miR-9-5p promotes the invasion and migration of endometrial stromal cells in endometriosis patients through the SIRT1/NF-κB pathway

摘要

Objective: The present study was designed to investigate the expression of miR-9-5p and to study the effect of miR-9-5p expression on the invasion and migration of endometrial stromal cells in endometriosis patients. Methods: We recruited 17 eutopic endometrium patients, 19 ectopic endometrium patients, and 13 normal endometrium patients, and we measured their miR-9-5p and SIRT1 expressions. Western blot was used to measure the protein expressions, and cellular immunofluorescence was used to check the positions of the p65 position protein in cells. A Transwell chamber and cell scratch tests were used to test cell invasion and migration, respectively. Results: miR-9-5p was highly expressed, and SIRT1 was lowly expressed in the endometria of the endometriosis patients, and there was a negative correlation between miR-9-5p and SIRT1 mRNA in the endometriosis patients. A dual luciferase reporter gene system showed that miR-9-5p targeted the inhibition of SIRT1 expression in the endometrial stromal cells. Moreover, the up-regulation of miR-9-5p expression using the miR-9-5p-mimics significantly increased the distance of endometrial stromal cell migration and the number of cells that entered into the lower chamber of the Transwell chamber, and the down-regulation of miR-9-5p using the miR-9-5p-inhibitor significantly decreased the distance of endometrial stromal cell migration and the number of cells that entered into the lower chamber of the Transwell chamber. Moreover, the miR-9-5p-mimics significantly increased the expressions of the P-p65/p65 protein and the 65 protein in the nuclei, and the miR-9-5p-inhibitor significantly decreased the expressions of the P-p65/p65 protein and the 65 protein in the nuclei. Conclusion: miR-9-5p is highly expressed in the endometria of endometriosis patients, and miR-9-5p can promote the invasion and migration of endometrial stromal cells in vitro by targeting the SIRT1 expression via the NF-κB pathway.