Effect of lysophosphatidylglycerol on several signaling molecules in OVCAR-3 human ovarian cancer cells: Involvement of pertussis toxin-sensitive G-protein coupled receptor

2007 ◽  
Vol 73 (5) ◽  
pp. 675-681 ◽  
Author(s):  
Kyoung Sun Park ◽  
Mi-Kyoung Kim ◽  
Dong-Soon Im ◽  
Yoe-Sik Bae
Keyword(s):  
Ovarian Cancer ◽  
Cancer Cells ◽  
G Protein ◽  
Pertussis Toxin ◽  
Signaling Molecules ◽  
Ovarian Cancer Cells ◽  
Human Ovarian Cancer ◽  
G Protein Coupled Receptor ◽  
G Protein Coupled

GRP137 promotes cell proliferation and metastasis through regulation of the PI3K/AKT pathway in human ovarian cancer

2018 ◽  
Vol 104 (5) ◽  
pp. 330-337 ◽  
Author(s):  
Li-qian Zhang ◽  
Su-qing Yang ◽  
Xiang-dong Qu ◽  
Xian-jun Chen ◽  
Hong-sheng Lu ◽  
...  
Keyword(s):  
Ovarian Cancer ◽  
G Protein ◽  
Biological Activities ◽  
Xenograft Model ◽  
Akt Pathway ◽  
Ovarian Cancer Cells ◽  
Human Ovarian Cancer ◽  
G Protein Coupled Receptor ◽  
Skov3 Cells ◽  
G Protein Coupled

Purpose: Ovarian cancer is one of the leading causes of death for women worldwide. The present study aims to investigate the role of G protein-coupled receptor 137 (GPR137) in the biological activities of ovarian cancer cells. Methods: (QUERY: Please supply Methods for Abstract) Results: G protein-coupled receptor 137 was highly expressed in clinical ovarian cancer tissues and exhibited the highest protein levels in SKOV3 cells and OVCAR3 cells. Knockdown of GPR137 caused significant decreases in cell proliferative rates and colony formation abilities in SKOV3 cells and OVCAR3 cells and also inhibited the in vivo tumorigenesis in a xenograft model. It was observed that knockdown of GPR137 inhibited cell motility by up to 40% in SKOV3 cells and approximately 65% in OVCAR3 cells in wound-healing assay. Cell migration abilities were consistently inhibited by 68.2% in SKOV3 cells and 59.3% in OVCAR3 cells, whereas cell invasion abilities were inhibited by 64.0% and 74.2% in SKOV3 and OVCAR3 cells, respectively, after knockdown of GPR137. When GPR137 was depleted, epithelial markers were increased, while mesenchymal markers decreased. Conclusions: Our data suggest that GPR137 plays pro-oncogenic roles in ovarian cancer via regulation of the PI3K/AKT pathway. These observations might pave new insights into therapeutic strategies against human ovarian cancer.

Estradiol Attenuates EGF-Induced Rapid uPAR Mobilization and Cell Migration via the G-protein-Coupled Receptor 30 in Ovarian Cancer Cells

2009 ◽  
Vol 19 (2) ◽  
pp. 214-222 ◽  
Author(s):  
Emir Henic ◽  
Vera Noskova ◽  
Gunilla Høyer-Hansen ◽  
Stefan Hansson ◽  
Bertil Casslén
Keyword(s):  
Ovarian Cancer ◽  
Cell Migration ◽  
Growth Factor ◽  
Epidermal Growth Factor ◽  
Cancer Cells ◽  
G Protein ◽  
Ovarian Cancer Cells ◽  
Upar Expression ◽  
Epidermal Growth ◽  
G Protein Coupled

Epidermal growth factor (EGF) stimulates proliferation and migration in ovarian cancer cells, and high tumor expression of the EGF system correlates with poor prognosis. Epidermal growth factor upregulates urokinase plasminogen activator receptor (uPAR) on the cell surface via 3 distinct mechanisms: rapid mobilization of uPAR from detergent-resistant domains, increased mRNA, and decreased degradation. G-protein-coupled receptor 30 (GPR30) is a newly identified membrane estrogen receptor (ER).The objective of this study was to explore the effects of 17β-estradiol (E2) on uPAR expression and cell migration in ovarian cancer cells and further to identify the ER involved.We used 7 ovarian cancer cell lines, cell migration assay, cellular binding of 125I-uPA, cellular degradation of 125I-uPA/PAI-1 complex, enzyme-linked immunosorbent assay for uPAR, solid-phase enzyme immunoassay for ERα, and quantitative polymerase chain reaction.Estradiol attenuates the stimulatory effect of EGF on cell migration and uPAR expression. Specifically, E2 reduces the very rapid increase of detergent extractable uPAR, which occurs within minutes of EGF stimulation and probably represents mobilization of uPAR from detergent-resistant domains such as lipid rafts. Estradiol influenced neither the amount of uPAR mRNA nor the rate of uPAR degradation or solubilization. The nuclear ER antagonists ICI 182780 and tamoxifen, which are GPR30 agonists, as well as the specifically constructed GPR30 agonist G1, mimicked the effect of E2 on uPAR expression and cell migration. OVCAR-3 cells express mRNA for GPR30.Estradiol attenuates EGF-induced mobilization of ligated uPAR from detergent-resistant domains and subsequent migration in ovarian cancer cells. The response to various ER ligands indicates that this effect is mediated via the membrane ER GPR30.

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