Exposure to a specific time‐varying electromagnetic field inhibits cell proliferation via cAMP and ERK signaling in cancer cells
| Autor: | Carly A. Buckner, Stan A. Koren, Robert M. Lafrenie, Alison L. Buckner, Michael A. Persinger |
|---|---|
| Rok vydání: | 2017 |
| Předmět: |
MAPK/ERK pathway
Cell signaling Time Factors animal structures MAP Kinase Signaling System Physiology Biophysics Mice 03 medical and health sciences chemistry.chemical_compound Electromagnetic Fields 0302 clinical medicine Cell Line Tumor Cyclic AMP Animals Humans Radiology Nuclear Medicine and imaging Phosphorylation Extracellular Signal-Regulated MAP Kinases Protein kinase A Cell Proliferation Forskolin Kinase Cell growth General Medicine Cyclic AMP-Dependent Protein Kinases Cell biology chemistry 030220 oncology & carcinogenesis Cancer cell Signal transduction 030217 neurology & neurosurgery |
| Zdroj: | Bioelectromagnetics. 39:217-230 |
| ISSN: | 1521-186X 0197-8462 |
| DOI: | 10.1002/bem.22096 |
| Popis: | 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. 39;217-230, 2018. © 2017 Wiley Periodicals, Inc. |
| Databáze: | OpenAIRE |
| Externí odkaz: |
|
Plný text