Although, an increasing body of evidence has linked estrogen receptor beta (ERß) to prostate cancer, the function of estrogen receptor alpha (ERα) in prostate cancer is not very well studied.
These findings suggest that CCND1 expression is possibly regulated by estrogens via ERβ and that this signaling pathway may influence prostate cancer development.
Our results support the conclusion that C/EBPβ down-regulated ERβ expression through increasing its promoter methylation, and then regulated proliferation and apoptosis in PCa.
Taken together, our data demonstrated that bakuchiol inactivated NF-κB signaling via AR and ERβ, which contributes to inhibition of PC-3 cell proliferation and migration, indicating that bakuchiol is one of the key component from P. corylifolia L for PCa treatment and has a potential as anti-prostate cancer drug candidates.
Using a new monoclonal antibody, the current study reports on the differential expression of the ERbeta in tissue sections from 132 patients with prostate cancer.
Differential expression profile analysis of ERβ was analyzed by quantitative immunohistochemistry using ethnicity-based tissue microarray encompassing 300 PCa tissue cores.
In ovarian cancer, the role of estrogen receptors (ERs), particularly of ERβ, being suggested as tumor suppressor in breast and prostate cancer, remains unclear.
The analysis of several immortalized cell lines derived from freshly explants of prostate cancer specimens showed that Nup153 protein was higher and present in multimeric complexes with eNOS and ERβ as compared to normal/hyperplastic prostate epithelial cells.
The mechanism of inactivation of the ERbeta gene in prostate carcinoma was CpG methylation because the degree of methylation at all CpG sites within the promoter region between -376 and -117 was higher in prostate carcinoma samples compared with BPH tissues.
We identify two independent susceptibility loci for prostate cancer at 11p15.4 (rs12791447, P=3.59 × 10(-8); PPFIBP2) and 14q23.2 (rs58262369, P=6.05 × 10(-10); ESR2).
Based on our recent finding of anti-estrogen/ER-beta-mediated growth inhibition of prostate cancer cells in vitro, the presence of ER-beta in metastatic cells may have important implications for the treatment of late-stage disease.
In addition, transfection experiment of ERβ-siRNA further indicated that diosicn showed excellent activity against PCa in vitro and in vivo by increasing ERβ expression level.
In addition, ARs; estrogen receptors (ERs; ERα and ERβ); and estrogen-related receptors (ERRs; ERRα, ERRβ, and ERRγ) have been reported to be involved in the development or regulation of PC.
The androgen-sensitive human prostate cancer cell line LNCaP expresses the estrogen receptor beta and androgen receptor and can be stimulated by androgens to secrete prostate-specific antigen (PSA).
Taken together, our results support the conclusion that abnormal methylation of the ERβ promoter may increase genetic susceptibility to prostate cancer.
Moreover, distinct ERβ dynamics in various cellular bio-settings such as prostate cancer (DU-145) or triple-negative breast cancer (MDA-MB-231) cells were directly observed for the first time viaFPNM staining.