Activation of estrogen receptor beta (ERβ) regulates the expression of N-cadherin, E-cadherin and β-catenin in androgen-independent prostate cancer cells

The Effects of Trifolium pratense L. Sprouts’ Phenolic Compounds on Cell Growth and Migration of MDA-MB-231, MCF-7 and HUVEC Cells

“…That allowed us to suppose that observed migration inhibition is not regulated at the transcription level of receptors, but rather by isoflavones binding to the ERβ receptor. Studies performed with PC-3 cells revealed that ERβ-selective agonist DPN decreased the expression of N-cadherin [52] which is consistent with what was observed by us-downregulation of N-cadherin in the presence of isoflavones. Because ERβ activation was also related with the induction of apoptosis in PC-3M cells, apoptotic cell death may result not only from cytotoxic activity of extract components, but also could be used as functional link for agonistic aglycons binding to ERβ protein [53].…”

Estrogen Receptors Promote Migration, Invasion and Colony Formation of the Androgen-Independent Prostate Cancer Cells PC-3 Through β-Catenin Pathway

“…The cells were wounded using 200 µl sterile pipette tips and then washed to remove detached cells and debris (28) and incubated in the absence (control, basal level of cellular function) and presence of 17β-estradiol (E2, 0.1 and 10 nM; Sigma Chemical Co.); ERβ-selective agonist DPN [10 nM; 2,3-bis(4-hydroxyphenyl)-propionitrile, Tocris Bioscience, Bristol, United Kingdom] and ERB-041 (10 nM; Sigma Chemical Co.) or ERα-selective agonist PPT [10 nM; 4,4' ,4"-(4-propyl-(1H)-pyrazole-1,3,5-triyl)trisphenol, Tocris Bioscience] for 24 h at 37 • C. The cells were also untreated or pretreated with ERβ-selective antagonist PHTPP [10 nM; 4-(2-phenyl-5,7-bis(trifluoromethyl)pyrazolo(1,5-a)pyrimidin-3-yl)phenol, Tocris Bioscience] or with a compound that disrupts the complex β-catenin-TCF/LEF transcription factor, PKF 118-310 (100 nM, Sigma-Aldrich Co) for 30 min. Incubation was continued in the absence and presence of DPN (10 nM) or ERB-041 (10 nM), for 24 h at 37 • C (18,21,22). The agonists and antagonists are highly selective, at these concentrations, as previously reported [(29, 30), (31), (20)].…”

“…The human androgen-independent prostate cancer cell line (PC-3) (derived from bone metastasis) was obtained from the American Type Culture Collection (Manassas, VA, United States). PC-3 cells cultures were carried out as previously described (18,(20)(21)(22).…”

“…These chambers were placed in 24-well plates containing culture medium with 10% FBS in the lower chamber. PC-3 cells in upper chambers were incubated in the absence (control) and presence of E2 (10 nM), DPN (10 nM) or PPT (10 nM) for 48 h at 37 • C. The cells were also untreated or pretreated with PHTPP (10 nM), MPP [10 nM; 1,3-bis(4-hydroxyphenyl)-4-methyl-5-(4-(2piperidinylethoxy)phenol)-1H-pyrazole dihydrochloride, Tocris Bioscience], PKF 118-310 (100 nM) (18,21,22) or VEGF specific inhibitor Bevacizumab (Avastin R , 25 ng) (35) for 30 min. Incubation was continued in the absence and presence of E2 (10 nM), DPN (10 nM) or PPT (10 nM), for 48 h at 37 • C. The membranes were washed thoroughly with 10 mM PBS, fixed in 4% paraformaldehyde for 30 min, and stained with 0.2% crystal violet for 10 min (28).…”

“…The role of these pathways through activation of estrogen receptors (ERs) remains to be explored in both cells. Furthermore, in PC-3 cells, the activation of ERβ decreases N-cadherin (22) and increases non-phosphorylated β-catenin levels (18). However, the molecular mechanisms of the crosstalk between ER and WNT/β-catenin pathways in this cell have not been well studied.…”