Cited by 158Estrogen and related hormone effectsReceptor Mechanisms and SignalingEffects and risks of endocrine disrupting chemicals

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Stimulating the GPR30 Estrogen Receptor with a Novel Tamoxifen Analogue Activates SF-1 and Promotes Endometrial Cell Proliferation

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Lin, Benjamin C., Suzawa, Miyuki, Blind, Raymond D., Tobias, Sandra C., Bulun, Serdar E., Scanlan, Thomas S., Ingraham, Holly A.·2009·Cancer Research

DOI 10.1158/0008-5472.can-08-1622PMC PMC2756996

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Abstract

Estrogens and selective estrogen receptor (ER) modulators such as tamoxifen are known to increase uterine cell proliferation. Mounting evidence suggests that estrogen signaling is mediated not only by ERα and ERβ nuclear receptors, but also by GPR30 (GPER), a seven transmembrane (7TM) receptor. Here, we report that primary human endometriotic H-38 cells express high levels of GPR30 with no detectable ERα or ERβ. Using a novel tamoxifen analogue, STX, which activates GPR30 but not ERs, significant stimulation of the phosphatidylinositol 3-kinase (PI3K) and mitogen-activated protein kinase (MAPK) pathways was observed in H-38 cells and in Ishikawa endometrial cancer cells expressing GPR30; a similar effect was observed in JEG3 choriocarcinoma cells. STX treatment also increased cellular pools of phosphatidylinositol (3,4,5) triphosphate, a proposed ligand for the nuclear hormone receptor SF-1 (NR5A1). Consistent with these findings, STX, tamoxifen, and the phytoestrogen genistein were able to increase SF-1 transcription, promote Ishikawa cell proliferation, and induce the SF-1 target gene aromatase in a GPR30-dependent manner. Our findings suggest a novel signaling paradigm that is initiated by estrogen activation of the 7TM receptor GPR30, with signal transduction cascades (PI3K and MAPK) converging on nuclear hormone receptors (SF-1/LRH-1) to modulate their transcriptional output. We propose that this novel GPR30/SF-1 pathway increases local concentrations of estrogen, and together with classic ER signaling, mediate the proliferative effects of synthetic estrogens such as tamoxifen, in promoting endometriosis and endometrial cancers. [Cancer Res 2009;69(13):5415–23]

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1 retracted

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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Authors: Lin, B. C., Suzawa, M., Blind, R. D., Tobias, S. C., Bulun, S. E., Scanlan, T. S., & Ingraham, H. A.
Affiliations: 1Pharmaceutical Chemistry and Departments of
University of California, San Francisco (US)
Northwestern University (US)
Oregon Health & Science University (US)
ORCID: Suzawa, Miyuki
Blind, Raymond D.
Bulun, Serdar E.
Scanlan, Thomas S.
Ingraham, Holly A.
Venue: Cancer Research
Publisher: American Association for Cancer Research (AACR)
Published: 2009-07-01
Volume: 69
Issue: 13
Pages: 5415-5423
ISSN: 0008-5472 (ISSN-L)
1538-7445
DOI: 10.1158/0008-5472.can-08-1622
PMC: PMC2756996
OpenAlex: W2103019385
Cited by: 157
References: 51
Citations by year: 2026: 4 · 2025: 7 · 2024: 3 · 2023: 9 · 2022: 8 · 2021: 5 · 2020: 8 · 2019: 11 · 2018: 5 · 2017: 2 · 2016: 13 · 2015: 18 · 2014: 15 · 2013: 11 · 2012: 11
FWCI: 7.56
Type: journal article
Language: en
Open access: bronze
doi.org
Locations: Cancer Research (publishedVersion)
PubMed (publishedVersion)
Europe PMC (PubMed Central) (acceptedVersion)
PubMed Central (acceptedVersion)
Funders: University of California, San Francisco
National Institute of General Medical Sciences
National Institute of Diabetes and Digestive and Kidney Diseases (R01DK063592, R01DK072246)
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: GPR30, G protein-coupled estrogen receptor, tamoxifen analogues, SF-1, steroidogenic factor 1, endometrial proliferation, endometriosis, endometrial cancer, PI3K signaling, MAPK signaling, phosphatidylinositol 3,4,5-trisphosphate, aromatase, genistein, estrogen signaling, choriocarcinoma
MeSH terms: Animals, Breast Neoplasms, Cell Division, Choriocarcinoma, Endometriosis, Estrogens, Female, Humans, Luciferases, Pregnancy, Receptors, Estrogen, Uterine Neoplasms, Endometrial Neoplasms, Genes, Reporter, Mice, Knockout, Receptors, G-Protein-Coupled, Cell Line, Tumor, Mice, Steroidogenic Factor 1

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Stimulating the GPR30 Estrogen Receptor with a Novel Tamoxifen Analogue Activates SF-1 and Promotes Endometrial Cell Proliferation

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