Extremely low frequency electromagnetic fields affect proliferation and mitochondrial activity of human cancer cell lines.

Purpose: To date, the effects of electromagnetic fields on cell metabolism have been overlooked. The objective of the present study was to investigate the influence of extremely low frequency electromagnetic fields (ELF-EMF) over mitochondrial metabolism and the consequent impact on cancer cell growth.

Materials And Methods: The effects of ELF-EMF on cancer growth were investigated in several human cancer cell lines by crystal violet assay.

The vitamin D receptor inhibits the respiratory chain, contributing to the metabolic switch that is essential for cancer cell proliferation.

We recently described the mitochondrial localization and import of the vitamin D receptor (VDR) in actively proliferating HaCaT cells for the first time, but its role in the organelle remains unknown. Many metabolic intermediates that support cell growth are provided by the mitochondria; consequently, the identification of proteins that regulate mitochondrial metabolic pathways is of great interest, and we sought to understand whether VDR may modulate these pathways. We genetically silenced VDR in HaCaT cells and studied the effects on cell growth, mitochondrial metabolism and biosynthetic pathways.

Mitochondrial translocation of vitamin D receptor is mediated by the permeability transition pore in human keratinocyte cell line.

Background: Vitamin D receptor (VDR) is a well known transcriptional regulator, active as heterodimer in association with coactivators and corepressors. In addition it has been described the extranuclear distribution of the receptor and in particular the recently reported mitochondrial localization in platelets and megakaryocytes is intriguing because it appears to be a common feature of steroid receptors. Whereas for other members of the steroid receptor family the mitochondrial function has been explored, up to now nothing is known about a mitochondrial form of VDR in human proliferating cells.