IMR Press / FBL / Volume 12 / Issue 1 / DOI: 10.2741/2056

Frontiers in Bioscience-Landmark (FBL) is published by IMR Press from Volume 26 Issue 5 (2021). Previous articles were published by another publisher on a subscription basis, and they are hosted by IMR Press on as a courtesy and upon agreement with Frontiers in Bioscience.

Signature of mitochondria of steroidal hormones-dependent normal and cancer cells: potential molecular targets for cancer therapy
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1 Department of Environmental & Occupational Health, Robert Stempel School of Public Health, HLS591, Florida International University, 11200 SW 8th Street, Miami, FL 33199, USA
2 Department of Anatomy and Cell Biology and UF Shands Cancer Center, University of Florida, College of Medicine, Gainesville, FL 32610, USA
3 Neuroscience Program, Miami Children Hospital, Miami, USA
Front. Biosci. (Landmark Ed) 2007, 12(1), 154–173;
Published: 1 January 2007

The cross-talk between the cell nucleus and mitochondria appears to control hormone-induced signaling involved in the apoptosis, proliferation, and differentiation of both normal and malignant cells. Evaluation of the defects in genetics and physiology of human endocrine diseases, such as cancer, may manifest as a result of mitochondrial physiologic and metabolic compensation of genetic defects. Steroidal agents control biogenesis and maintenance of mitochondria through the crosstalk between nuclear and mitochondrial genomes. The regulation of mitochondrial transcription by steroidal hormones, presumably occurring through pathways similar to those that take place in the nucleus, opens a new way to better understand steroid hormone and vitamin action at the cellular level. In addition to the steroid hormone receptors, estrogen generated mitochondrial oxidants together with an estrogen-driven increase in epithelial cell proliferation have been shown to participate in the initiation and promotion of the neoplastic lesions in estrogen-sensitive tissues. Mitochondria generation of ROS appears to transduce signals to the nucleus for the activation of transcription factors involved in the cell cycle progression of estrogen-dependent cancer cells. Therefore, an in-depth analysis of such redox regulatory mechanisms is pertinent to the development of novel drugs and gene therapy strategies for the treatment of steroid hormone-dependent diseases related to mitochondrial disorders including cancer.

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