|
Endometrial Carcinoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
Chronic BDE-47 Exposure Aggravates Malignant Phenotypes and Chemoresistance by Activating ERK Through ERα and GPR30 in Endometrial Carcinoma.
|
31737560 |
2019 |
|
Endometrial Carcinoma
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
Immunohistochemistry was performed to assess AMF and GPER-1 expression in endometrial cancer specimens and normal endometrium.
|
30836961 |
2019 |
|
Endometrial Carcinoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
MicroRNA‑195 inhibits epithelial‑mesenchymal transition by targeting G protein‑coupled estrogen receptor 1 in endometrial carcinoma.
|
31545414 |
2019 |
|
Endometrial Carcinoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
Our study demonstrated that MDH2, stimulated by estrogen, was involved in the development of PTEN-regulated endometrial carcinoma through GPR30-related pathway.
|
28189066 |
2017 |
|
Endometrial Carcinoma
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
TET1 mediated GPER up-regulation was another mechanism that insulin promotes EC cell proliferation.
|
27889612 |
2017 |
|
Endometrial Carcinoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
Menopausal status was not associated with the positivity of GPR30 in both type 1 and type 2 endometrial cancer.
|
29207611 |
2017 |
|
Endometrial Carcinoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
In addition, the results suggest that miR-424 up-regulation inactivated the PI3K/AKT signaling, which was mediated by G-protein-coupled estrogen receptor-1 (GPER) in endometrial cancer.
|
26638889 |
2015 |
|
Endometrial Carcinoma
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
E2 stimulated cell proliferation and induced GPR30 expression and PI3K/Akt pathway activation in endometrial cancer cells, Ishikawa cells, and HEC-1A cells, whereas the expression of ERs remained unchangeable.
|
23235274 |
2013 |
|
Endometrial Carcinoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
We evaluated the expression of Gankyrin in endometrial tissues and further explored its roles in estrogen-driven and GPR30-mediated endometrial cancer cell proliferation.
|
23142288 |
2013 |
|
Endometrial Carcinoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
These results provided new insights for understanding the pathophysiological functions of GPR30 in human endometrial cancers.
|
24039841 |
2013 |
|
Endometrial Carcinoma
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
GPER mediates the Egr-1 expression induced by 17β-estradiol and 4-hydroxitamoxifen in breast and endometrial cancer cells.
|
22147081 |
2012 |
|
Endometrial Carcinoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
Nuclear estrogen receptor-mediated Notch signaling and GPR30-mediated PI3K/AKT signaling in the regulation of endometrial cancer cell proliferation.
|
22075757 |
2012 |
|
Endometrial Carcinoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
These results support that GPER status adds clinically relevant information to ERα status in endometrial carcinoma and suggest a potential for new inhibitors in the treatment of metastatic endometrial cancers with ERα expression and GPER loss.
|
22415229 |
2012 |
|
Endometrial Carcinoma
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
GPR30 expression was also found in two human endometrial cancer cell lines: RL95-2 (estrogen receptor positive) and KLE (estrogen receptor negative).
|
19432902 |
2009 |
|
Endometrial Carcinoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
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.
|
19549922 |
2009 |
|
Endometrial Carcinoma
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
GPR30 represents an alternative estrogen-responsive receptor that is overexpressed in tumors where estrogen and progesterone receptors are downregulated, and in high-risk endometrial cancer patients with lower survival rates.
|
17403429 |
2007 |
|
Endometrial Carcinoma
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
Transfecting a GPR30 antisense expression vector in both endometrial cancer cell lines, OHT was no longer able to induce growth effects, whereas the proliferative response to E2 was completely abrogated only in HEC1A cells.
|
16239258 |
2006 |