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Estrogen receptor‐β in mitochondria: implications for mitochondrial bioenergetics and tumorigenesis
Author(s) -
Liao TienLing,
Tzeng ChiiRuey,
Yu ChaoLan,
Wang YiPei,
Kao ShuHuei
Publication year - 2015
Publication title -
annals of the new york academy of sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.712
H-Index - 248
eISSN - 1749-6632
pISSN - 0077-8923
DOI - 10.1111/nyas.12872
Subject(s) - mitochondrial biogenesis , mitochondrion , carcinogenesis , microbiology and biotechnology , bioenergetics , estrogen receptor , biology , oxidative phosphorylation , estrogen receptor beta , apoptosis , cancer research , biochemistry , cancer , genetics , breast cancer
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.