Cross‐talk between signal transducer and activator of transcription 3 and estrogen receptor signaling

FEBS Letters

Kishi, Hiroyuki¹  Muraguchi, Atsushi¹  Matsuda, Tadashi¹  Yamamoto, Tetsuya¹  Junicho, Akira³  Saatcioglu, Fahri² 

[1] Department of Immunology, Faculty of Medicine, Toyama Medical and Pharmaceutical University, 2630 Sugitani, Toyama 930-0194, Japan;Biotechnology Centre of Oslo, University of Oslo, Gaustadalleen 21, 0349 Oslo, Norway;Department of Urology, Faculty of Medicine, Toyama Medical and Pharmaceutical University, 2630 Sugitani, Toyama 930-0194, Japan

关键词: Interleukin-6;    Signal transducer and activator of transcription 3;    17β-Estradiol;    Estrogen receptor;    Cross-talk;    Transcription;    IL;    interleukin;    ER;    estrogen receptor;    STAT;    signal transducer and activator of transcription;    E2;    17β-estradiol;    LUC;    luciferase;    LIF;    leukemia inhibitory factor;   

DOI  :  10.1016/S0014-5793(00)02296-1

学科分类：生物化学/生物物理

来源: John Wiley & Sons Ltd.

【 摘 要 】

Interleukin-6 (IL-6) is a multifunctional cytokine that plays important roles in the immune system, hematopoiesis, and acute phase reactions. Estrogens have significant roles in a variety of biological events, such as the development and maintenance of female reproductive organs, and bone and lipid metabolism. Previous studies demonstrated that estrogens suppress IL-6-induced osteoporosis and the growth of multiple myeloma cells by repressing IL-6 and IL-6 receptor gene expression. Here we present a novel mechanism for the inhibitory effect of estrogens on IL-6 function. IL-6-induced activation of signal transducer and activator of transcription 3 (STAT3) activity and STAT3-mediated gene expression were suppressed by 17β-estradiol (E2) in breast cancer cells. E2-mediated inhibition of STAT3 activation was reversed by tamoxifen, an estrogen receptor (ER) antagonist. We provide evidence that the inhibitory action of ER on STAT3 activity was due to direct physical interactions between STAT3 and ER which represents a novel form of cross-talk between STAT3 and ER signaling pathways.

【 授权许可】

Unknown