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

Hengwei Liu, Yu Du, Zhibing Zhang, Liqun Lv, Wenqian Xiong, Ling Zhang, Na Li, Haitang He, Qi Li, Yi Liu
Biology of reproduction · 2018 · vol. 99(5) , pp. 968–981 · doi:10.1093/biolre/ioy128 · PMID:29860279 · W2807648383
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Hypoxia induces autophagy and epithelial-mesenchymal transition in endometrial cells, promoting migration and invasion, with HIF-1α mediating this process.

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Abstract

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.

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Condition tags

mesh:D004715endometriosis

MeSH descriptors

Autophagy Endometriosis Endometrium Epithelial Cells Epithelial-Mesenchymal Transition Hypoxia Adult Cadherins Cadherins Cell Line Cell Movement Endometriosis Endometrium Epithelial Cells Female Humans Hypoxia Hypoxia-Inducible Factor 1, alpha Subunit Hypoxia-Inducible Factor 1, alpha Subunit Microtubule-Associated Proteins

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Papers in the corpus that this work cites (lower rings, blue) and that cite this one (upper rings, green). Dot size scales with the paper's in-corpus citation count — bigger dot = more influential within the endo/adeno field. Click a dot to open that paper. [ expand to 2 hops ] — adds papers reached through this work's immediate citers/citees. Heavier; up to 60 extra dots.

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