scholarly journals The activation of G protein-coupled receptor 30 (GPR30) inhibits proliferation of estrogen receptor-negative breast cancer cells in vitro and in vivo

2014 ◽  
Vol 5 (10) ◽  
pp. e1428-e1428 ◽  
Author(s):  
W Wei ◽  
Z-J Chen ◽  
K-S Zhang ◽  
X-L Yang ◽  
Y-M Wu ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Estrogen Receptor ◽  
Cancer Cells ◽  
G Protein ◽  
Breast Cancer Cells ◽  
G Protein Coupled Receptor ◽  
G Protein Coupled ◽  
Estrogen Receptor Negative

Hydrogen sulfide-releasing aspirin suppresses NF-κB signaling in estrogen receptor negative breast cancer cells in vitro and in vivo

2012 ◽  
Vol 83 (6) ◽  
pp. 723-732 ◽  
Author(s):  
Mitali Chattopadhyay ◽  
Ravinder Kodela ◽  
Niharika Nath ◽  
Arpine Barsegian ◽  
Daniel Boring ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Estrogen Receptor ◽  
Hydrogen Sulfide ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Estrogen Receptor Negative

scholarly journals Nitric Oxide-Releasing Aspirin Suppresses NF-κB Signaling in Estrogen Receptor Negative Breast Cancer Cells in Vitro and in Vivo

Molecules ◽  
2015 ◽  
Vol 20 (7) ◽  
pp. 12481-12499 ◽  
Author(s):  
Niharika Nath ◽  
Mitali Chattopadhyay ◽  
Deborah Rodes ◽  
Anna Nazarenko ◽  
Ravinder Kodela ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Nitric Oxide ◽  
Estrogen Receptor ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Nitric Oxide Releasing ◽  
Estrogen Receptor Negative

scholarly journals The G Protein–Coupled Receptor GPR30 Inhibits Proliferation of Estrogen Receptor–Positive Breast Cancer Cells

2010 ◽  
Vol 70 (3) ◽  
pp. 1184-1194 ◽  
Author(s):  
Eric A. Ariazi ◽  
Eugen Brailoiu ◽  
Smitha Yerrum ◽  
Heather A. Shupp ◽  
Michael J. Slifker ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Estrogen Receptor ◽  
Cancer Cells ◽  
G Protein ◽  
Breast Cancer Cells ◽  
G Protein Coupled Receptor ◽  
Estrogen Receptor Positive ◽  
G Protein Coupled ◽  
Positive Breast Cancer

scholarly journals Regulation of ERRα Gene Expression by Estrogen Receptor Agonists and Antagonists in SKBR3 Breast Cancer Cells: Differential Molecular Mechanisms Mediated by G Protein-Coupled Receptor GPR30/GPER-1

2010 ◽  
Vol 24 (5) ◽  
pp. 969-980 ◽  
Author(s):  
Yin Li ◽  
Lutz Birnbaumer ◽  
Christina T. Teng
Keyword(s):  
Breast Cancer ◽  
Estrogen Receptor ◽  
Cancer Cells ◽  
G Protein ◽  
Breast Cancer Cells ◽  
Molecular Mechanisms ◽  
Cellular Proliferation ◽  
G Protein Coupled Receptor ◽  
Ici 182,780 ◽  
G Protein Coupled

Abstract In selected tissues and cell lines, 17β-estradiol (E2) regulates the expression of estrogen-related receptor α (ERRα), a member of the orphan nuclear receptor family. This effect is thought to be mediated by the estrogen receptor α (ERα). However in the ERα- and ERβ-negative SKBR3 breast cancer cell line, physiological levels of E2 also stimulate ERRα expression. Here, we explored the molecular mechanism that mediates estrogen action in ER-negative breast cancer cells. We observed that E2, the ERα agonist, as well as the ERα antagonists ICI 182,780 and tamoxifen (TAM), a selective ER modulator, stimulate the transcriptional activity of the ERRα gene and increase the production of ERRα protein in SKBR3 cells. Moreover, the ERRα downstream target genes expression and cellular proliferation are also increased. We show further that the G protein-coupled receptor GPR30/GPER-1 (GPER-1) mediates these effects. The GPER-1 specific ligand G-1 mimics the actions of E2, ICI 182,780, and TAM on ERRα expression, and changing the levels of GPER-1 mRNA by overexpression or small interfering RNA knockdown affected the expression of ERRα accordingly. Utilizing inhibitors, we delineate a different downstream pathway for ER agonist and ER antagonist-triggered signaling through GPER-1. We also find differential histone acetylation and transcription factor recruitment at distinct nucleosomes of the ERRα promoter, depending on whether the cells are activated with E2 or with ER antagonists. These findings provide insight into the molecular mechanisms of GPER-1/ERRα-mediated signaling and may be relevant to what happens in breast cancer cells escaping inhibitory control by TAM.

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