Extremely Low Frequency Magnetic Fields Induce mTOR and Hsa_Circ_100338 Expression Changes in Gastric Cancer and
Fereshteh Mansoury1, Nahid Babaei1, Soheila Abdi2
1Department of Cell Biology and Genetics, Bushehr Branch, Islamic Azad University, Bushehr, Iran.
Objective:
Extremely low-frequency magnetic field (ELF-MF) exposure, as a targeted tumor therapy, presents several potential advantages. In this research, we investigated effects of different ELF-MF intensities on cell viability and expression levels of the mammalian target of rapamycin (mTOR) and hsa_circ_100338 in the normal fibroblast (Hu02) and human gastric adenocarcinoma (AGS) cell lines.
Materials And Methods:
In this experimental study, cell lines of AGS and Hu02, were cultured under the exposure of ELFMF with magnetic flux densities (MFDs) of 0.25, 0.5, 1 and 2 millitesla (mT) for 18 hours. The 3-(4, 5-dimethylthiazoyl-2- yl)-2, 5-diphenyltetrazolium bromide (MTT) assay was used to evaluate the cell viability. Relative expression of mTOR and hsa_circ_100338 RNAs was estimated by quantitative real-time polymerase chain reaction (qRT-PCR) technique.
Results:
Viability of the normal cells was significantly increased at MFDs of 0.5, 1 and 2 mT, while viability of the tumor cells was significantly decreased at MFD of 0.25 and increased at MFD of 2 mT. Expression level of mTOR was significantly increased at the all applied MFDs in the normal cells, while it was significantly decreased at MFDs of 0.25 and 0.5mT in the tumor cells. MFDs of 1 and 2 mT in tumor cells inversely led to the increase in mTOR expression. hsa_circ_100338 was downregulated in MFD of 0.25 mT and then it was increased parallel to the increase of MFD in the normal and tumor cells.
Conclusion:
Results of the present study indicated that ELF-MF at MFDs of 0.25 and 0.5 mT can lead to decrease in the both mTOR and hsa_circ_100338 expression levels. Given the role of mTOR in cell growth, proliferation and differentiation, in addition to the potential role of hsa_circ_100338 in metastasis, expression inhibition of these two genes could be a therapeutic target in cancer treatment.
