Autophagy contributes to hypoxia-induced epithelial to mesenchymal transition of endometrial epithelial cells in endometriosis†
| Autor: | Zhibing Zhang, Yi Liu, Ling Zhang, Qi Li, Haitang He, Wenqian Xiong, Yu Du, Liqun Lv, Hengwei Liu, Na Li |
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| Rok vydání: | 2018 |
| Předmět: |
Adult
0301 basic medicine Epithelial-Mesenchymal Transition Endometriosis Vimentin Biology Cell Line Endometrium 03 medical and health sciences Cell Movement Autophagy medicine Humans S100 Calcium-Binding Protein A4 Epithelial–mesenchymal transition Hypoxia Mesenchymal stem cell Epithelial Cells Cell migration Cell Biology General Medicine Middle Aged Hypoxia (medical) Cadherins Hypoxia-Inducible Factor 1 alpha Subunit medicine.disease 030104 developmental biology Reproductive Medicine Cell culture Cancer research biology.protein Female medicine.symptom Microtubule-Associated Proteins Research Article |
| Zdroj: | Biology of Reproduction. 99:968-981 |
| ISSN: | 1529-7268 0006-3363 |
| Popis: | Endometriosis is a benign gynecologic disorder, and presents with malignant characteristics, such as migration and invasion. Hypoxia has been implicated in triggering epithelial–mesenchymal transition (EMT). Hypoxia is also known to induce autophagy. However, the relationship between autophagy and EMT under hypoxia conditions in endometriosis remains unknown. In the present study, we found that the expression of hypoxia-inducible factor-1α (HIF-1α), microtubule associated protein light chain 3 (LC3), and mesenchymal cell marker vimentin was significantly higher in ectopic endometrium from patients with endometriosis, along with decreased expression of epithelial cell marker E-cadherin. After hypoxia treatment, endometrial epithelial cells exhibited enhanced migration and invasion abilities, as well as promoted autophagy and the EMT phenotype. Our analyses also show that HIF-1α was responsible for induction of autophagy. Moreover, inhibition of autophagy by chemical or genetic approaches suppressed hypoxia triggered EMT and reduced cell migration and invasion. Collectively, our findings identify that autophagy is critical for the migration and invasion of endometrial cells through the induction of EMT and indicate that inhibition of autophagy may be a novel useful strategy in the treatment of endometriosis. |
| Databáze: | OpenAIRE |
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