許多文獻指出，細胞生理會受到電場和磁場的電磁力影響。另外，細胞會受磁場不同的 物理參數而影響癌細胞的生長，如磁場頻率、梯度和強度等。靜磁場常被用於研究特定 磁場強度下的生物效應，然而靜磁場影響細胞的生理機制仍懸而待解且存在爭議。因此， 本研究要探討靜磁場如何調控癌細胞生理機制。在本研究中，細胞實驗結果顯示靜磁場 會調控癌細胞的生長速率及細胞週期。根據細胞生長速率的實驗結果指出，受磁組細胞 的數量增加一倍所需時間比對照組長。此外，細胞週期的實驗結果顯示在靜磁場(static magnetic field，SMF)下暴露 24 小時後，與對照組相比受磁組有更多累積於分裂期的 比例（% of G2/M，SMF：控制組= 5.50 : 0.25）。在免疫螢光染色及西方點墨法的結 果發現，受磁組的細胞素 B1 和 E1 表現量上升且受磁組 ATM-NBS1-CHK 信號傳導途徑也 因磁場而活化。在次世代定序的結果發現，靜磁場主要影響了細胞移動、免疫和發育相 關基因表現。在活細胞影像分析的結果中發現，暴露於靜磁場下的癌細胞有較多細胞累 積在有絲分裂期，細胞型態較收縮且周圍突起較短，細胞的移動頻率較高，這顯示靜磁 場可能影響細胞中微管絲與機動蛋白的組合，使受磁組的細胞附著能力較差。在斑馬魚 生物毒性測試結果中也發現，靜磁場影響了黑色素的移動和生成，但控制組和受磁組於 受孕後 96 小時之生長率，以及幼魚的外型並沒有明顯差異。本研究意旨在理解靜磁場 調控的癌細胞效應，並評估利用此生物效應的特點，作為輔助性療法的潛能;Previous reports have demonstrated that exposure of electromagnetic force could affect cellular physiology. Others have shown that static magnetic field (SMF) has impacts on cell proliferation, particularly in cancer cells. Several physical parameters, such as magnetic frequency, gradient, and magnitude, were reported to affect the biological consequences. However, discrepancies exist between the SMF and cancer cell responses and the mechanisms underlying the SMF-mediated effects remained largely unexplored. The main purpose of this study is to investigate the mechanisms of SMF-mediated effects in cancer cells. Our results showed that the exposure of SMF affected cancer cell proliferation and cell cycle distribution. The doubling time for cells exposed to SMF was longer than that of control group. The results of flow cytometry showed that SMF induced higher percentage of cells accumulated in the mitotic phase compared to that of control group after 24-hour exposures (% of G2/M，SMF： control= 5.50 : 0.25). Results of immune-fluorescent staining and western blotting found higher expressions of cyclin B1 and cyclin E1 SMF-treated cells. Furthermore, the activation of ATM-NBS1-CHK signaling pathway was enhanced. The results of Next Generation Sequencing (NGS) analysis showed that the SMF primarily regulated genes involved in functions of motility, immune and embryonic development related pathways. From the time-lapse fluorescent microscope observations, more cancer cells exposed to SMF were accumulated in mitotic phase. The SMF-treated cells exhibited a shrinkage phenotype, faster motion frequency, and shorter peripheral protrusions. These observations indicate that the v
SMF may affect polymerizations of microtubules and F-actin, as well as cell adhesion. To test the SMF-mediated effects on development, we used zebrafish as the model and evaluated the phenotypic alterations during development. We found that SMF exposures evidently affected the distribution of melanin. Some embryonic malformations were also observed under SMF treatment. However, there’s no difference on the survival ratio between SMF-treated group and control group. The presented study helps to understand more molecular mechanisms of the SMF-mediated effects on cancer cells. This may provide an opportunity to utilize the features of SMF to tailor therapeutic strategy.
