Cytotoxicity of temozolomide on human glioblastoma cells is enhanced by the concomitant exposure to an extremely low-frequency electromagnetic field (100 Hz, 100 G)

Akbarnejad, Zeinab; Eskandary, Hossein; Dini, Luciana; Vergallo, Cristian; Nematollahi-Mahani, Seyed Noureddin; Farsinejad, Alireza; Abadi, Maryam Fekri Soofi; Ahmadi, Meysam

doi:10.1016/j.biopha.2017.05.050

Cited by 48 publications

(37 citation statements)

References 58 publications

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“…Taken together, such findings seem to suggest that MF can elevate the effects of DNA-damaging redox-active agents without affecting significantly cell viability or growth, and this could induce genomic instability and the accumulation of further genetic mutations, thus allowing cancer cells to accumulate further oncogenic mutations in order to progress toward increased aggressiveness ( 134 ). Interestingly, Akbarnejad et al ( 90 ) demonstrated that the cytotoxic effect of temozolomide on two lines of human glioblastoma cells was enhanced by a 6-day square-wave 100 Hz, 10 mT MF, and this was associated with the potentiation of the TMZ-induced activation of oxidative stress-responsive genes. However, the authors failed to demonstrate that such a response was dependent on a different modulation of TMZ-induced ROS overproduction.…”

Section: Considerations On Multiple Endpoint-based Studiesmentioning

confidence: 99%

Extremely Low-Frequency Magnetic Fields and Redox-Responsive Pathways Linked to Cancer Drug Resistance: Insights from Co-Exposure-Based In Vitro Studies

Falone

Santini

Cordone

et al. 2018

Front. Public Health

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Electrical devices currently used in clinical practice and common household equipments generate extremely low-frequency magnetic fields (ELF-MF) that were classified by the International Agency for Research on Cancer as “possible carcinogenic.” Assuming that ELF-MF plays a role in the carcinogenic process without inducing direct genomic alterations, ELF-MF may be involved in the promotion or progression of cancers. In particular, ELF-MF-induced responses are suspected to activate redox-responsive intracellular signaling or detoxification scavenging systems. In fact, improved protection against oxidative stress and redox-active xenobiotics is thought to provide critical proliferative and survival advantage in tumors. On this basis, an ever-growing research activity worldwide is attempting to establish whether tumor cells may develop multidrug resistance through the activation of essential cytoprotective networks in the presence of ELF fields, and how this might trigger relevant changes in tumor phenotype. This review builds a framework around how the activity of redox-responsive mediators may be controlled by co-exposure to ELF-MF and reactive oxygen species-generating agents in tumor and cancer cells, in order to clarify whether and how such potential molecular targets could help to minimize or neutralize the functional interaction between ELF-MF and malignancies.

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Section: Considerations On Multiple Endpoint-based Studiesmentioning

confidence: 99%

Extremely Low-Frequency Magnetic Fields and Redox-Responsive Pathways Linked to Cancer Drug Resistance: Insights from Co-Exposure-Based In Vitro Studies

Falone

Santini

Cordone

et al. 2018

Front. Public Health

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“…The exposure system has been described in greater detail elsewhere [17]. Briefly, ELF-EMF was generated by a clinically approved magnetotherapy device Fisiofield Mini (Fisioline Co., Verduno, Italy) that could generate square or sinusoidal waves with frequencies of 0-100 Hz and amplitudes of 0 − 100 G. The device was set to generate continuous square waves with a frequency of 100 Hz and amplitude of 100 G. In addition, the device contained four coils that could apply magnetic fields to two groups as simultaneously and individually.…”

Section: Exposure Systemmentioning

confidence: 99%

“…There is a direct relationship between ROS and hem-oxygenase-1and SOD. Our previous study showed an increase in ROS, HO-1 and P53 [17]. Through redox system, over-expression of the superoxide dismutase (SODs) in vitro increases cell differentiation, decreases cell growth and proliferation and can reverse a malignant phenotype to a nonmalignant one [58,64].…”

Section: Differentiationmentioning

confidence: 99%

“…Pulse electromagnetic field in the 0-300 H z range as a therapeutic tool extensively used for the treatment of cancer [15,16]. Some studies have suggested that static magnetic fields (SMFs) and pulse electromagnetic fields have the potential as the adjunctive treatment method for chemotherapy [17][18][19]. Previous studies have demonstrated that the cellular effects of extremely pulsed electromagnetic fields (ELF-EMFs) depend, in large part, on their intensity and exposure time, as well as on the phenotype of the cellular target and interactions with intracellular structure [1 7,20,21].…”

Section: Introductionmentioning

confidence: 99%

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Electromagnetic Field and Temozolomide Increase Differentiation of Human Glioblastoma Cell Line; concise view of mechanism

Ahmadi-Zeidabadi

Akbarnejad

Esmaeeli

et al. 2018

Preprint

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Glioblastoma is a highly malignant brain tumor with an extremely dismal prognosis, with a median survival of 12 months. Promoting glioma stem cell (GSC) differentiation is a crucial therapeutic strategy in treating glioblastoma to improve survival. We combine standard chemotherapy drug Temozolomide (TMZ) with Electromagnetic Field to evaluate their differentiation effects on glioma U87 cell line. Human glioma U87 cells exposed to electromagnetic field (EMF), Temozolomide (TMZ) alone and a combination of both were compared to control group. Nestin and CD133 were detected to identify stem-like cells (SLCs) changes during the experiment. The differentiation was found through detecting the expression of the glial fibrillary acidic protein (GFAP), and Notch4. We evaluated Ca + , SOD, and Notch as important chemical mediators in signal transduction to elucidate the mechanism of actions in the processes of differentiation. The expression of cancer SLC markers CD133, and neural stem/progenitor Nestin decreased in EMF/ Drug combined group compared to control which shows depletion of stem-like cell pool. In contrast, the differentiation of SLCs was increased by detecting the expression of the glial fibrillary acidic protein (GFAP), but, Notch4 decreased in Electromagnetic field/Drug combined group compared to control which shows a benign process of treatment. The differentiation was also confirmed by light microscopy. Morphological changes such as an elongated shape with elongated neurites, intercellular connection, and neurite branching were observed. Superoxide dismutase (SOD), Ca + and Notch were also increased as important chemical mediators in signal transduction. Here, we found the combination of pulsed electromagnetic fields (PEMFs) and TMZ significantly resulted in differentiation and glioma stem cells (GSCs) pool reduction that could have a profound therapeutic implication.

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“…It has been established that cell apoptosis increases after exposure to EMR [16,17], accompanied by upregulation of a series of apoptosis-related genes such as p53, bax, and caspase-3 [18,19]. p53 is a tumor suppressor gene and it plays an important role in DNA damage, the cell cycle, and apoptosis [20,21].…”

Section: Introductionmentioning

confidence: 99%

Apoptotic Effect of 1800 MHz Electromagnetic Radiation on NIH/3T3 Cells

Song

Liang

et al. 2020

IJERPH

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To investigate the effect of 1800 MHz electromagnetic radiation (EMR) on apoptosis, we exposed NIH/3T3 cells at 1800 MHz with a specific absorption rate (SAR) of 2 W/kg intermittently for 12, 24, 36, and 48 h. After exposure, Cell Counting Kit-8 (CCK-8) and flow cytometry were used to detect cell viability and apoptosis; the expression of p53, a molecule with the key role in apoptosis, was measured by real-time qPCR, western blot, and immunofluorescence; and images of the structure of the mitochondria, directly reflecting apoptosis, were captured by electron microscopy. The results showed that the viability of cells in the 12, 36, and 48 h exposure groups significantly decreased compared with the sham groups; after 48 h of exposure, the percentage of late apoptotic cells in the exposure group was significantly higher. Real-time qPCR results showed that p53 mRNA in the 48 h exposure group was 1.4-fold of that in the sham group; significant differences of p53 protein fluorescence expression were observed between the exposure groups and the sham groups after 24 h and 48 h. The mitochondrial swelling and vesicular morphology were found in the electron microscopy images after 48 h exposure. These findings demonstrated 1800 MHz, SAR 2 W/kg EMR for 48 h may cause apoptosis in NIH/3T3 cells and that this apoptosis might be attributed to mitochondrial damage and upregulation of p53 expression.

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Cytotoxicity of temozolomide on human glioblastoma cells is enhanced by the concomitant exposure to an extremely low-frequency electromagnetic field (100 Hz, 100 G)

Cited by 48 publications

References 58 publications

Extremely Low-Frequency Magnetic Fields and Redox-Responsive Pathways Linked to Cancer Drug Resistance: Insights from Co-Exposure-Based In Vitro Studies

Extremely Low-Frequency Magnetic Fields and Redox-Responsive Pathways Linked to Cancer Drug Resistance: Insights from Co-Exposure-Based In Vitro Studies

Electromagnetic Field and Temozolomide Increase Differentiation of Human Glioblastoma Cell Line; concise view of mechanism

Apoptotic Effect of 1800 MHz Electromagnetic Radiation on NIH/3T3 Cells

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