Expression Study of Estrogen Receptor-related Receptors and Steroid Hormone Receptors in Human Prostatic Cells

2006 ◽  
pp. 501-507
Author(s):  
C. P. Cheung ◽  
Lung-Wai Chan ◽  
Ki Lui ◽  
Uwe Borgmeyer ◽  
Shiuan Chen ◽  
...  
Cancers ◽  
2020 ◽  
Vol 12 (8) ◽  
pp. 2155
Author(s):  
Hiroki Ide ◽  
Hiroshi Miyamoto

Preclinical and/or clinical evidence has indicated a potential role of steroid hormone-mediated signaling pathways in the development of various neoplastic diseases, while precise mechanisms for the functions of specific receptors remain poorly understood. Specifically, in urothelial cancer where sex-related differences particularly in its incidence are noted, activation of sex hormone receptors, such as androgen receptor and estrogen receptor-β, has been associated with the induction of tumor development. More recently, glucocorticoid receptor has been implied to function as a suppressor of urothelial tumorigenesis. This article summarizes and discusses available data suggesting that steroid hormone receptors, including androgen receptor, estrogen receptor-α, estrogen receptor-β, glucocorticoid receptor, progesterone receptor and vitamin D receptor, as well as their related signals, contribute to modulating urothelial tumorigenesis.


2017 ◽  
Author(s):  
Jeffery M. Vahrenkamp ◽  
Chieh-Hsiang Yang ◽  
Adriana C. Rodriguez ◽  
Aliyah Almomen ◽  
Kristofer C. Berrett ◽  
...  

SummarySteroid hormone receptors are simultaneously active in many tissues and are capable of altering each other’s function. Estrogen receptor α (ER) and glucocorticoid receptor (GR) are expressed in the uterus and their ligands have opposing effects on uterine growth. In endometrial tumors with high ER expression, we surprisingly found that expression of GR is associated with poor prognosis. Dexamethasone reduced normal uterine growth in vivo; however, this growth inhibition was abolished in estrogen-induced endometrial hyperplasia. We observed low genomic binding site overlap when ER and GR are induced with their respective ligands; however, upon simultaneous induction they co-occupy more sites. GR binding is significantly altered by estradiol with GR recruited to ER bound loci that become more accessible upon estradiol induction. Gene expression responses to co-treatment were more similar to estradiol, but with novel regulated genes. Our results suggest phenotypic and molecular interplay between ER and GR in endometrial cancer.


2000 ◽  
pp. 247-258
Author(s):  
R. Rex Denton ◽  
Samir K. Ghosh ◽  
Roland Baron ◽  
Anuradha Ray

2009 ◽  
Vol 89 (4) ◽  
pp. 467-473 ◽  
Author(s):  
R Singh ◽  
T Pretheeban ◽  
R Rajamahendran

The local modulatory role of gonadotropin releasing hormone (GnRH), gonadotropin releasing hormone receptor (GnRH-R) system in regulating steroid hormone receptors at the endometrial level is still not known. Estrogen and progesterone maintain uterine functions by acting through their corresponding receptors; estrogen receptors (ERα and ERβ) and progesterone receptors (PR). We recently demonstrated GnRH-R in bovine endometrium and find the co-existence of GnRH and steroid hormone receptors in endometrium as interesting. Our objective was to determine the effect of a GnRH agonist (buserelin), on the expression of ERα, ERβ, and PR messenger RNA (mRNA) in bovine endometrium. Reproductive tracts were collected from slaughtered cows at a local abattoir, and endometrial explants were treated with buserelin (0, 200, 500, 1000 ng mL-1 respectively), GnRH antagonist-antide (500 ng mL-1) and antide + buserelin (500+200 ng mL-1) for 6 h and stored at -80°C for RNA extraction. Two micrograms of total RNA was subjected to reverse transcription polymerase chain reaction, PCR products electrophoresed (2% agrose gel); visualized and statistically analyzed. The results showed that buserelin (200 ng mL-1) increased the expression of ERα in the luteal phase endometrium. In addition, the expression of endometrial ERα was greater during the follicular than luteal phase. This up regulation of ERα mRNA in luteal phase endometrium suggests that GnRH administration may influence pregnancy in bovines. Key words: GnRH, bovine, endometrium, estrogen receptors, progesterone receptors


1995 ◽  
Vol 15 (4) ◽  
pp. 1847-1857 ◽  
Author(s):  
W L Kraus ◽  
K E Weis ◽  
B S Katzenellenbogen

Although estrogen receptor (ER) and progestin receptor (PR) are members of different steroid hormone receptor subfamilies, there is considerable biological evidence for cross-talk between the estrogen and progestin hormone-receptor signaling pathways. We have developed a model system to analyze the mechanisms underlying this cross-talk, specifically the repression of ER-mediated transcriptional activity by PR complexed with agonistic or antagonistic ligands. Estrogen- and progestin-responsive reporter vectors containing a variety of promoters were transfected into primary cultures of rat uterine cells and 3T3 mouse fibroblasts with expression vectors for PR (the A and/or B isoforms) as well as ER. Our results demonstrate that both PR isoforms can act as potent ligand-dependent repressors of ER activity. The magnitude of the repression was dependent on the PR isoform (i.e., PR A or PR B), ligand type (i.e., agonist or antagonist), PR levels, and ligand concentration but was unaffected by the ER levels. The promoter context was important in determining both the magnitude and PR isoform specificity of the repression for agonist-occupied PR but not for antagonist-occupied PR. Ligand-occupied PR A was a stronger repressor of ER-mediated transcriptional activity than was ligand-occupied PR B, and antagonist-occupied PR was a more effective repressor than agonist-occupied PR. Mechanistic studies suggest that liganded PR represses ER activity by interfering with its ability to interact productively with the transcriptional machinery, a process known as quenching. The data do not support competitive repression, direct repression, or squelching as the mechanism of PR's inhibitory effect. Experiments with ER mutants demonstrated that the N-terminal portion of ER was required for repression by agonist-occupied PR but not by antagonist-occupied PR. These results, as well as other differences between the two PR-ligand complexes, suggest that they differentially target ER when repressing ER transcriptional activity. These findings underscore the mounting evidence for the importance of interactions between members of the steroid hormone receptor family.


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