scholarly journals Estrogen receptor β upregulates FOXO3a and causes induction of apoptosis through PUMA in prostate cancer

Oncogene ◽  
2013 ◽  
Vol 33 (33) ◽  
pp. 4213-4225 ◽  
Author(s):  
P Dey ◽  
A Ström ◽  
J-Å Gustafsson
Keyword(s):  
Prostate Cancer ◽  
Estrogen Receptor ◽  
Estrogen Receptor Β ◽  
Induction Of Apoptosis

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

scholarly journals The Role of Estrogen Receptor β in Prostate Cancer

2014 ◽  
Vol 20 (1) ◽  
pp. 427-434 ◽  
Author(s):  
Paraskevi Christoforou ◽  
Panagiotis F. Christopoulos ◽  
Michael Koutsilieris
Keyword(s):  
Prostate Cancer ◽  
Estrogen Receptor ◽  
Estrogen Receptor Β

Current concepts and significance of estrogen receptor β in prostate cancer

Steroids ◽  
2012 ◽  
Vol 77 (12) ◽  
pp. 1262-1266 ◽  
Author(s):  
Johan Hartman ◽  
Anders Ström ◽  
Jan-Åke Gustafsson
Keyword(s):  
Prostate Cancer ◽  
Estrogen Receptor ◽  
Estrogen Receptor Β

scholarly journals Estrogen receptor β and the progression of prostate cancer: role of 5α-androstane-3β,17β-diol

2010 ◽  
Vol 17 (3) ◽  
pp. 731-742 ◽  
Author(s):  
Donatella Dondi ◽  
Margherita Piccolella ◽  
Andrea Biserni ◽  
Sara Della Torre ◽  
Balaji Ramachandran ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Estrogen Receptor ◽  
Cultured Cells ◽  
Estrogen Receptor Β ◽  
Continuous Administration ◽  
Ablation Therapy ◽  
Androgen Ablation ◽  
Androgen Ablation Therapy

Prostate cancer (PC) develops in response to an abnormal activation of androgen receptor induced by circulating androgens and, in its initial stages, is pharmacologically controlled by androgen blockade. However, androgen ablation therapy often allows androgen-independent PC development, generally characterized by increased invasiveness. We previously reported that 5α-androstane-3β,17β-diol (3β-Adiol) inhibits the migration of PC cell lines via the estrogen receptor β (ERβ) activation. Here, by combining in vitro assays and in vivo imaging approaches, we analyzed the effects of 3β-Adiol on PC proliferation, migration, invasiveness, and metastasis in cultured cells and in xenografts using luciferase-labeled PC3 (PC3-Luc) cells. We found that 3β-Adiol not only inhibits PC3-Luc cell migratory properties, but also induces a broader anti-tumor phenotype by decreasing the proliferation rate, increasing cell adhesion, and reducing invasive capabilities in vitro. All these 3β-Adiol activities are mediated by ERβ and cannot be reproduced by the physiological estrogen, 17β-estradiol, suggesting the existence of different pathways activated by the two ERβ ligands in PC3-Luc cells. In vivo, continuous administration of 3β-Adiol reduces growth of established tumors and counteracts metastasis formation when PC3-Luc cells are engrafted s.c. in nude mice or are orthotopically injected into the prostate. Since 3β-Adiol has no androgenic activity, and cannot be converted to androgenic compounds, the effects here described entail a novel potential application of this agent against human PC.

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