHz RF-EMR exposure. The effects of RF-EMR exposure on neuronal development in infants and children deserve greater focus.

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The effect of exposure to radiofrequency LTE signal and coexposure to mitomycin‐C in Chinese hamster lung fibroblast V79 cells

Sannino

Romeo

Scarfì

et al. 2023

Bioelectromagnetics

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This study aims to investigate the cellular effects of radiofrequency exposure, 1950 MHz, long‐term evolution (LTE) signal, administered alone and in combination with mitomycin‐C (MMC), a well‐known cytotoxic agent. Chinese hamster lung fibroblast (V79) cells were exposed/sham exposed in a waveguide‐based system under strictly controlled conditions of both electromagnetic and environmental parameters, at specific absorption rate (SAR) of 0.3 and 1.25 W/kg. Chromosomal damage (micronuclei formation), oxidative stress (reactive oxygen species [ROS] formation), and cell cycle progression were analyzed after exposure and coexposure. No differences between exposed samples and sham‐controls were detected following radiofrequency exposure alone, for all the experimental conditions tested and biological endpoints investigated. When radiofrequency exposure was followed by MMC treatment, 3 h pre‐exposure did not modify MMC‐induced micronuclei. Pre‐exposure of 20 h at 0.3 W/kg did not modify the number of micronuclei induced by MMC, while 1.25 W/kg resulted in a significant reduction of MMC‐induced damage. Absence of effects was also detected when CW was used, at both SAR levels. MMC‐induced ROS formation resulted significantly decreased at both SAR levels investigated, while cell proliferation and cell cycle progression were not affected by coexposures. The results here reported provide no evidence of direct effects of 1950 MHz, LTE signal. Moreover, they further support our previous findings on the capability of radiofrequency pre‐exposure to induce protection from a subsequent toxic treatment, and the key role of the modulated signals and the experimental conditions adopted in eliciting the effect.

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Exposure to long-term evolution radiofrequency electromagnetic fields decreases neuroblastoma cell proliferation via Akt/mTOR-mediated cellular senescence

Cited by 6 publications

References 48 publications

The Role of lncRNAs and miRNAs in Therapy-Induced Senescence in Neuroblastoma

The Role of lncRNAs and miRNAs in Therapy-Induced Senescence in Neuroblastoma

1,800 MHz Radiofrequency Electromagnetic Irradiation Impairs Neurite Outgrowth With a Decrease in Rap1-GTP in Primary Mouse Hippocampal Neurons and Neuro2a Cells

The effect of exposure to radiofrequency LTE signal and coexposure to mitomycin‐C in Chinese hamster lung fibroblast V79 cells

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