Knockdown of miR-150-5p reduces hypoxia-induced autophagy and epithelial-mesenchymal transition of endometriotic cells via regulating the PDCD4/NF-?B signaling pathway

Background: Hypoxia is an important microenvironmental factor that induces Endometriosis (EMs), but its mechanism remains unclear. Our study aims to investigate the mechanisms of miR-150-5p on hypoxia-induced EMs.Methods: Ovarian endometriosis cyst wall stromal cell lines CRL-7566 cells were treated with hypoxia. Cell migration ability was measured by Transwell assay. qRT-PCR was performed to detect miR-150-5p and PDCD4 expression. The autophagy-related proteins (LC3-I, LC3-II, Beclin-1, and p62), epithelial-mesenchymal transition (EMT) related proteins (E-cadherin, N-cadherin, and Vimentin) and NF-Kappa B signaling pathway related proteins p65 expression were measured by western blot. Dual-luciferase reporter gene assay verified the binding rela-tionship between miR-150-5p and PDCD4. Results: After hypoxia treatment, the miR-150-5p expression was up-regulated in CRL-7566 cells, while the expression of PDCD4 was down-regulated. In CRL-7566 cells, autophagy, migration and EMT were increased after hypoxia treatment. The autophagy inhibitor 3-MA inhibited hypoxia-induced the autophagy, migration and EMT of CRL-7566 cells. Hypoxia-induced autophagy and EMT of CRL-7566 cells were inhibited after knocking down miR-150-5p. Then miR-150-5p negatively regulated PDCD4 expression. PDCD4 knockdown reversed the inhibitory effect of miR-150-5p silencing on hypoxia-induced autophagy and EMT of CRL-7566 cells. Inhibiting the NF-Kappa B signaling pathway weakened the effect of PDCD4 knockdown on hypoxia-induced autophagy and EMT of CRL-7566 cells.Conclusion: MiR-150-5p silencing inhibited hypoxia-induced autophagy and EMT of endometriotic cells by regulating the PDCD4/NF-Kappa B signaling pathway.