Effect of GPER on the activation of PI3K/Akt induced by 17β-estradiol in endometrial carcinoma cells
10.3760/cma.j.issn.0529-567x.2012.04.011
- VernacularTitle:GPER在雌激素激活的子宫内膜癌细胞内PI3K/Akt信号通路中的作用
- Author:
Yancai ZHANG
;
Ruixia GUO
;
Xin GE
;
Yuhuan QIAO
- Publication Type:Journal Article
- Keywords:
Endometrial neoplasms;
Receptors,estrogen;
Receptors,G-protein-coupled;
Estradiol;
1-Phosphatidylinositol 3-kinase;
Proto-oncogene proteins c-akt
- From:
Chinese Journal of Obstetrics and Gynecology
2012;47(4):292-296
- CountryChina
- Language:Chinese
-
Abstract:
ObjectiveTo investigate the expression of G protein-coupled ER (GPER) and ER in the activation of phosphatidylinositol 3-kinase (PI3K)/protein kinase B (Akt) induced by 17β-estradiol (17β-E2 )in endometrial carcinoma cells,Ishikawa and HEC-1A.Methods Expressions of GPER,Erα and Erβ protein in Ishikawa and HEC-1A cells were detected by immunohistochemical SP method.Levels of GPER,Erα and Erβ were examined by western blot in Ishikawa and HEC-1A cells after treated with 1 ×10-6 mol/L 17β-E2 at different time (0,15,30,60,120 minutes).ResultsGPER was positive expressed in Ishikawa and HEC-1A cells.Erα and Erβ were both positive expressed in Ishikawa cells.While,Erα was weakly expressed and Erβ was almost negatively expressed in HEC-1A cells.Western blot analysis showed that 1× 10-6 mol/L 17β-E2 treatment,the Ishikawa and HEC-1A cells GPER protein level for 15 minutes markedly increased (P ＜ 0.05 ),which Ishikawa 30 minutes,when cells reached the highest level (0.192 ± 0.004),HEC-1A cells for 15 minutes and reached the highest level (0.184 ±0.006) ; Ishikawa and HEC-1A cells,Akt,activation of 15 minutes from the treatment start was significantly increased (P ＜ 0.05 ),which Ishikawa cells for 30 minutes and reached the highest level (0.666 ± 0.021 ),HEC-1A cells for 15 minutes and reached maximum (0.788 ± 0.035); Ishikawa and HEC-1 A cells,Erα and Erβ protein expression did not change significantly ( P ＞ 0.05 ).Conclusion GPER likely involved in non-nuclear activation of PI3K/Akt signaling pathways in endometrial carcinoma cells,Ishikawa and HEC-1A.
