Different effects of magnetic field on drug activity in human uterine sarcoma cell lines MES-SA and MES-SA/Dx5

ABSTRACT

Previous studies reported that combined effect of magnetic field (MF) on cytotoxic drugs in human cancer cells. We focused on the effects of 60 Hz MF on drug activity in human uterine sarcoma MES-SA and drug-resistant variant MES-SA/Dx5 cells that overexpressed the membrane protein MDR1(P-glycoprotein), a drug efflux transporter for doxorubicin, daunorubicin, and etoposide, but not cisplatin. The cisplatin with MF caused 60% decrease in cell viability when compared with no MF treatment, cisplatin alone in MES-SA cells. Even in MES-SA/Dx5 cells, MF exposure equally enhanced cisplatin activity. Then, MF enhanced doxorubicin and daunorubicin activity in MES-SA cells and caused 60% decrease in the cell viability compared with these drugs only but had less effect on these drugs in MES-SA/Dx5 cells. Etoposide activity was unaffected by MF exposure in both cell lines, although etoposide is a MDR1 substrate as with doxorubicin and daunorubicin. Thus, MF had no direct impact on MDR1 in the cell membrane. However, the differences in doxorubicin and daunorubicin activity between MES-SA and MES-SA/Dx5 data revealed that the presence of MDR1 in abundance prevented the enhancing effects of MF on doxorubicin and daunorubicin activity. These results suggested that MF may act in the opposite direction of MDR1, affect the drug influx transporters for doxorubicin and daunorubicin, and facilitate anticancer drug uptake into the cells.

KEYWORDS:

• Magnetic field (MF)
• MDR1
• drug transporter
• doxorubicin
• daunorubicin
• etoposide
• cisplatin

Acknowledgments

We would like to thank S. Yamada and Y. Ikehata for technical assistance with magnetic field device. This work was supported by Japan Society for the promotion of Science (JSPS), Grant-in Aid for Scientific Research (C) under Grant 19K12819.

Disclosure statement

No potential conflict of interest was reported by the author(s).

Additional information

Funding

This work was supported by KAKENHI JSPS [19K12819].