LINC01541 Functions as a ceRNA to Modulate the Wnt/β-Catenin Pathway by Decoying miR-506-5p in Endometriosis.

Abstract

Endometriosis is one of the most common gynecological diseases that adversely effects the lives of women. Our previous studies showed that LINC01541 plays a key role in 17β-estradiol (17β-E2)-stimulated endometrial stromal cells (ESCs); however, the mechanism by which LINC01541 exerts if effects requires further elaboration. Here, we report that LINC01541 serves to reduce the bioavailability of miR-506-5p by acting as a molecular sponge. Samples of control endometrial tissue and ectopic endometrial tissue were obtained from 10 healthy volunteers and 18 patients with endometriosis, respectively, and the levels of LINC01541 and miR-506-5p expressions in those tissues were measured. The relationship between LINC01541 and miR-506-5p was verified in 17β-E2-stimulated ESCs. Overexpression or silencing of miR-506-5p in ESCs was performed explore its role in endometriosis, and we also investigated whether WNT inhibitory factor 1 (WIF1) might be a target gene of miR-506-5p. Our results showed that LINC01541 was expressed at low levels and miR-506-5p was expressed at high levels in ectopic tissues. LINC01541 expression was negatively correlated with miR-506-5p expression. We also found that miR-506-5p activated the Wnt/β-catenin pathway by inhibiting WIF1 expression, and thereby induced the proliferation, migration, and invasion of ESCs. Furthermore, silencing of miR-506-5p promoted apoptosis and suppressed the proliferation of 17β-E2-treated ESCs. Overexpression of miR-506-5p could reverse the inhibitory effect of LINC01541 in endometriosis. In summary, this study found that in endometriosis, LINC01541 functions as a ceRNA that modulates the Wnt/β-catenin pathway by decoying miR-506-5p.