| In recent years, along with the rapid development of communication technology, public health effects induced by electromagnetic radiation have been increasingly concerned. Though domestic and foreign scholars have conducted studies about the effects of electromagnetic radiation, the results by far were not consistent because of the different samples, irradiation parameters, irradiation time, etc. In 2011, the International Agency for Research on Cancer(IARC) has classified the electromagnetic radiation as group 2B carcinogen(possible human carcinogen).Our previous study have found that long-term electromagnetic radiation could increase the levels of ROS and change p53 gene expression. Our previous studies found that long-term electromagnetic radiation could increase the intracellular level of ROS and change p53 gene expression. Acting at the hub of cell signaling networks, p53 is related to more than hundred genes upstream and downstream. The study of major pathway involved in p53 signaling network induced by electromagnetic radiation contributes to investigate the effects of electromagnetic radiation on cell electromagnetic radiation to expose NIH/3T3 cells for long-term radiation at SAR of 2 W/kg, intermittent exposure mode(5 min on/10 min off), 5 h/d. We detected the expression of p53 and related genes, also studied cells proliferation induced by longterm exposure. The results showed that: under the influence of 1800 MHz electromagnetic radiation, p53 expression presented a fluctuated trend. When cells were exposed as long as 60 days, p53 gene expression was significantly increased. Irradiated for 60 days, the cells were detected by p53 PCR Array. The results showed that 13 genes’ expression fold change was over two times in 84 genes, 11 up-regulated genes, 2 down-regulated genes. Pathway analysis showed, 60 days of electromagnetic radiation perhaps mainly through ATM-CHK2/ATR-CHK1-p53 pathway led to cell cycle arrest and apoptosis in p53 signaling network. In irradiation 60 days cells, P53 and related protein were used Western Blot assay to determine, results in line with the PCR Array. Irradiation to 138 days, p53 expression decreased compared with shamexposed cells. The study on p53 gene sequencing of 60 days and 138 days cells found that: 138 days of exposure of p53 gene have a base mutation in 1601 position located in the non-coding regions,occurring G→T mutation. The role of the base need further research.We all know p53 gene is a key core of cellular signal networks, which is an important role in cell survival and proliferation. In this study, cloning experiments were detected two irradiation time 60 days and 138 days respectively about NIH/3T3 cells proliferation radiation. The results showed that: plate cloning experiments, exposed to 60 days, exposure group cells was significantly lower than that in the sham exposure group(p<0.05), however colony rate exposed to 138 days did not change significantly. Soft agar cloning experiments, 138 days exposure group formation significantly, whereas, there was no significant difference in 60 days exposure group and control groups. Telomerase and p53 play key roles in tumor formation and cells senescence. Irradiation to 60 days and 138 days, telomerase expression was detected by ELISA methods. The results showed that the expression of telomerase was no significant difference in 60 days cells, which was significantly higher in the 138 days exposure group than that in the sham exposure group(p<0.05).In summary, 60 days electromagnetic radiation may be due to the generation of ROS or other factors started the ATM-CHK2/ATR-CHK1-p53 DNA damage repair pathway, which leads to the cell cycle arrest or apoptosis. The longer term exposure may cause mutations in p53 gene non-coding region in the process of DNA damage repair, then affect the ability of cells proliferation even induced NIH/3T3 cells transformation. The mechanism of electromagnetic radiation impacting on p53 signaling network need to be further studied. |
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