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. 2017 Sep;14(3):2796-2802.
doi: 10.3892/ol.2017.6544. Epub 2017 Jul 8.

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

Affiliations

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

Long Xiao et al. Oncol Lett. 2017 Sep.

Abstract

Previous studies have suggested that changes in sex hormone receptor expression may be associated with the initiation and progression of prostate cancer (PCa). Therefore, the present study aimed to investigate the association and possible pathways between two sex hormone receptors and PCa by measuring the expression levels of the androgen receptor (AR) and the estrogen receptor subtypes alpha (ERα) and beta (ERβ) in prostatic cancer PC-3 cell lines. The pcDNA3.1-hERβ plasmid was transfected into PC-3 cell lines. The expression levels of AR, ERα and ERβ were detected at the mRNA level by reverse transcription-polymerase chain reaction (RT-PCR) and quantitative PCR (qPCR). The results demonstrated that the expression levels of AR, ERβ and ERα were downregulated to different degrees: ERβ test group vs. PC-3 cell group (P=0.000; 95% confidence interval: 0.9803-1.6331). ERβ and AR expression was detected continuously in the PC-3 cells, but the expression of ERα was not. AR expression levels exhibited an upward trend whilst the expression of ERβ demonstrated a marked downward trend. There is a correlation between the expression levels of ERβ and the incidence of PCa, and ERβ may inhibit the growth of PC-3 cell lines by regulating the expression levels of AR. ERβ may provide a novel target for PCa therapies.

Keywords: androgen receptor; estrogen receptor α; estrogen receptor β; prostatic cancer.

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Figures

Figure 1.
Figure 1.
(A) PC-3 cells prior to transfection with the pcDNA3.1-hERβ-plasmid examined using inverted phase contrast microscopy (magnification, ×200). Cells were seeded in 6 orifice plates and grown for 48 h. Cells are distributed over ~80–90% of the bottom of the dish. The cells are fusiform, in orderly rows, a medium and uniform size with larger nuclei and less cytoplasm. Silk phase separation was observed occasionally. (B) PC-3 cells subsequent to pcDNA3.1-hERβ plasmid transfection at magnification, ×200. Rates of cell apoptosis were marked. Contraction of nuclei, less cytoplasm, few synapses and poor rates of growth were observed.
Figure 2.
Figure 2.
The ΔΔCq value of AR. Test, ΔΔCq value of AR in the test group; Lipofectamine® 2000, ΔΔCq value of AR in the Lipofectamine® 2000-transfected group; Blank plasmid, ΔΔCq value of AR in the blank plasmid-transfected group; Control cell, ΔΔCq value of AR in the control groups; AR, androgen receptor.
Figure 3.
Figure 3.
The ΔΔCq value of ERβ. Test, ΔΔCq value of ERβ in the test group; Lipofectamine® 2000, ΔΔCq value of ERβ in the Lipofectamine® 2000-transfected group; Blank plasmid, ΔΔCq value of ERβ in the blank plasmid-transfected group; Control cell, ΔΔCq value of ERβ in the control groups; ERβ, estrogen receptor β.
Figure 4.
Figure 4.
The ΔΔCq value of ERα. Test, ΔΔCq value of ERα in the test group; Lipofectamine® 2000 ΔΔCq value of ERα in the Lipofectamine® 2000-transfected group; Blank plasmid, ΔΔCq value of ERα in the blank plasmid-transfected group; Control cell, ΔΔCq value of ERα in the control groups; ERα, estrogen receptor α.
Figure 5.
Figure 5.
AR, ERβ, ERα ΔΔCq value content ratio diagram. The proportion of AR, ERβ and ERα in each group is demonstrated. AR, androgen receptor; ERβ, estrogen receptor β; ERα, estrogen receptor α.
Figure 6.
Figure 6.
Value of AR, ERβ, ERα Content Ratio Diagram. The proportion of AR, ERβ and ERα in each group is demonstrated. AR, androgen receptor; ERβ, estrogen receptor β; ERα, estrogen receptor α.

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