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17 beta-Estradiol activates PI3K/Akt signaling pathway by estrogen receptor (ER)-dependent and ER-independent mechanisms in endometrial cancer cells
Guo, RX; Wei, LH; Tu, Z; Sun, PM; Wang, JL; Zhao, D; Li, XP; Tang, JM
关键词endometrial carcinoma estradiol PI3K-Akt signal transduction pathway estrogen receptor
刊名JOURNAL OF STEROID BIOCHEMISTRY AND MOLECULAR BIOLOGY
2006-04-01
DOI10.1016/j.jsbmb.2005.11.013
99期:1页:9-18
收录类别SCI
文章类型Article
WOS标题词Science & Technology
类目[WOS]Biochemistry & Molecular Biology ; Endocrinology & Metabolism
研究领域[WOS]Biochemistry & Molecular Biology ; Endocrinology & Metabolism
关键词[WOS]NITRIC-OXIDE SYNTHASE ; STEROID-HORMONES ; KINASE-B ; ESTRADIOL ; GROWTH ; AKT ; PHOSPHORYLATION ; INHIBITION ; APOPTOSIS ; NEURONS
英文摘要

Cellular response to estrogen is mediated both by estrogen receptor (ER) binding to estrogen response element (ERE) and by non-nuclear actions like activation of signal transducing pathways. The main aims are to study if PI3K/Akt signaling pathway can be activated by 17 beta-estradiol (E2) via non-nuclear action and to investigate the relationship of the action of E2 and ER in endometrial cancer cells expressing with different status of ER. The levels of phosphorylated Akt (Ser(473)) (P-Akt) and total Akt were examined by western blot and Akt kinase activity was measured in cells after stimulation with 1 mu M E2 at different time points. Inhibitory role of LY294002 on activation of Akt induced by E2 and its estrogen antagonist, ICI182780 were also tested. P-Akt/Akt was used as a measure of activation of Akt. We found that maximum P-Akt/Akt and Akt kinase activity took place at 30 min in Ishikawa cells and 15 min in HEC-1A cells and the activation persisted for at least 2 h after stimulation with 1 mu M E2. The activation of Akt elicited gradually with increasing doses of E2. PI3K inhibitor, LY294002, stopped the activating Akt in a dose-dependent manner and 50 mu M LY294002 completely blocked the activation of Akt induced by E2. ICI182 780 could block the activation of PI3K/Akt in ER-positive Ishikawa cells but not in HEC-1A cells with poor-expressed ER. This study demonstrated that E2 is able to promptly activate PI3K/Akt signal pathway in Ishikawa cells in an ER-dependent manner and ER-independent in HEC-1A cells. Blockage of PI3K/Akt cascade may become a potential and effective way to control endometrial carcinoma, especially in ER-negative cancers, which show no response to endocrinal therapy. (c) 2006 Elsevier Ltd. All rights reserved.

语种英语
WOS记录号WOS:000237585200002
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被引频次:49[WOS]   [WOS记录]     [WOS相关记录]
文献类型期刊论文
条目标识符http://ir.bjmu.edu.cn/handle/400002259/63345
专题北京大学第二临床医学院_妇科
作者单位1.Peking Univ, Peoples Hosp 11, Dept Gynecol, Beijing 100044, Peoples R China
2.Zhengzhou Univ, Teaching Hosp 1, Dept Obstet & Gynecol, Zhengzhou 450052, Peoples R China
3.Peking Univ, Peoples Hosp, Dept Internal Med, Beijing 100044, Peoples R China
4.Charite Univ, Dept Gynecol & Obstet, Tumor Ovarian Canc Grp, D-13353 Berlin, Germany
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Guo, RX,Wei, LH,Tu, Z,et al. 17 beta-Estradiol activates PI3K/Akt signaling pathway by estrogen receptor (ER)-dependent and ER-independent mechanisms in endometrial cancer cells[J]. JOURNAL OF STEROID BIOCHEMISTRY AND MOLECULAR BIOLOGY,2006,99(1):9-18.
APA Guo, RX.,Wei, LH.,Tu, Z.,Sun, PM.,Wang, JL.,...&Tang, JM.(2006).17 beta-Estradiol activates PI3K/Akt signaling pathway by estrogen receptor (ER)-dependent and ER-independent mechanisms in endometrial cancer cells.JOURNAL OF STEROID BIOCHEMISTRY AND MOLECULAR BIOLOGY,99(1),9-18.
MLA Guo, RX,et al."17 beta-Estradiol activates PI3K/Akt signaling pathway by estrogen receptor (ER)-dependent and ER-independent mechanisms in endometrial cancer cells".JOURNAL OF STEROID BIOCHEMISTRY AND MOLECULAR BIOLOGY 99.1(2006):9-18.
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