{"paper_id":"36e4930e-f126-4474-8587-db5f441b1304","body_text":"Abstract\nEndometriosis is a common benign gynecological disease defined as the presence of endometrial tissue outside the uterine cavity. The aim of this study was to identify the molecular mechanism underlying hypoxia-induced increases in invasive ability of human endometrial stromal cells (HESCs). Herein, we show that the expression levels of hypoxia-inducible factor lα (HIF-1α) and β-catenin were greater in ectopic endometriotic tissue compared with eutopic tissue from controls. Exposure of eutopic endometrial stromal cells under hypoxic conditions or treated with desferrioxamine (DFO, chemical hypoxia) resulted in a time-dependent increase in β-catenin expression and its dephosphorylation. Hypoxia/HIF-1α also activated the β-catenin/T-cell factor (TCF) signaling pathway and the expression of target genes, vascular endothelial growth factor and matrix metalloproteinase 9, and knockdown of HIF-1α or β-catenin abrogated hypoxia-induced increases in HESC invasiveness. These results suggest that HIF-1α interacting with β-catenin/TCF signaling pathway, which is activated by hypoxia, may provide new insights into the etiology of endometriosis.\nSimilar content being viewed by others\nReferences\nGiudice LC, Kao LC. Endometriosis. Lancet. 2004; 364(9447):1789–1799.\nHalme J, Hammond MG, Hulka JF, Raj SG, Talbert LM. Retrograde menstruation in healthy women and in patients with endometriosis. Obstet Gynecol. 1984; 64(2):151–154.\nOlive DL, Pritts EA. Treatment of endometriosis. N Engl J Med. 2001; 345(4):266–275.\nFigueira PG, Abrao MS, Krikun G, Taylor HS. Stem cells in endometrium and their role in the pathogenesis of endometriosis. 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