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

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.