Molecular and cellular endocrinology, 2010-04, Vol.317 (1-2), p.31
2010
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- Autor(en) / Beteiligte
- Titel
- 17betaE2 promotes cell proliferation in endometriosis by decreasing PTEN via NFkappaB-dependent pathway
- Ist Teil von
- Molecular and cellular endocrinology, 2010-04, Vol.317 (1-2), p.31
- Ort / Verlag
- Ireland
- Erscheinungsjahr
- 2010
- Quelle
- MEDLINE
- Beschreibungen/Notizen
- 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 (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. 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.
- Sprache
- Englisch
- Identifikatoren
- eISSN: 1872-8057DOI: 10.1016/j.mce.2009.11.009Titel-ID: cdi_pubmed_primary_19932734
- Format
- –
- Schlagworte
- Adult, Cell Nucleus - drug effects, Cell Nucleus - enzymology, Cell Proliferation - drug effects, DNA - metabolism, Endometriosis - enzymology, Endometriosis - pathology, Enzyme Activation - drug effects, Epithelial Cells - drug effects, Epithelial Cells - enzymology, Epithelial Cells - pathology, Estradiol - pharmacology, Female, Humans, MAP Kinase Signaling System - drug effects, NF-kappa B - metabolism, Phosphatidylinositol 3-Kinases - metabolism, Phosphorylation - drug effects, Protein Binding - drug effects, Protein Transport - drug effects, Proto-Oncogene Proteins c-akt - metabolism, PTEN Phosphohydrolase - deficiency, PTEN Phosphohydrolase - genetics, PTEN Phosphohydrolase - metabolism, Signal Transduction - drug effects, Subcellular Fractions - drug effects, Subcellular Fractions - metabolism, Transcription, Genetic - drug effects