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Estrogen's Effects on Mitochondrial Gene Expression: Mechanisms and Potential Contributions to Estrogen Carcinogenesis
JIN-QIANG CHENa AND
JAMES D. YAGER
Department of Environmental Health Sciences, Division of Toxicological Sciences, The Johns Hopkins Bloomberg School of Public Health, Baltimore, Maryland 21285, USA
Address for correspondence: Dr. James D. Yager, Department of Environmental Health Sciences, Division of Toxicological Sciences, The Johns Hopkins Bloomberg School of Public Health, Baltimore, MD, 21285. Voice: 410-955-3348; fax: 410-955-0116. jyager{at}jhsph.edu
aCurrent address: Breast Cancer Research Laboratory, Fox Chase Cancer Center, 7701 Burholme Ave., Philadelphia, PA 19111.
Estrogen receptor (ER)  and ERß are localized in the nucleus and involved in the regulation of nuclear estrogen-responsive genes by 17ß estradiol (E2). In addition, recently others have shown that upon E2 binding, ER localizes to the plasma membrane and initiates mitogen-activated protein kinase (MAPK)-mediated signal transduction. Previously, we reported that in liver, cultured rat hepatocytes and human HepG2 cells, estrogen treatment enhanced mitochondrial DNA (mtDNA)-encoded gene transcript levels. These effects were blocked by a specific antiestrogen, suggesting a role for the ER. Others have reported the presence of putative estrogen-responsive elements in mtDNA. These observations suggested the hypothesis that the ER localized in mitochondria and functioned directly to enhance the levels of mtDNA-encoded transcripts, analogous to what has been observed for the glucocorticoid hormone receptor. Using Western blot analysis, confocal immunofluorescence, immunogold electron microscopy, and gel electrophoresis mobility shift assays, we have demonstrated the estrogen-dependent presence of ERß and ER within mitochondria of HepG2 and MCF-7 human breast tumor cells. Together, these results suggest that the ERs may act as transcription factors directly involved in the regulation by E2 of mtDNA transcription.
Key Words: estrogen receptor • estrogen • mitochondria • HepG2 cells • MCF-7 cells
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