GnRH agonist (buserelin) up regulates estrogen receptor α mRNA but not estrogen receptor β and progesterone receptor mRNA in bovine endometrium in vitro

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

2020 ◽  
Vol 19 (5) ◽  
pp. 13-21
Author(s):  
S.V. Shramko ◽  
◽  
L.F. Gulyaeva ◽  
V.N. Zorina ◽  
T.V. Tretyakova ◽  
...  

Objective. To perform comparative analysis of clinical data, serum levels of acute-phase proteins, cytokines, steroid hormones, and expression of genes encoding sex hormone receptors in tissues of patients with proliferative diseases of the uterus. Patients and methods. We analyzed clinical data of 349 patients with various proliferative diseases of the uterus. We also evaluated their serum levels of α2-macroglobulin, pregnancy-associated α2-glycoprotein, their immunocomplexes with IgG, lactoferrin, VEGF, IL-6, TNFa, IL-8, and sex hormones. Uterine tissue samples were tested for the expression of genes encoding estrogen receptors α and β (ЕRα, ЕRβ) and progesterone receptors (PGR). Data analysis was performed using the statistical packages of SAS 9.4, STATISTICA12, and IBM-SPSS Statistics 22. Results. The changes in the level of acute-phase proteins indicated inflammation. In isolated uterine fibroids, expression of genes encoding progesterone receptors prevailed, whereas in isolated adenomyosis, expression of genes encoding estrogen receptors prevailed. Patients with both uterine fibroids and adenomyosis demonstrated similar levels of expression of genes encoding sex steroid hormone receptors. Tissues of uterine leiomyosarcoma were characterized by downregulated expression of genes encoding sex steroid hormone receptors. Conclusion. Upregulation of genes encoding progesterone receptors in isolated uterine fibroids confirms that therapy with progesterone receptor blockers is appropriate in this case. The predominance of expression of genes encoding estrogen receptors in isolated adenomyosis indicates local hyperestrogenism, justifying the use of progestogens and antiestrogens. Equal expression of genes encoding estrogen and progesterone receptors in patients with combined disease, as wells as high frequency of inflammatory changes in tissues and increased serum levels of inflammatory markers, proves the need for antiinflammatory therapy. Key words: adenomyosis, inflammation, steroid receptor genes, leiomyosarcoma, uterine fibroids, gene expression


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 ◽  
Vol 124 (2) ◽  
pp. 276-280 ◽  
Author(s):  
Mojgan Devouassoux-Shisheboran ◽  
David P. Schammel ◽  
Yan-Gao Man ◽  
Fattaneh A. Tavassoli

Abstract Objective.—To predict if antiestrogenic agents are useful in the treatment of breast fibromatoses, we undertook an immunohistochemical study of sex steroid hormone receptors (estrogen receptor, progesterone receptor, and androgen receptor) and protein pS2 in 33 cases. Methods.—The morphologic and immunohistochemical findings were correlated to patient menstrual status, which was categorized as childbearing age (n = 15), perimenopausal (n = 8), and postmenopausal (n = 10). Results.—Fibromatoses in women of childbearing age were more cellular, more mitotically active, and displayed a larger proportion of cells with mild atypia than those in perimenopausal and postmenopausal women. The hormonal status of these 3 groups does not explain the morphologic variations observed in these groups, inasmuch as no immunostaining for any of the hormone receptors was detected in the tumors. Conclusions.—The absence of estrogen receptor and pS2 in breast fibromatoses suggests that antiestrogenic agents are unlikely to be beneficial in the management of these tumors. Assessment of the hormone receptor profile is a useful adjunct in the diagnosis of spindle cell lesions of the breast. Although most spindle cell carcinomas as well as fibromatoses of the breast do not express estrogen or progesterone receptors, the absence of androgen receptor reactivity would favor a diagnosis of fibromatosis over that of myofibroblastoma.


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

2011 ◽  
Vol 5 ◽  
pp. BCBCR.S7707 ◽  
Author(s):  
R. Jahanban Esfahlan ◽  
N. Zarghami ◽  
A. Jahanban Esfahlan ◽  
M. Mollazadeh ◽  
K. Nejati ◽  
...  

Background Obesity has been associated with increased mortality from hormone dependant cancers such as breast cancer which is the most prevalent cancer in women. The link between obesity and breast cancer can be attributed to excess estrogen produced through aromatization in adipose tissue. The role of steroid hormone receptors in breast cancer development is well studied but how obesity can affect the expression pattern of steroid hormones in patients with different grades of breast cancer was the aim of this study. Methods In this case-control study, 70 women with breast cancer participated with different grades of obesity (36 none obese, BMI < 25 kg/m2 and 34 obese, BMI ≥ 25 kg/m2). The mean age of participants was 44.53 ± 1.79 yr (21–70 yr). The serum level of estrogen, progesterone and androgen determined by ELISA. Following quantitative expression of steroid hormone receptors mRNA in tumor tissues evaluated by Real-time PCR. Patients with previous history of radiotherapy or chemotherapy were excluded. SPSS 16 was used for data analysis and P < 0.05 considered statistically significant. Results The difference in ERα, ERβ and PR mRNA level between normal and obese patients was significant ( P < 0.001). In addition, the expression of AR mRNA was found to be higher than other steroid receptors. There was no significant relation between ERβ gene expression in two groups ( P = 0.68). We observed a significant relationship between ERα and AR mRNA with tumor stage and tumor grade, respectively ( P = 0.023, P = 0.015). Conclusion According to the obtained results, it is speculated that obesity could paly a significant role in estrogen receptors gene expression and also could affect progression and proliferation of breast cancer cells.


Neurosurgery ◽  
1989 ◽  
Vol 25 (4) ◽  
pp. 541-545 ◽  
Author(s):  
Liang-Shong Lee ◽  
Chin-Wen Chi ◽  
Tai-Jay Chang ◽  
Min-Deh Chou ◽  
Hsiu-Chih Liu ◽  
...  

Abstract Meningioma is a hormone-related intracranial tumor. Brain tumor samples were collected from 32 Chinese patients, 20 of whom had meningiomas. Estrogen receptors were present in 6 of 17 meningiomas, 1 hemangioblastoma, 1 gemistocytic astrocytoma, and 1 neurilemoma. Of the 26 samples assayed for progesterone receptors, measurable bindings were found in 14 of 17 meningiomas, 1 of 2 astrocytomas, 1 malignant lymphoma, 1 hemangioblastoma, 1 ganglioglioma, 1 glioblastoma multiforme, 1 anaplastic ependymoma, 1 small cell sarcoma, and 1 neurilemoma. Androgen receptors were found in 8 of 19 meningiomas, but not in the 11 other brain tumors examined. Measurable glucocorticoid receptors were found in 15 of 19 meningiomas, 1 malignant lymphoma, 1 hemangioblastoma, 2 craniopharyngiomas, 1 neurilemoma, 1 of 2 glioblastomas, and 1 of 2 astrocytomas. Of the 10 samples examined for tyrosine aminotransferase activity, measurable enzyme activity was found in 7 of the 8 meningiomas, but not in the single hemangioblastoma nor in the single craniopharyngioma. In accordance with other published studies, the results from this study also suggest that the growth of meningiomas may be regulated by hormones, and that the role steroid hormones and their receptors play in the meningioma is worthy of further investigation.


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