title: Estrogen receptor-β in mitochondria: implications for mitochondrial bioenergetics and tumorigenesis.
abstract: Estrogen enhances mitochondrial function by enhancing mitochondrial biogenesis and sustaining mitochondrial energy-transducing capacity. Shifts in mitochondrial bioenergetic pathways from oxidative phosphorylation to glycolysis have been hypothesized to be involved in estrogen-induced tumorigenesis. Studies have shown that mitochondria are an important target of estrogen. Estrogen receptor-β (ERβ) has been shown to localize to mitochondria in a ligand-dependent or -independent manner and can affect mitochondrial bioenergetics and anti-apoptotic signaling. However, the functional role of mitochondrial ERβ in tumorigenesis remains unclear. Clinical studies of ERβ-related tumorigenesis have shown that ERβ stimulates mitochondrial metabolism to meet the high energy demands of processes such as cell proliferation, cell survival, and transformation. Thus, in elucidating the precise role of mitochondrial ERβ in cell transformation and tumorigenesis, it will be particularly valuable to explore new approaches for the development of medical treatments targeting mitochondrial ERβ-mediated mitochondrial function and preventing apoptosis.
authors: Graduate Institute of Medical Science, College of Medicine, Taipei Medical University, Taipei, Taiwan.|School of Medical Laboratory Science and Biotechnology, College of Medical Science and Technology, Taipei Medical University, Taipei, Taiwan.
authors: Tien-Ling
authors: TL
authors: Liao
authors: Department of Obstetrics and Gynecology, Taipei Medical University Hospital, Taipei, Taiwan.|Center for Reproductive Medicine and Sciences, Taipei Medical University Hospital, Taipei, Taiwan.|Department of Obstetrics and Gynecology, College of Medicine, Taipei Medical University, Taipei, Taiwan.
authors: Chii-Ruey
authors: CR
authors: Tzeng
authors: Department of Microbiology and Immunology, Rosalind Franklin University of Medicine and Science, North Chicago, Illinois.
authors: Chao-Lan
authors: CL
authors: Yu
authors: Graduate Institute of Medical Science, College of Medicine, Taipei Medical University, Taipei, Taiwan.|School of Medical Laboratory Science and Biotechnology, College of Medical Science and Technology, Taipei Medical University, Taipei, Taiwan.
authors: Yi-Pei
authors: YP
authors: Wang
authors: School of Medical Laboratory Science and Biotechnology, College of Medical Science and Technology, Taipei Medical University, Taipei, Taiwan.|Center for Reproductive Medicine and Sciences, Taipei Medical University Hospital, Taipei, Taiwan.
authors: Shu-Huei
authors: SH
authors: Kao
mesh_terms: D000818:Animals; D017209:Apoptosis / Q000187:drug effects; D063646:Carcinogenesis / Q000139:chemically induced / Q000378:metabolism*; D002274:Carcinogens, Environmental / Q000378:metabolism / Q000633:toxicity; D004734:Energy Metabolism / Q000187:drug effects; D047629:Estrogen Receptor beta / Q000819:agonists* / Q000378:metabolism; D004967:Estrogens / Q000009:adverse effects / Q000378:metabolism*; D006801:Humans; D008024:Ligands; D008928:Mitochondria / Q000187:drug effects / Q000201:enzymology / Q000378:metabolism*; D063269:Mitochondrial Turnover / Q000187:drug effects; D008954:Models, Biological; D021381:Protein Transport / Q000187:drug effects; D015398:Signal Transduction / Q000187:drug effects
chemical_list: D002274:Carcinogens, Environmental; C000600034:ESR2 protein, human; D047629:Estrogen Receptor beta; D004967:Estrogens; D008024:Ligands
keywords: bioenergetics; endometriosis; estrogen; estrogen receptor-β; mitochondrial estrogen receptor-β; tumorigenesis