Cited by 366Estrogen and related hormone effectsReceptor Mechanisms and SignalingEffects and risks of endocrine disrupting chemicals

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Minireview: G Protein-Coupled Estrogen Receptor-1, GPER-1: Its Mechanism of Action and Role in Female Reproductive Cancer, Renal and Vascular Physiology

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Filardo, Edward J., Thomas, Peter·2012·Endocrinology

DOI 10.1210/en.2012-1061PMC PMC3380306

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Abstract

Using cDNA cloning strategies commonly employed for G protein-coupled receptors (GPCR), GPCR-30 (GPR30), was isolated from mammalian cells before knowledge of its cognate ligand. GPR30 is evolutionarily conserved throughout the vertebrates. A broad literature suggests that GPR30 is a Gs-coupled heptahelical transmembrane receptor that promotes specific binding of naturally occurring and man-made estrogens but not cortisol, progesterone, or testosterone. Its “pregenomic” signaling actions are manifested by plasma membrane-associated actions familiar to GPCR, namely, stimulation of adenylyl cyclase and Gβγ-subunit protein-dependent release of membrane-tethered heparan bound epidermal growth factor. These facts regarding its mechanism of action have led to the formal renaming of this receptor to its current functional designate, G protein-coupled estrogen receptor (ER) (GPER)-1. Further insight regarding its biochemical action and physiological functions in vertebrates is derived from receptor knockdown studies and the use of selective agonists/antagonists that discriminate GPER-1 from the nuclear steroid hormone receptors, ERα and ERβ. GPER-1-selective agents have linked GPER-1 to physiological and pathological events regulated by estrogen action, including, but not limited to, the central nervous, immune, renal, reproductive, and cardiovascular systems. Moreover, immunohistochemical studies have shown a positive association between GPER-1 expression and progression of female reproductive cancer, a relationship that is diametrically opposed from ER. Unlike ER knockout mice, GPER-1 knockout mice are fertile and show no overt reproductive anomalies. However, they do exhibit thymic atrophy, impaired glucose tolerance, and altered bone growth. Here, we discuss the role of GPER-1 in female reproductive cancers as well as renal and vascular physiology.

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RETRACTED: 17β-Estradiol, Genistein, and 4-Hydroxytamoxifen Induce the Proliferation of Thyroid Cancer Cells through the G Protein-Coupled Receptor GPR30
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Retracted
Retracted: G-Protein–Coupled Receptor 30 and Estrogen Receptor-α Are Involved in the Proliferative Effects Induced by Atrazine in Ovarian Cancer Cells
Albanito, L., Lappano, R., Madeo, A., Chimento, A., Prossnitz, E. R., Cappello, A. R., Dolce, V., Abonante, S., Pezzi, V., & Maggiolini, M. (2008) · Environmental Health Perspectives · doi:10.1289/ehp.11297 · Cited by 105
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Self-citation
Estrogen-Induced Activation of Erk-1 and Erk-2 Requires the G Protein-Coupled Receptor Homolog, GPR30, and Occurs via Trans-Activation of the Epidermal Growth Factor Receptor through Release of HB-EGF
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“Excellent reviews have been written about the use of GPER-1-selective ligands, including the GPER-1 agonist G-1 and the GPER-1 antagonist G-15, to investigate disease models (8, 36).”
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Filardo, 2007, Activation of the novel estrogen receptor G protein coupled receptor 30 (GPR30) at the plasma membrane., Endocrinology, 148, 3236, 10.1210/en.2006-1605 · DOI

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Authors: Filardo, E. J., & Thomas, P.
Affiliations: Brown University (US)
University of Texas at Austin Marine Science Institute (US)
Corresponding author: Filardo, Edward J.
ORCID: Filardo, Edward J.
Thomas, Peter
Venue: Endocrinology
Publisher: The Endocrine Society
Published: 2012-04-11
Volume: 153
Issue: 7
Pages: 2953-2962
ISSN: 0013-7227 (ISSN-L)
1945-7170
DOI: 10.1210/en.2012-1061
PMC: PMC3380306
OpenAlex: W2137207319
Cited by: 366
References: 83
Citations by year: 2026: 16 · 2025: 10 · 2024: 24 · 2023: 16 · 2022: 18 · 2021: 28 · 2020: 31 · 2019: 30 · 2018: 29 · 2017: 26 · 2016: 28 · 2015: 36 · 2014: 36 · 2013: 29 · 2012: 9
FWCI: 4.34
Type: journal article
Language: en
Open access: green
europepmc.org
Locations: Endocrinology (publishedVersion)
Europe PMC (PubMed Central) (publishedVersion)
PubMed Central (publishedVersion)
PubMed (publishedVersion)
Funders: National Cancer Institute (R01CA119165)
Topics: Life Sciences › Biochemistry, Genetics and Molecular Biology › Endocrinology › Estrogen and related hormone effects
Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Receptor Mechanisms and Signaling
Physical Sciences › Environmental Science › Health, Toxicology and Mutagenesis › Effects and risks of endocrine disrupting chemicals
Keywords: G protein-coupled estrogen receptor, GPR30, estrogen signaling, female reproductive cancers, renal physiology, vascular physiology, adenylate cyclase, Gβγ subunits, estrogen receptor knockout mice, thymic atrophy, glucose tolerance, bone growth
MeSH terms: Animals, Biopsy, Female, Genital Neoplasms, Female, Humans, Kidney, Ligands, Models, Biological, Models, Genetic, Receptors, Estrogen, Transcriptional Activation, Gene Expression Regulation, Neoplastic, Receptors, G-Protein-Coupled, Mice, ErbB Receptors

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Minireview: G Protein-Coupled Estrogen Receptor-1, GPER-1: Its Mechanism of Action and Role in Female Reproductive Cancer, Renal and Vascular Physiology

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