A mechanistically approached review upon assorted cell lines stimulated by athermal electromagnetic irradiation.

The probable influence of electromagnetic irradiation on cancer treatment has been deduced from the interaction of artificial electromagnetic emissions with biological organisms. Nonetheless, the suspected health effects induced by electromagnetic-based technology imply that such a treatment may contaminate the adjacent healthy cells. Thus, gaining mechanistic insights into the problem is required to avoid athermal health hazards. To tackle that, the current review, based upon in vitro studies into assorted cell lines, depicts the alterations in physiological processes triggered by electromagnetic irradiation via addressing gene regulatory cascades. Furthermore, decisive factors in the hypothesized cause-effect linkage in terms of the cell line-associated, exposure-associated, or endpoint-associated parameters are highlighted. As a result, subcellular structures such as aberrant Ca(2+) channels, rich glycocalyx charge, or high water content in cancerous cells, which have attracted a great deal of attention, can explain their higher susceptibility compared with healthy cells under irradiation. Affected by cell components or geometry, the cellular biological window correlates with the metabolic or cell cycle status and determines the irradiation that causes the maximum influence. For instance, correlations between the frequency (or intensity) of irradiation and cell excitability or between the duration of irradiation and cell doubling time are observed. There are unspecified signaling pathways such as the pathway of PPAR-γ or MAPKs, and also proteins devoid of any investigation such as p14, or S phase-related and G2 phase-related proteins. Other chains, such as the cAMP connection with mitochondrial ATP or ERK signaling, the association of Hsps releases with signaling pathways of MAPKs, or the role of different ion channels in regulating various cell processes, require further investigation.