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Repression of interleukin‐6 gene expression by 17β‐estradiol:
Author(s) -
Ray Prabir,
Ghosh Samir K,
Zhang Dong-Hong,
Ray Anuradha
Publication year - 1997
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/s0014-5793(97)00487-0
Subject(s) - psychological repression , gene expression , gene , interleukin , microbiology and biotechnology , chemistry , genetics , biology , cytokine
The cytokine interleukin‐6 (IL‐6), a key mediator of immune and acute phase responses of the liver, has also been implicated in uterine functions. Estrogens are potent repressors of IL‐6 production by uterine stromal cells. In the endometrial adenocarcinoma cell line Ishikawa, phorbol ester‐induced activation of the IL‐6 promoter was inhibited to basal levels by 17β‐estradiol (E 2 ) in a wild‐type receptor‐dependent fashion. Although tamoxifen has been shown to have estrogenic effects on the endometrium, it did not inhibit induction of the IL‐6 promoter. We previously showed that inhibition of IL‐6 gene expression by E 2 does not involve high‐affinity binding of the estrogen receptor (ER) to IL‐6 DNA. We now report that the ER can directly interact with the transcription factors NF‐IL6 and NF‐κB and can inhibit their ability to bind DNA which might be the molecular basis for repression of IL‐6 gene expression by estrogens.