GPR30 predicts poor survival for ovarian cancer

Smith, Harriet O.; Arias-Pulido, Hugo; Kuo, Dennis Yi-Shin; Howard, Tamara; Qualls, Clifford; Lee, Sang Joon; Verschraegen, Claire F.; Hathaway, Helen J.; Joste, Nancy E.; Prossnitz, Eric R.

doi:10.1016/j.ygyno.2009.05.015

Cited by 188 publications

(179 citation statements)

References 49 publications

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“…Surprisingly, a member of the GPCR family, GPR30/GPER, was recently shown to mediate the multifaceted actions of estrogens in different tissues including cancer cells [135] . Importantly, GPER overexpression was associated with lower survival rates in endometrial and ovarian cancer patients and with an elevated risk of developing metastases in patients with breast cancer [136][137][138] . GPER by transactivating EGFR triggers numerous transduction pathways including the intracellular cAMP, calcium mobilization, MAPK, PI3-K and phospholipase C activation in a variety of cell types [139] .…”

Section: Gpcrs Activated By Hormonesmentioning

confidence: 99%

GPCRs and cancer

Lappano

2012

Acta Pharmacol Sin

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G-protein-coupled receptors (GPCRs), which represent the largest gene family in the human genome, play a crucial role in multiple physiological functions as well as in tumor growth and metastasis. For instance, various molecules like hormones, lipids, peptides and neurotransmitters exert their biological effects by binding to these seven-transmembrane receptors coupled to heterotrimeric G-proteins, which are highly specialized transducers able to modulate diverse signaling pathways. Furthermore, numerous responses mediated by GPCRs are not dependent on a single biochemical route, but result from the integration of an intricate network of transduction cascades involved in many physiological activities and tumor development. This review highlights the emerging information on the various responses mediated by a selected choice of GPCRs and the molecular mechanisms by which these receptors exert a primary action in cancer progression. These findings provide a broad overview on the biological activity elicited by GPCRs in tumor cells and contribute to the identification of novel pharmacological approaches for cancer patients.

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Section: Gpcrs Activated By Hormonesmentioning

confidence: 99%

GPCRs and cancer

Lappano

2012

Acta Pharmacol Sin

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“…GPR30 expression was discovered in the vascular smooth muscle cells of patients with atherosclerosis [23]. Subsequently, it was found that GPR30 expression mediated the proliferation of ovarian [24], endometrial [10], breast [13], and sperm cell [25] tumors. Tian et al [19] investigated the potential proliferative effect of estrogen-driven GPR30 signaling on uterine smooth muscle cells in samples of leiomyoma and adjacent myometrium.…”

Section: Discussionmentioning

confidence: 99%

G-protein-coupled estrogen receptor-30 gene polymorphisms are associated with uterine leiomyoma risk

Kasap

Turhan

Edgünlü

et al. 2015

Bosn J of Basic Med Sci

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The G-protein-coupled estrogen receptor , GPER-1) is a member of the G-protein-coupled receptor 1 family and is expressed significantly in uterine leiomyomas. To understand the relationship between GPR30 single nucleotide polymorphisms and the risk of leiomyoma, we measured the follicle-stimulating hormone (FSH) and estradiol (E2) levels of 78 perimenopausal healthy women and 111 perimenopausal women with leiomyomas. The participants' leiomyoma number and volume were recorded. DNA was extracted from whole blood with a GeneJET Genomic DNA Purification Kit. An amplification-refractory mutation system polymerase chain reaction approach was used for genotyping of the GPR30 gene (rs3808350, rs3808351, and rs11544331). The differences in genotype and allele frequencies between the leiomyoma and control groups were calculated using the chi-square (χ2) and Fischer' s exact test. The median FSH level was higher in controls (63 vs. 10 IU/L, p=0.000), whereas the median E2 level was higher in the leiomyoma group (84 vs. 9.1 pg/mL, p=0.000). The G allele of rs3808351 and the GG genotype of both the rs3808350 and rs3808351 polymorphisms and the GGC haplotype increased the risk of developing leiomyoma. There was no significant difference in genotype frequencies or leiomyoma volume. However, the GG genotype of the GPR30 rs3808351 polymorphism and G allele of the GPR30 rs3808351 polymorphism were associated with the risk of having a single leiomyoma. Our results suggest that the presence of the GG genotype of the GPR30 rs3808351 polymorphism and the G allele of the GPR30 rs3808351 polymorphism affect the characteristics and development of leiomyomas in the Turkish population.

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“…GPR30 expression is not only associated with cancer growth, but also with metastases development (61). In primary breast tumors (10), epithelial ovarian cancer (62) and endometrial cancer (7), tumors with higher GPR30 expression are more metastastic compared to GPR30-negative tumors. Likewise, aggressive cancer cell lines express high GPR30 levels, whereas their associated normal cell lines show little or no GPR30 expression (63,64).…”

Section: Discussionmentioning

confidence: 99%

Regulation of HRG-β1-induced proliferation, migration and invasion of MCF-7 cells by upregulation of GPR30 expression

Zhang

2012

Mol Med Report

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Abstract. The cooperation and communication between different cell signaling transduction pathways are considered critical in the development of various types of cancer as well as drug resistance. There is evidence of crosstalk between the G protein-coupled receptor 30 (GPR30), the newly discovered estrogen receptor (ER), and the ErbB family. Heregulin (HRG)-β1, the ligand for ErbB3 and ErbB4, upregulates GPR30 expression in MCF-7, T-47D and BT-474 breast cancer cell lines that express ERα. In the present study, recombinant human HRG-β1 was used to investigate the upregulation of GPR30 expression by HRGs in MCF-7 breast cancer cells which were ERα-positive. In MCF-7 cells, the ErbB2 inhibitor, AG825, the MAPK inhibitor, PD98059, and the MEK1/2 inhibitor, U0126, blocked the HRG-β1-induced GPR30 expression. 17-β-estradiol (E2) boosted the HRG-β1-induced proliferation, migration and invasion of MCF-7 cells. Similar to E2, the specific GPR30 agonist, G-1, promoted HRG-β1-induced migration and invasion, but inhibited growth. Using the specific GPR30 antagonist, G-15, or the small interfering RNA for GPR30, the functions of GPR30 after treatment with HRG-β1 were further investegated. The results from our study indicate that the interruption between GPR30 signaling and the ErbB family system may serve as a promising therapeutic strategy for breast cancer.

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GPR30 predicts poor survival for ovarian cancer

Cited by 188 publications

References 49 publications

GPCRs and cancer

GPCRs and cancer

G-protein-coupled estrogen receptor-30 gene polymorphisms are associated with uterine leiomyoma risk

Regulation of HRG-β1-induced proliferation, migration and invasion of MCF-7 cells by upregulation of GPR30 expression

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