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Static magnetic field (SMF) has a potential as a cancer therapeutic modality due to its specific inhibitory effects on the proliferation of multiple cancer cells. However, the underlying mechanism remains unclear, and just a few studies have examined the effects of SMF on metastasis, an important concern in cancer treatment. In this study, we evaluated the effects of moderate SMF (~150 mT) on the proliferation and migration of 4T1 breast cancer cells. Our results showed that SMF treatment accelerated cell proliferation but inhibited cell migration. Further, SMF treatment shortened the telomere length, decreased telomerase activity, and inhibited the expression of the cancer-specific marker telomerase reverse transcriptase (TERT), which may be related to expression upregulation of e2f1, a transcription repressor of TERT and positive regulator of the mitotic cell cycle. Our results revealed that SMF repressed both, cell migration and telomerase function. The telomerase network is responsive to SMF and may be involved in SMF-mediated cancer-specific effects; moreover, it may function as a therapeutic target in magnetic therapy of cancers.

Accumulative evidence has shown the adverse effects of a geomagnetic field shielded condition, so called a hypomagnetic field (HMF), on the metabolic processes and oxidative stress in animals and cells. However, the underlying mechanism remains unclear. In this study, we evaluate the role of HMF on the regulation of cellular reactive oxygen species (ROS) in human neuroblastoma SH-SY5Y cells. We found that HMF exposure led to ROS decrease, and that restoring the decrease by additional H2O2 rescued the HMF-enhanced cell proliferation. The measurements on ROS related indexes, including total anti-oxidant capacity, H2O2 and superoxide anion levels, and superoxide dismutase (SOD) activity and expression, indicated that the HMF reduced H2O2 production and inhibited the activity of CuZn-SOD. Moreover, the HMF accelerated the denaturation of CuZn-SOD as well as enhanced aggregation of CuZn-SOD protein, in vitro. Our findings indicate that CuZn-SOD is able to response to the HMF stress and suggest it a mediator of the HMF effect. Electronic supplementary material The online version of this article (doi:10.1007/s13238-017-0403-9) contains supplementary material, which is available to authorized users.