17βE2 promotes cell proliferation in endometriosis by decreasing PTEN via NFκB-dependent pathway

Zhang H, Hui Zhang, Zhao X, Xingbo Zhao, Xingbo Ζhao, Liu S, Shu Liu, Jijun Li, Li J, Zeqing Wen, Wen Z, Mingjiang Li, Li M
Molecular and cellular endocrinology · 2009 · vol. 317(1-2) , pp. 31–43 · doi:10.1016/j.mce.2009.11.009 · PMID:19932734 · W2017190024
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⚙ AI-generated summary by claude@2026-06, 2026-06-09 ⓘ

17β estradiol (E2) accelerates endometriosis cell growth by reducing PTEN expression, a process mediated by the NFκB signaling pathway.

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Abstract

UnlabelledThe 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 (NFkappaB) signaling overactivities coexisted in endometriosis. In vitro, 17beta-estradiol rapidly activated the 3 pathways in endometriotic cells and specific inhibitions on the 3 pathways respectively blocked 17beta-estradiol-induced cell proliferation. 17beta-estradiol suppressed PTEN transcription and expression in endometriotic cells which was abolished by specific NFkappaB inhibition.Conclusion(s)Total/nuclear PTEN-loss and MAPK/ERK, PI3K/AKt, and NFkappaB signal overactivities coexist in endometriosis. In vitro, 17beta-estradiol can promotes cell proliferation in endometriosis by activating PI3K/AKt pathway via an NFkappaB/PTEN-dependent pathway. For the first time we propose the possibility of the presence of a positive feedback-loop: 17beta-estradiol-->high NFkappaB-->low PTEN-->high PI3K-->high NFkappaB, in endometriosis, which may finally promote the proliferation of ectopic endometrial epithelial cells and in turn contributes to the progression of the disease.

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Condition tags

endometriosis

MeSH descriptors

Endometriosis Endometriosis Estradiol NF-kappa B PTEN Phosphohydrolase Signal Transduction Adult Cell Nucleus Cell Nucleus Cell Nucleus Cell Proliferation Cell Proliferation DNA DNA Endometriosis Enzyme Activation Enzyme Activation Epithelial Cells Epithelial Cells Epithelial Cells

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