Co-expression of steroid hormone receptors (estrogen receptor α and/or progesterone receptors) and Her2/neu (c-erbB-2) in breast cancer: Clinical outcome following tamoxifen-based adjuvant therapy

2006 ◽  
Vol 98 (1) ◽  
pp. 36-40 ◽  
Author(s):  
Francisco E. Gago ◽  
Mariel A. Fanelli ◽  
Daniel R. Ciocca
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.


2010 ◽  
Vol 21 (9) ◽  
pp. 1620-1628 ◽  
Author(s):  
Senad Medunjanin ◽  
Sönke Weinert ◽  
Alexander Schmeisser ◽  
Doris Mayer ◽  
Ruediger C. Braun-Dullaeus

Estrogens are suggested to play a role in the development and progression of proliferative diseases such as breast cancer. Like other steroid hormone receptors, the estrogen receptor-α (ERα) is a substrate of protein kinases, and phosphorylation has profound effects on its function and activity. Given the importance of DNA-dependent protein kinase (DNA-PK) for DNA repair, cell cycle progression, and survival, we hypothesized that it modulates ERα signaling. Here we show that, upon estrogen stimulation, DNA-PK forms a complex with ERα in a breast cancer cell line (MELN). DNA-PK phosphorylates ERα at Ser-118. Phosphorylation resulted in stabilization of ERα protein as inhibition of DNA-PK resulted in its proteasomal degradation. Activation of DNA-PK by double-strand breaks or its inhibition by siRNA technology demonstrated that estrogen-induced ERα activation and cell cycle progression is, at least, partially dependent on DNA-PK.


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


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