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

Abstract

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 (P < 0.05). 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.

Correlation of neuroendocrine features with prognosis of non-small cell lung cancer

“…NSCLC are often diagnosed at late stages [ 8 ]. For patients with advanced stages of NSCLC when surgical excision is not an option, the adjuvant chemotherapy and radiotherapy has been extensively used [ 9 ]. However, unlike small-cell lung cancer (SCLC) that often has neuroendocrine (NE) features, NSCLC is usually chemoresistant.…”

Biological effects of static magnetic field exposure in the context of MR-guided radiotherapy

“…62 In the last 5 years, three studies have been published on the topic of combined SMF and ionising radiation exposure in human cancer in vitro models. [63][64][65] Viability of lung adrenocarcinoma cells (cell line A549) treated with 0.5 T SMF alone for 1 to 4 h was significantly inhibited by approximately 10% relative to untreated cells (p < 0.05). 63 Gene chip analysis revealed that SMF exposure of 1 h produced alterations in gene expression associated with the promotion of cell cycle arrest and apoptosis.…”

“…[63][64][65] Viability of lung adrenocarcinoma cells (cell line A549) treated with 0.5 T SMF alone for 1 to 4 h was significantly inhibited by approximately 10% relative to untreated cells (p < 0.05). 63 Gene chip analysis revealed that SMF exposure of 1 h produced alterations in gene expression associated with the promotion of cell cycle arrest and apoptosis. A549 clonogenic survival following X-ray irradiation was significantly impaired in cells exposed to SMF (p < 0.05), e.g.…”

“…the survival fraction at 10 Gy was 0.24 for B = 0 T and 0.02 for B = 0.5 T. Flow cytometry analysis linked SMF exposure with an increase in the proportion of cells in phase G2 and M, the most radiosensitive phases, suggesting that SMF may act to radiosensitize A549 cells by influencing cell cycle progression via an unidentified interaction mechanism. 63 Teodori et al 64 studied the impact of 0.08 T SMF in combination with orthovoltage X-ray irradiation on DNA damage (comet assay) and mitochondrial membrane potential (JC-1 probe) in human primary glioblastoma cells in vitro. SMF exposure (24 h) without irradiation was associated with a significant increase in DNA damage (p < 0.01), 64 which concords with the SMF-related viability reduction observed by Feng et al 63 Intriguingly, glioblastoma DNA damage was significantly reduced by 6 and 20 h SMF exposure post-irradiation (p < 0.001), while the inclusion of an additional 6 h SMF pre-treatment did not impact this result.…”

“…63 Teodori et al 64 studied the impact of 0.08 T SMF in combination with orthovoltage X-ray irradiation on DNA damage (comet assay) and mitochondrial membrane potential (JC-1 probe) in human primary glioblastoma cells in vitro. SMF exposure (24 h) without irradiation was associated with a significant increase in DNA damage (p < 0.01), 64 which concords with the SMF-related viability reduction observed by Feng et al 63 Intriguingly, glioblastoma DNA damage was significantly reduced by 6 and 20 h SMF exposure post-irradiation (p < 0.001), while the inclusion of an additional 6 h SMF pre-treatment did not impact this result. 64 X-ray induced loss of mitochondrial membrane potential was diminished by exposure to SMFs during recovery, suggesting a potential link between the protection of mitochondria by SMF (possibly via SMF perturbation of the electron transport chain in mitochondria) and a reduction in radiation-induced genotoxicity.…”