Static magnetic field （SMF） has been known to affect cell proliferation in a cell-type-dependent manner, while the mechanism still remains unclear. We found that 1 T moderate intensity SMF inhibits cell proliferatio...Static magnetic field （SMF） has been known to affect cell proliferation in a cell-type-dependent manner, while the mechanism still remains unclear. We found that 1 T moderate intensity SMF inhibits cell proliferation of nasopharyngeal carcinoma CNE-2Z cells and the Akt/ mTOR signaling pathway, which is upregulated in many cancers, roTOR inhibitors are potential chemodrugs, but their clinical effects are limited by the feedback reactiva- tion of other signaling components such as EGFR and Akt. We showed that 1 T SMF increases the antitumor efficacy of mTOR inhibitor Torin 2. In addition, 1 T SMF increases the inhibition efficiency on roTOR substrates phosphorylation and represses the mTOR inhibitor-induced feedback reactivation of EGFR and Akt. Our study not only demonstrates that mTOR/Akt pathway is one of the molecular targets of SMFs in cells, but also reveals the clinical potentials of combinations of roTOR inhibitors and SMFs in cancer treatment.展开更多
基金supported by the Chinese Academy of Sciences‘‘Hundred Talent Program’’and the National Natural Science Foundation of China(U1532151)the Chinese High Magnetic Field Laboratory facility
文摘Static magnetic field （SMF） has been known to affect cell proliferation in a cell-type-dependent manner, while the mechanism still remains unclear. We found that 1 T moderate intensity SMF inhibits cell proliferation of nasopharyngeal carcinoma CNE-2Z cells and the Akt/ mTOR signaling pathway, which is upregulated in many cancers, roTOR inhibitors are potential chemodrugs, but their clinical effects are limited by the feedback reactiva- tion of other signaling components such as EGFR and Akt. We showed that 1 T SMF increases the antitumor efficacy of mTOR inhibitor Torin 2. In addition, 1 T SMF increases the inhibition efficiency on roTOR substrates phosphorylation and represses the mTOR inhibitor-induced feedback reactivation of EGFR and Akt. Our study not only demonstrates that mTOR/Akt pathway is one of the molecular targets of SMFs in cells, but also reveals the clinical potentials of combinations of roTOR inhibitors and SMFs in cancer treatment.
