北京大学医学部机构知识库
Advanced  
IR@PKUHSC  > 北京大学第二临床医学院  > 妇科  > 期刊论文
学科主题: 临床医学
题名:
17 beta-Estradiol activates PI3K/Akt signaling pathway by estrogen receptor (ER)-dependent and ER-independent mechanisms in endometrial cancer cells
作者: 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
发表日期: 2006-04-01
DOI: 10.1016/j.jsbmb.2005.11.013
卷: 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
Citation statistics:
内容类型: 期刊论文
URI标识: http://ir.bjmu.edu.cn/handle/400002259/63345
Appears in Collections:北京大学第二临床医学院_妇科_期刊论文

Files in This Item:

There are no files associated with this item.


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

Recommended Citation:
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.
Service
Recommend this item
Sava as my favorate item
Show this item's statistics
Export Endnote File
Google Scholar
Similar articles in Google Scholar
[Guo, RX]'s Articles
[Wei, LH]'s Articles
[Tu, Z]'s Articles
CSDL cross search
Similar articles in CSDL Cross Search
[Guo, RX]‘s Articles
[Wei, LH]‘s Articles
[Tu, Z]‘s Articles
Related Copyright Policies
Null
Social Bookmarking
Add to CiteULike Add to Connotea Add to Del.icio.us Add to Digg Add to Reddit
所有评论 (0)
暂无评论
 
评注功能仅针对注册用户开放,请您登录
您对该条目有什么异议,请填写以下表单,管理员会尽快联系您。
内 容:
Email:  *
单位:
验证码:   刷新
您在IR的使用过程中有什么好的想法或者建议可以反馈给我们。
标 题:
 *
内 容:
Email:  *
验证码:   刷新

Items in IR are protected by copyright, with all rights reserved, unless otherwise indicated.

 

 

Valid XHTML 1.0!
Copyright © 2007-2017  北京大学医学部 - Feedback
Powered by CSpace