标题:17 beta E-2 promotes cell proliferation in endometriosis by decreasing PTEN via NF kappa B-dependent pathway
作者:Zhang, Hui; Zhao, Xingbo; Liu, Shu; Li, Jijun; Wen, Zeqing; Li, Mingjiang
作者机构:[Zhang, Hui; Zhao, Xingbo; Liu, Shu; Li, Jijun; Wen, Zeqing; Li, Mingjiang] Shandong Univ, Dept Obstet & Gynecol, Prov Hosp, Jinan 250021, Shandong, P 更多
通讯作者:Li, MJ
通讯作者地址:[Li, MJ]Shandong Univ, Dept Obstet & Gynecol, Prov Hosp, 324 Jingwu Rd, Jinan 250021, Shandong, Peoples R China.
来源:MOLECULAR AND CELLULAR ENDOCRINOLOGY
出版年:2010
卷:317
期:1-2
页码:31-43
DOI:10.1016/j.mce.2009.11.009
关键词:PTEN; MAPK/ERK/p-ERK; PI2K/AKt/p-AKt; NF kappa B; 17 beta-Estradiol;; Endometriosis
摘要:The objective of this study was to explore the mechanism of phosphatase and tensin homolog (PTEN) loss in endometriosis. We found that aberrant PTEN expression and mitogen-activated protein kinases (MAPK)/ERK, phosphoinositide 3-kinase (PI3K)/AKt, and nuclear factor-kappaB (NF kappa B) signaling overactivities coexisted in endometriosis. In vitro, 17 beta-estradiol rapidly activated the 3 pathways in endometriotic cells and specific inhibitions on the 3 pathways respectively blocked 17 beta-estradiol-induced cell proliferation. 17 beta-estradiol suppressed PTEN transcription and expression in endometriotic cells which was abolished by specific NF kappa B inhibition.; Conclusion(s): Total/nuclear PTEN-loss and MAPK/ERK, PI3K/AKt, and NF kappa B signal overactivities coexist in endometriosis. In vitro, 17 beta-estradiol can promotes cell proliferation in endometriosis by activating PI3K/AKt pathway via an NF kappa B/PTEN-dependent pathway. For the first time we propose the possibility of the presence of a positive feedback-loop: 17 beta-estradiol -> high NF kappa B -> low PTEN -> high PI3K -> high NF kappa B, in endometriosis, which may finally promote the proliferation of ectopic endometrial epithelial cells and in turn contributes to the progression of the disease. (C) 2009 Elsevier Ireland Ltd. All rights reserved.
收录类别:SCIE
WOS核心被引频次:45
资源类型:期刊论文
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