Background
Endometriosis is a gynecological non-malignant disease that is manifested by the presence of extrauterine ectopic endometrial cells and stroma. The
Conclusions
Our results indicated that the overexpression of TRADD prohibited migration, invasion, EMT, M1/M2 polarization and ectopic endometrial cysts formation in endometriosis, and this might due to regulating NF-κB and MAPK signaling.
Methods
Cell migration, invasion, and the expression of epithelial-mesenchymal transition (EMT) inducers in TRADD silencing or overexpression in eutopic endometrial stromal cells (EuSCs) and ectopic endometrial stromal cells (EcSCs) were analyzed by wound healing assay, transwell assay, quantitative reverse transcription polymerase chain reaction (qRT-PCR), western blotting and rat endometriosis model. A cell line derived from THP-1 macrophages was used to measure M1/M2 polarization in endometriosis by flow cytometry and enzyme-linked immunosorbent assay (ELISA).
Results
The mRNA level and protein expression of TRADD, keratin, E-cadherin, N-cadherin, vascular endothelial growth factor, matrix metalloproteinase-9, CD40, and CD206 were abnormally expressed in ectopic endometrial tissues and EcSCs. TRADD silencing promoted migration, invasion, and EMT in EuSCs, while TRADD overexpression restrained migration, invasion, and EMT in EcSCs. TRADD knockdown prohibited M1/M2 polarization in normal endometrial homogenization-treated THP-1-derived macrophages, whereas TRADD upregulation facilitated M1/M2 polarization in patients with endometrial homogenization-treated THP-1-derived macrophages. In addition, TRADD overexpression suppressed ectopic endometrial cysts formation in a rat endometriosis model. TRADD overexpression activated NF-κB and MAPK signaling in EcSCs and rat models. Conclusions: Our results indicated that the overexpression of TRADD prohibited migration, invasion, EMT, M1/M2 polarization and ectopic endometrial cysts formation in endometriosis, and this might due to regulating NF-κB and MAPK signaling.