Exposure to a specific time-varying electromagnetic field inhibits cell proliferation via cAMP and ERK signaling in cancer cells.


Author: Buckner CA1,2, Buckner AL1,2, Koren SA3, Persinger MA1,3, Lafrenie RM1,2

Affiliation: <sup>1</sup>Department of Biomolecular Sciences, Laurentian University, Sudbury, Ontario, Canada.

<sup>2</sup>Department of Behavioural Neurosciences, Laurentian University, Sudbury, Ontario, Canada.

<sup>3</sup>Regional Cancer Program, Health Sciences North, Sudbury, Ontario, Canada.
Conference/Journal: Bioelectromagnetics.
Date published: 2017 Nov 10
Other:
  Special Notes: doi: 10.1002/bem.22096. [Epub ahead of print]   ,  Word Count: 258  
    Exposure to specific electromagnetic field (EMF) patterns can affect a variety of biological systems. We have shown that exposure to Thomas-EMF, a low-intensity, frequency-modulated (25-6 Hz) EMF pattern, inhibited growth and altered cell signaling in malignant cells. Exposure to Thomas-EMF for 1 h/day inhibited the growth of malignant cells including B16-BL6 mouse melanoma cells, MDA-MB-231, MDA-MB-468, BT-20, and MCF-7 human breast cancer and HeLa cervical cancer cells but did not affect non-malignant cells. The Thomas-EMF-dependent changes in cell proliferation were mediated by adenosine 3',5'-cyclic monophosphate (cAMP) and extracellular-signal-regulated kinase (ERK) signaling pathways. Exposure of malignant cells to Thomas-EMF transiently changed the level of cellular cAMP and promoted ERK phosphorylation. Pharmacologic inhibitors (SQ22536) and activators (forskolin) of cAMP production both blocked the ability of Thomas-EMF to inhibit cell proliferation, and an inhibitor of the MAP kinase pathway (PD98059) was able to partially block Thomas-EMF-dependent inhibition of cell proliferation. Genetic modulation of protein kinase A (PKA) in B16-BL6 cells also altered the effect of Thomas-EMF on cell proliferation. Cells transfected with the constitutively active form of PKA (PKA-CA), which interfered with ERK phosphorylation, also interfered with the Thomas-EMF effect on cell proliferation. The non-malignant cells did not show any EMF-dependent changes in cAMP levels, ERK phosphorylation, or cell growth. These data indicate that exposure to the specific Thomas-EMF pattern can inhibit the growth of malignant cells in a manner dependent on contributions from the cAMP and MAP kinase pathways. Bioelectromagnetics. 2017;9999:XX-XX. © 2017 Wiley Periodicals, Inc.



© 2017 Wiley Periodicals, Inc.



KEYWORDS: ERK; Thomas-EMF; cAMP; cancer; cell signaling



PMID: 29125193  DOI: 10.1002/bem.22096