Abstract
Background. Prolonged exposure to oestrogens (17β‐estradiol)(E2), xenoestrogens, hormone replacement therapy and contraceptives has been recognized as a key aetiological factor of human breast cancer. The biological and carcinogenic effects of E2 and xenoestrogens are mediated via oestrogen receptors alpha (ERα) and beta (ERβ). Both receptors are localized in the nucleus of E2‐targeted cells including human breast cells where they are involved in the regulation of nuclear gene expression. There is increasing evidence indicating that a small fraction of total cellular ERs, particularly ERα, are localized in the membrane of E2‐targeted cells where they mediate E2‐dependent and/or E2‐independent rapid and non‐nuclear genomic signal pathways.
Results. The present work will present evidence that: (1) there is mitochondrial localization of ERs in human breast cancer cells; (2) there is a functional role of the mitochondrial ERs in the regulation of mitochondrial genes encoding respiratory chain proteins.
Conclusions. The potential implications of the mitochondrial ER‐mediated pathways in oestrogen carcinogenesis, particularly in stimulation of cell proliferation and inhibition of apoptosis, in human breast cancer and the potential nutritional and environmental perspectives of these effects will be addressed.