| Pulsed electromagnetic field potentiates etoposide-induced MCF-7 cell death |
Sung-Hun Woo  1,# (Graduate student), Bohee Kim 1,# (Graduate student), Sung Hoon Kim 1,2 (Professor), Byung Chul Jung 1,3 (Research worker), Yongheum Lee 4 (Professor), Yoon Suk Kim 1,* (Professor) |
1Department of Biomedical Laboratory Science, College of Software and Digital Healthcare Convergence, Yonsei University, Wonju, Gangwon-do 26493, Republic of Korea,
2Department of Biomedical Laboratory Science, Korea Nazarene University, Cheonan, Chungcheongnam-do 31172, Republic of Korea,
3Department of Nutritional Sciences and Toxicology, University of California, Berkeley, State of California 94720, United States,
4Department of Biomedical Engineering, College of Software and Digital Healthcare Convergence, Yonsei University, Wonju, Gangwon-do 26493, Republic of Korea |
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Abstract
Etoposide is a chemotherapeutic medication used to treat various types of cancer, including breast cancer. It is established that pulsed electromagnetic field (PEMF) therapy can enhance the effects of anti-cancer chemotherapeutic agents. In this study, we investigated whether PEMFs influence the anti-cancer effects of etoposide in MCF-7 cells and determined the signal pathways affected by PEMFs. We observed that co-treatment with etoposide and PEMFs led to a decrease in viable cells compared with cells solely treated with etoposide. PEMFs elevated the etoposide-induced PARP cleavage and caspase-7/9 activation and enhanced the etoposide-induced down-regulation of survivin and up-regulation of Bax. PEMF also increased the etoposide-induced activation of DNA damage-related molecules. In addition, the reactive oxygen species (ROS) level was slightly elevated during etoposide treatment and significantly increased during co-treatment with etoposide and PEMF. Moreover, treatment with ROS scavenger restored the PEMF-induced decrease in cell viability in etoposide-treated MCF-7 cells. These results combined indicate that PEMFs enhance etoposide-induced cell death by increasing ROS induction–DNA damage–caspase-dependent apoptosis.
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| Abstract, Accepted Manuscript(in press) [Submitted on August 23, 2021, Accepted on September 27, 2021] |
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