scholarly journals Involvement of estrogen receptor β in androgen receptor-induced growth inhibition in prostate cancer PC-3 cells

2017 ◽  
Vol 14 (3) ◽  
pp. 2796-2802 ◽  
Author(s):  
Long Xiao ◽  
Minhui Xiao ◽  
Linbo Gao ◽  
Wanchao Xu
Keyword(s):  
Prostate Cancer ◽  
Estrogen Receptor ◽  
Androgen Receptor ◽  
Growth Inhibition ◽  
Estrogen Receptor Β

scholarly journals Estrogen receptor β exerts tumor suppressive effects in prostate cancer through repression of androgen receptor activity

PLoS ONE ◽  
2020 ◽  
Vol 15 (5) ◽  
pp. e0226057
Author(s):  
Surendra Chaurasiya ◽  
Scott Widmann ◽  
Cindy Botero ◽  
Chin-Yo Lin ◽  
Jan-Åke Gustafsson ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Estrogen Receptor ◽  
Androgen Receptor ◽  
Estrogen Receptor Β ◽  
Receptor Activity ◽  
Androgen Receptor Activity

scholarly journals Estrogen receptor β exerts tumor suppressive effects in prostate cancer through repression of androgen receptor activity

2019 ◽  
Author(s):  
Surendra Chaurasiya ◽  
Scott Widmann ◽  
Cindy Botero ◽  
Chin-Yo Lin ◽  
Anders M. Strom ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Estrogen Receptor ◽  
Androgen Receptor ◽  
Estrogen Receptor Β ◽  
Rna Seq ◽  
Protein Levels ◽  
Synthetic Ligand ◽  
Androgen Receptor Activity ◽  
Mutant Phenotypes ◽  
Prostate Epithelium

AbstractEstrogen receptor β (ERβ) was first identified in the rodent prostate and is abundantly expressed in human and rodent prostate epithelium, stroma, immune cells and endothelium of the blood vessels. In the prostates of mice with inactivated ERβ, mutant phenotypes include epithelial hyperplasia and increased expression of androgen receptor (AR)-regulated genes, most of which are also upregulated in prostate cancer (PCa). ERβ is expressed in both basal and luminal cells in the prostate while AR is expressed in luminal but not in the basal cell layer which harbors the prostate stem cells. To investigate the mechanisms of action of ERβ and its potential cross-talk with AR, we used RNA-seq to study the effects of estradiol or the synthetic ligand, LY3201, in AR-positive LNCaP PCa cells which had been engineered to express ERβ. Transcriptomic analysis indicated relatively few changes in gene expression with ERβ overexpression, but robust responses following ligand treatments. There is significant overlap of responsive genes between the two ligands, as well as ligand-specific alterations. Gene set analysis of down-regulated genes identified an enrichment of androgen-responsive genes, such as FKBP5, CAMKK2, and TBC1D4. Consistently, AR transcript, protein levels, and transcriptional activity were down-regulated following ERβ activation. In agreement with this, we find that the phosphorylation of the CAMKK2 target, AMPK, was repressed by ligand-activated ERβ. Down-regulation of TBC1D4, a major regulator of glucose uptake in prostate, indicates that ERβ is changing glucose metabolism in the prostate. These findings suggest that ERβ-mediated signaling pathways are involved in the negative regulation of AR expression and activity, thus supporting a tumor suppressive role for ERβ in PCa.

Androgen receptor or estrogen receptor-β blockade alters DHEA-, DHT-, and E2-induced proliferation and PSA production in human prostate cancer cells

The Prostate ◽  
2007 ◽  
Vol 67 (11) ◽  
pp. 1152-1162 ◽  
Author(s):  
Julia T. Arnold ◽  
Xunxian Liu ◽  
Jeffrey D. Allen ◽  
Hanh Le ◽  
Kimberly K. McFann ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Estrogen Receptor ◽  
Androgen Receptor ◽  
Cancer Cells ◽  
Estrogen Receptor Β ◽  
Human Prostate ◽  
Human Prostate Cancer ◽  
Prostate Cancer Cells

scholarly journals Dioscin induces prostate cancer cell apoptosis through activation of estrogen receptor-β

2017 ◽  
Vol 8 (8) ◽  
pp. e2989-e2989 ◽  
Author(s):  
Xufeng Tao ◽  
Lina Xu ◽  
Lianhong Yin ◽  
Xu Han ◽  
Yan Qi ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Estrogen Receptor ◽  
Cancer Cell ◽  
Cell Apoptosis ◽  
Prostate Cancer Cell ◽  
Estrogen Receptor Β ◽  
Cancer Cell Apoptosis
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