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BioMed Research International
Volume 2013 (2013), Article ID 657259, 6 pages
Research Article

Effect of Adjuvant Magnetic Fields in Radiotherapy on Non-Small-Cell Lung Cancer Cells In Vitro

1Cancer Research Institute, Zhejiang Cancer Hospital, No. 38 Guangji Road, Hangzhou, Zhejiang 310022, China
2Key Laboratory Diagnosis and Treatment Technology on Thoracic Oncology, Hangzhou, Zhejiang 310022, China
3Department of Oncology, Affiliated Hangzhou Hospital (Hangzhou First People’s Hospital), Nanjing Medical University, No. 261 Huansha Road, Hangzhou 310006, China

Received 18 April 2013; Revised 12 July 2013; Accepted 12 July 2013

Academic Editor: Maria F. Chan

Copyright © 2013 Jianguo Feng et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Objectives. To explore sensitization and possible mechanisms of adjuvant magnetic fields (MFs) in radiotherapy (RT) of non-small-cell lung cancer. Methods. Human A549 lung adenocarcinoma cells were treated with MF, RT, and combined MF-RT. Colony-forming efficiency was calculated, cell cycle and apoptosis were measured, and changes in cell cycle- and apoptosis-related gene expression were measured by microarray. Results. A 0.5 T, 8 Hz stationary MF showed a duration-dependent inhibitory effect lasting for 1–4 hours. The MF-treated groups had significantly greater cell inhibition than did controls ( ). Surviving fractions and growth curves derived from colony-forming assay showed that the MF-only, RT-only, and MF-RT groups had inhibited cell growth; the MF-RT group showed a synergetic effect. Microarray of A549 cells exposed for 1 hour to MF showed that 19 cell cycle- and apoptosis-related genes had 2-fold upregulation and 40 genes had 2-fold downregulation. MF significantly arrested cells in G2 and M phases, apparently sensitizing the cells to RT. Conclusions. MF may inhibit A549 cells and can increase their sensitivity to RT, possibly by affecting cell cycle- and apoptosis-related signaling pathways.