Overexpression of TAFI promotes epithelial mesenchymal transition in endometriosis.

OBJECTIVE: Endometriosis is a disease that occurs in women. Thrombin-activated fibrinolytic inhibitor (TAFI) is mainly secreted by stem cells and acts as a regulatory role in the body. Epithelial leaf transition plays a leading role in cell growth and invasion. Our study focuses on the mechanism of TAFI in patients with endometriosis. PATIENTS AND METHODS: The expression of TAFI was determined by immunohistochemistry. Reverse transcriptase-polymerase chain reaction (RT-PCR) served to detect the expression of TAFI and the effect of TAFI on overall survival (OS) and progression-free survival (PFS) levels. The changes of primary cytology in patients with endometriosis were observed under a microscope. The cell source was further determined by immunofluorescence labeling of vimentin and cytokeratin, and the expression of TAFI was detected by Western-blot. 3-4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide (MTT) and cell invasion assay were utilized to detect the viability and aggressiveness of cells after epithelial mesenchymal transition (EMT). RESULTS: TAFI was overexpressed in endometriosis tissues and no expression of TAFI was found in normal tissues, which is consistent with RT-PCR results. TAFI overexpressed endometriosis patients had low levels of overall OS and PFS. There were statistically significant differences. Cell morphology shows that endometriosis primary cells are mainly composed of epithelial cells and fibroblasts. Immunofluorescence assay showed that vimentin and cytokeratin were expressed in cells, and the expression of TAFI was detected by Western-blot. Compared with normal tissues, TAFI was considerably higher in patients with endometriosis. The results of Western-blot and RT-PCR showed that the expression of TAFI was significantly increased in patients with endometriosis and the cell proliferation and cell invasion were significantly accelerated. CONCLUSIONS: Our results show that TAFI is highly expressed in endometriosis and causes EMT, which accelerated the cell proliferation and cell invasion. Snail is an inhibitor of E-cadherin, which may participate in metastasis and invasion of endometriosis by mediating EMT. So, we suspect that Snail controls the occurrence of the EMT and then affects the cell metastasis and invasion, which requires further verification.