Estrogen Receptor (ER) β Regulates ERα Expression in Stromal Cells Derived from Ovarian Endometriosis
Author(s) -
Elena Trukhacheva,
Zhihong Lin,
Scott Reierstad,
You-Hong Cheng,
Magdy P. Milad,
Serdar E. Bulun
Publication year - 2008
Publication title -
the journal of clinical endocrinology and metabolism
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.206
H-Index - 353
eISSN - 1945-7197
pISSN - 0021-972X
DOI - 10.1210/jc.2008-1466
Subject(s) - stromal cell , estrogen receptor alpha , estrogen receptor , gene knockdown , estrogen , endocrinology , medicine , biology , progesterone receptor , estrogen receptor beta , cancer research , chromatin immunoprecipitation , promoter , gene expression , cell culture , gene , cancer , breast cancer , genetics , biochemistry
Estradiol and its nuclear receptors, estrogen receptor (ER) alpha and ERbeta, play critical roles in endometrium and endometriosis. Levels of ERbeta, due to pathological hypomethylation of its promoter, are significantly higher in endometriotic vs. endometrial tissue and stromal cells, whereas ERalpha levels are lower in endometriosis. Estradiol regulates ERalpha gene expression via its alternatively used promoters A, B, and C.
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