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Hypoxia‐inducible factor 1α activates and is inhibited by unoccupied estrogen receptor β
Author(s) -
Lim Wonchung,
Cho Jungyoon,
Kwon Hyeok-yi,
Park Yeomyeong,
Rhyu Mee-Ra,
Lee YoungJoo
Publication year - 2009
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/j.febslet.2009.03.028
Subject(s) - transactivation , estrogen receptor beta , estrogen receptor alpha , transcription factor , estrogen receptor , beta (programming language) , estrogen related receptor alpha , chemistry , alpha (finance) , hormone response element , hek 293 cells , reporter gene , microbiology and biotechnology , estrogen , transcription (linguistics) , endocrinology , biology , medicine , receptor , gene expression , gene , biochemistry , philosophy , cancer , linguistics , breast cancer , patient satisfaction , construct validity , computer science , programming language , nursing
Previously, we showed that hypoxia induces ligand‐independent estrogen receptor (ER)α activation. In this study, we found that hypoxia activated the ERβ‐mediated transcriptional response in HEK293 cells in the absence of estrogen. ERβ transactivation was induced by the expression of the hypoxia‐inducible factor 1α (HIF‐1α) under normoxia. ERβ interacted with HIF‐1α, and SRC1 and CBP potentiated the effect of HIF‐1α on ERβ‐mediated transcription. We then examined the effect of ERβ on HIF1‐α transactivation. Surprisingly, ERβ attenuated the transcriptional activity of HIF‐1α, as measured by HRE‐driven reporter gene expression and hypoxic induction of VEGF mRNA in HEK293 cells. Taken together, these data show that HIF‐1α activates ERβ‐mediated transcription in the absence of a ligand, and ERβ inhibits HIF‐1α‐mediated transcription.