Pulsed electromagnetic field potentiates etoposide-induced MCF-7 cell death
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Etoposide is a chemotherapeutic medication used to treat varioustypes of cancer, including breast cancer. It is established thatpulsed electromagnetic field (PEMF) therapy can enhance theeffects of anti-cancer chemotherapeutic agents. In this study,we investigated whether PEMFs influence the anti-cancer effectsof etoposide in MCF-7 cells and determined the signal pathwaysaffected by PEMFs. We observed that co-treatment with etoposideand PEMFs led to a decrease in viable cells comparedwith cells solely treated with etoposide. PEMFs elevated the etoposide-induced PARP cleavage and caspase-7/9 activation andenhanced the etoposide-induced down-regulation of survivinand up-regulation of Bax. PEMF also increased the etoposideinducedactivation of DNA damage-related molecules. In addition,the reactive oxygen species (ROS) level was slightly elevatedduring etoposide treatment and significantly increased duringco-treatment with etoposide and PEMF. Moreover, treatment withROS scavenger restored the PEMF-induced decrease in cell viabilityin etoposide-treated MCF-7 cells. These results combinedindicate that PEMFs enhance etoposide-induced cell death byincreasing ROS induction–DNA damage–caspase-dependentapoptosis.
Abstract
Etoposide is a chemotherapeutic medication used to treat varioustypes of cancer, including breast cancer. It is established thatpulsed electromagnetic field (PEMF) therapy can enhance theeffects of anti-cancer chemotherapeutic agents. In this study,we investigated whether PEMFs influence the anti-cancer effectsof etoposide in MCF-7 cells and determined the signal pathwaysaffected by PEMFs. We observed that co-treatment with etoposideand PEMFs led to a decrease in viable cells comparedwith cells solely treated with etoposide. PEMFs elevated the etoposide-induced PARP cleavage and caspase-7/9 activation andenhanced the etoposide-induced down-regulation of survivinand up-regulation of Bax. PEMF also increased the etoposideinducedactivation of DNA damage-related molecules. In addition,the reactive oxygen species (ROS) level was slightly elevatedduring etoposide treatment and significantly increased duringco-treatment with etoposide and PEMF. Moreover, treatment withROS scavenger restored the PEMF-induced decrease in cell viabilityin etoposide-treated MCF-7 cells. These results combinedindicate that PEMFs enhance etoposide-induced cell death byincreasing ROS induction–DNA damage–caspase-dependentapoptosis.
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