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Author  |
Caraglia, M.; Marra, M.; Mancinelli, F.; D'Ambrosio, G.; Massa, R.; Giordano, A.; Budillon, A.; Abbruzzese, A.; Bismuto, E. |
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Title |
Electromagnetic fields at mobile phone frequency induce apoptosis and inactivation of the multi-chaperone complex in human epidermoid cancer cells |
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Journal Article |
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Year |
2005 |
Publication |
Journal of Cellular Physiology |
Abbreviated Journal |
J Cell Physiol |
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Volume |
204 |
Issue |
2 |
Pages |
539-548 |
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Keywords |
Apoptosis/*radiation effects; Carcinoma, Squamous Cell/metabolism/pathology/*physiopathology; Cell Line, Tumor; Cell Survival; *Cellular Phone; *Electromagnetic Fields; Extracellular Signal-Regulated MAP Kinases/antagonists & inhibitors/metabolism; HSP90 Heat-Shock Proteins/antagonists & inhibitors/metabolism; Humans; Molecular Chaperones/*antagonists & inhibitors; Proteasome Endopeptidase Complex/metabolism; Proto-Oncogene Proteins c-raf/metabolism; Signal Transduction/radiation effects; Ubiquitin/metabolism; ras Proteins/metabolism |
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Abstract |
The exposure to non-thermal microwave electromagnetic field (MW-EMF) at 1.95 MHz, a frequency used in mobile communication, affects the refolding kinetics of eukaryotic proteins (Mancinelli et al., 2004). On these basis we have evaluated the in vivo effect of MW-EMF in human epidermoid cancer KB cells. We have found that MW-EMF induces time-dependent apoptosis (45% after 3 h) that is paralleled by an about 2.5-fold decrease of the expression of ras and Raf-1 and of the activity of ras and Erk-1/2. Although also the expression of Akt was reduced its activity was unchanged likely as a consequence of the increased expression of its upstream activator PI3K. In the same experimental conditions an about 2.5-fold increase of the ubiquitination of ras and Raf-1 was also found and the addition for 12 h of proteasome inhibitor lactacystin at 10 microM caused an accumulation of the ubiquitinated isoforms of ras and Raf-1 and counteracted the effects of MW-EMF on ras and Raf-1 expression suggesting an increased proteasome-dependent degradation induced by MW-EMF. The exposure of KB cells to MW-EMF induced a differential activation of stress-dependent pathway with an increase of JNK-1 activity and HSP70 and 27 expression and with a reduction of p38 kinase activity and HSP90 expression. The overexpression of HSP90 induced by transfection of KB cells with a plasmid encoding for the factor completely antagonized the apoptosis and the inactivation of the ras --> Erk-dependent survival signal induced by MW-EMF. Conversely, the inhibition of Erk activity induced by 12 h exposure to 10 mM Mek-1 inhibitor U0126 antagonized the effects induced by HSP90 transfection on apoptosis caused by MW-EMF. In conclusion, these results demonstrate for the first time that MW-EMF induces apoptosis through the inactivation of the ras --> Erk survival signaling due to enhanced degradation of ras and Raf-1 determined by decreased expression of HSP90 and the consequent increase of proteasome dependent degradation. |
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Address |
Department of Biochemistry and Biophysics, Second University of Naples, Italy |
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English |
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ISSN |
0021-9541 |
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Notes |
PMID:15754340 |
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Call Number |
IT'IS @ evaj @ |
Serial |
292 |
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