Overexpressed miR-106b-5p promotes epithelial-mesenchymal transition in endometriosis by targeting PTEN.

ABSTRACT

The miRNA miR-106b-5p expression is elevated in endometriotic lesions. This study aimed to detect miR-106b-5p expression in human endometrial stromal cells and explore the molecular mechanisms regulating proliferation, migration, and epithelial-mesenchymal transition (EMT) of these cells. Cell proliferation, migration, and EMT were compared after miR-106b-5p upregulation. The downstream target of miR-106b-5p was verified using bioinformatic, luciferase reporter, and rescue assays. The relationship between miR-106b-5p and the target genes was also analyzed. Results showed that the expression of miR-106b-5p in endometriotic lesions was higher than that in non-lesion tissues. Furthermore, upregulation of miR-106b-5p promoted the proliferation, migration, and EMT of human endometrial stromal cells. Additionally, phosphatase and tensin homolog ten (PTEN) was found to be negatively correlated with miR-106b-5p expression. Low expression levels of PTEN were significantly correlated with cell proliferation, migration, and EMT. High PTEN expression could rescue the effect of miR-106b-5p on cell capacity. In conclusion, miR-106b-5p modified human endometrial stromal cell function by sponging PTEN. These findings indicate that inhibition of miR-106b-5p may be an effective therapeutic strategy for endometriosis.