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1 T moderate intensity static magnetic field affects Akt/mTOR pathway and increases the antitumor efficacy of mTOR inhibitors in CNE-2Z cells
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  • 作者:Lei Zhang ; Xingxing Yang ; Juanjuan Liu ; Yan Luo ; Zhiyuan Li ; Xinmiao Ji…
  • 关键词:Static magnetic field ; Cell proliferation ; mTOR ; mTOR inhibitor ; Feedback reactivation ; 稳态磁场
  • 细胞增殖 ; mTOR ; mTOR抑制剂 负反馈
  • 刊名:Chinese Science Bulletin
  • 出版年:2015
  • 出版时间:December 2015
  • 年:2015
  • 卷:60
  • 期:24
  • 页码:2120-2128
  • 全文大小:3,399 KB
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  • 作者单位:Lei Zhang (1) (2)
    Xingxing Yang (1)
    Juanjuan Liu (1) (2)
    Yan Luo (1)
    Zhiyuan Li (1)
    Xinmiao Ji (1)
    Wenchao Wang (1)
    Xin Zhang (1)

    1. High Magnetic Field Laboratory, Chinese Academy of Sciences, Hefei, 230031, China
    2. University of Science and Technology of China, Hefei, 230026, China
  • 刊物主题:Science, general; Life Sciences, general; Physics, general; Chemistry/Food Science, general; Earth Sciences, general; Engineering, general;
  • 出版者:Springer Berlin Heidelberg
  • ISSN:1861-9541
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. mTOR inhibitors are potential chemodrugs, but their clinical effects are limited by the feedback reactivation 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 mTOR 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 mTOR inhibitors and SMFs in cancer treatment. Keywords Static magnetic field Cell proliferation mTOR mTOR inhibitor Feedback reactivation

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