MiR-20a contributes to endometriosis by regulating NTN4 expression.

Abstract

Endometriosis is a chronic disease that affects roughly 5-15 % of women of reproductive age. The pathophysiology of the disease occurrence and progression is unclear. MicroRNAs (miRNAs) are short, non-coding RNAs that have important regulatory function. It has been postulated that abnormal expression of miRNA is associated with ovarian endometriosis. Forty patients with ovarian endometriosis and 20 controls with benign ovarian tumor were included to examine the expression level of miR-20a. Quantitative real-time PCR (qPCR) was performed to detect the expression level of miR-20a. The target genes and pathways involved in aberrantly expressed miR-20a were identified by computational algorithms. Furthermore, selected target genes expression level were analyzed by qPCR. Significantly increased miR-20a expression level was observed in patients with ovarian endometriosis as compared with controls. Further stratified analysis showed that the increased expression level of miR-20a was only associated with advanced endometriosis (stage III-IV), but not mild endometriosis (stage I-II). The cell cycle was identified to be one of the most relevant pathways in the pathogenesis of endometriosis conducted by miR-20a. The expression level of target gene NTN4 (netrin-4) was significantly decreased in patients with ovarian endometriosis. The results of this study suggest that increased expression of miR-20a may play an important role in the pathogenesis of ovarian endometriosis by suppressing NTN4.