Autophagy contributes to hypoxia-induced epithelial to mesenchymal transition of endometrial epithelial cells in endometriosis.

摘要: Endometriosis is a benign gynecologic disorder, and presents with malignant characteristics, such as migration invasion. Hypoxia has been implicated in triggering epithelial-mesenchymal transition (EMT). also known to induce autophagy. However, the relationship between autophagy EMT under hypoxia conditions endometriosis remains unknown. In present study, we found that expression of hypoxia-inducible factor-1α (HIF-1α), microtubule associated protein light chain 3 (LC3), mesenchymal cell marker vimentin was significantly higher ectopic endometrium from patients endometriosis, along decreased epithelial E-cadherin. After treatment, endometrial cells exhibited enhanced invasion abilities, well promoted phenotype. Our analyses show HIF-1α responsible for induction Moreover, inhibition by chemical or genetic approaches suppressed triggered reduced Collectively, our findings identify critical through indicate may be novel useful strategy treatment endometriosis.