scholarly journals Intrinsic versus Extrinsic Aging: A Histopathological, Morphometric and Immunohistochemical Study of Estrogen Receptor β and Androgen Receptor

2016 ◽  
Vol 29 (4) ◽  
pp. 178-189 ◽  
Author(s):  
Iman Seleit ◽  
Ola Ahmed Bakry ◽  
Hala Saed El Repey ◽  
Raghdaa Ali
Keyword(s):  
Estrogen Receptor ◽  
Androgen Receptor ◽  
Immunohistochemical Study ◽  
Estrogen Receptor Β

Androgen Receptor Regulation by Physiological Concentrations of the Isoflavonoid Genistein in Androgen-Dependent LNCaP Cells Is Mediated by Estrogen Receptor β

2004 ◽  
Vol 45 (2) ◽  
pp. 245-251 ◽  
Author(s):  
Jasmin Bektic ◽  
Andreas P Berger ◽  
Karina Pfeil ◽  
Gabriele Dobler ◽  
Georg Bartsch ◽  
...  
Keyword(s):  
Estrogen Receptor ◽  
Androgen Receptor ◽  
Estrogen Receptor Β ◽  
Receptor Regulation ◽  
Lncap Cells

scholarly journals Estrogen receptor β, a regulator of androgen receptor signaling in the mouse ventral prostate

2017 ◽  
Vol 114 (19) ◽  
pp. E3816-E3822 ◽  
Author(s):  
Wan-fu Wu ◽  
Laure Maneix ◽  
Jose Insunza ◽  
Ivan Nalvarte ◽  
Per Antonson ◽  
...  
Keyword(s):  
Estrogen Receptor ◽  
Androgen Receptor ◽  
Rna Sequencing ◽  
Transforming Growth Factor ◽  
Expression Profiles ◽  
Estrogen Receptor Β ◽  
Orphan Receptor ◽  
Ventral Prostate ◽  
Caveolin 1 ◽  
Domain 3

As estrogen receptor β−/−(ERβ−/−) mice age, the ventral prostate (VP) develops increased numbers of hyperplastic, fibroplastic lesions and inflammatory cells. To identify genes involved in these changes, we used RNA sequencing and immunohistochemistry to compare gene expression profiles in the VP of young (2-mo-old) and aging (18-mo-old) ERβ−/−mice and their WT littermates. We also treated young and old WT mice with an ERβ-selective agonist and evaluated protein expression. The most significant findings were that ERβ down-regulates androgen receptor (AR) signaling and up-regulates the tumor suppressor phosphatase and tensin homolog (PTEN). ERβ agonist increased expression of the AR corepressor dachshund family (DACH1/2), T-cadherin, stromal caveolin-1, and nuclear PTEN and decreased expression of RAR-related orphan receptor c, Bcl2, inducible nitric oxide synthase, and IL-6. In the ERβ−/−mouse VP, RNA sequencing revealed that the following genes were up-regulated more than fivefold: Bcl2, clusterin, the cytokines CXCL16 and -17, and a marker of basal/intermediate cells (prostate stem cell antigen) and cytokeratins 4, 5, and 17. The most down-regulated genes were the following: the antioxidant gene glutathione peroxidase 3; protease inhibitors WAP four-disulfide core domain 3 (WFDC3); the tumor-suppressive genes T-cadherin and caveolin-1; the regulator of transforming growth factor β signaling SMAD7; and the PTEN ubiquitin ligase NEDD4. The role of ERβ in opposing AR signaling, proliferation, and inflammation suggests that ERβ-selective agonists may be used to prevent progression of prostate cancer, prevent fibrosis and development of benign prostatic hyperplasia, and treat prostatitis.

scholarly journals The Role of Steroid Hormone Receptors in Urothelial Tumorigenesis

Cancers ◽  
2020 ◽  
Vol 12 (8) ◽  
pp. 2155
Author(s):  
Hiroki Ide ◽  
Hiroshi Miyamoto
Keyword(s):  
Estrogen Receptor ◽  
Androgen Receptor ◽  
Glucocorticoid Receptor ◽  
Hormone Receptors ◽  
Steroid Hormone ◽  
Tumor Development ◽  
Estrogen Receptor Α ◽  
Estrogen Receptor Β ◽  
Steroid Hormone Receptors

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.

Fibromatosis of the Breast

2000 ◽  
Vol 124 (2) ◽  
pp. 276-280 ◽  
Author(s):  
Mojgan Devouassoux-Shisheboran ◽  
David P. Schammel ◽  
Yan-Gao Man ◽  
Fattaneh A. Tavassoli
Keyword(s):  
Estrogen Receptor ◽  
Androgen Receptor ◽  
Hormone Receptors ◽  
Spindle Cell ◽  
Immunohistochemical Study ◽  
Progesterone Receptors ◽  
Steroid Hormone Receptors ◽  
Childbearing Age ◽  
Sex Steroid Hormone ◽  
Receptor Profile

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.

scholarly journals Dehydroepiandrosterone-induces miR-21 transcription in HepG2 cells through estrogen receptor β and androgen receptor

2014 ◽  
Vol 392 (1-2) ◽  
pp. 23-36 ◽  
Author(s):  
Yun Teng ◽  
Lacey M. Litchfield ◽  
Margarita M. Ivanova ◽  
Russell A. Prough ◽  
Barbara J. Clark ◽  
...  
Keyword(s):  
Estrogen Receptor ◽  
Androgen Receptor ◽  
Hepg2 Cells ◽  
Estrogen Receptor Β

Human megakaryocytes and platelets contain the estrogen receptor β and androgen receptor (AR): testosterone regulates AR expression

Blood ◽  
2000 ◽  
Vol 95 (7) ◽  
pp. 2289-2296 ◽  
Author(s):  
Gopal Khetawat ◽  
Nauder Faraday ◽  
Michele L. Nealen ◽  
K. Vinod Vijayan ◽  
Everlie Bolton ◽  
...  
Keyword(s):  
Gender Differences ◽  
Estrogen Receptor ◽  
Androgen Receptor ◽  
Sex Hormones ◽  
Platelet Function ◽  
Messenger Rna ◽  
Ex Vivo ◽  
Estrogen Receptor Β ◽  
Human Cd34 ◽  
Hel Cells

Abstract Gender differences in vascular thromboses are well known, and there is evidence that platelets may be involved in these differences and that sex hormones affect platelet function. We characterized the expression of the estrogen receptor  (ER ), estrogen receptor β (ER β), progesterone receptor (PR), and androgen receptor (AR) in the megakaryocyte lineage. Megakaryocytes generated ex vivo from normal human CD34+ stem cells contained RNA for ER β and AR, which increased with cell differentiation. Platelets and human erythroleukemia (HEL) cells also contained ER β and AR transcripts. No ER  or PR messenger RNA or protein was detected in the megakaryocyte lineage. Immunofluorescence microscopy showed that ER β protein was present in glycoprotein (GP) IIb+ megakaryocytes and the HEL megakaryocytic cell line in a predominantly cytoplasmic location. AR showed a cytoplasmic and nuclear distribution in GPIIb+ and GPIIb− cells derived from CD34+ cells and in HEL cells. Western immunoblotting confirmed the presence of ER β and AR in platelets. Megakaryocyte and HEL AR expression was up-regulated by 1, 5, and 10 nmol/L testosterone, but down-regulated by 100 nmol/L testosterone. These findings indicate a regulated ability of megakaryocytes to respond to testosterone and suggest a potential mechanism through which sex hormones may mediate gender differences in platelet function and thrombotic diseases.

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