The role of miR-27b-3p/HOXA10 axis in the pathogenesis of endometriosis

Abstract

Background: To explore the effects of microRNA (miR)-27b-3p-mediated homeobox A10 (HOXA10) on the proliferation, migration, and invasion of endometriosis cells (hEM15A).Methods: First, quantitative polymerase chain reaction (qPCR) was performed for the measurement of miR-27b-3p and HOXA10 expression in hEM15A cells and human embryonic stem cells (hESC). Then, the targeted relationship of miR-27b-3p with HOXA10 was verified by conducting a dual-luciferase reporter experiment. Subsequently, qPCR and western blot were performed to determine the effect of miR-27b-3p on HOXA10 expression. Finally, Cell Counting Kit-8, Transwell, and scratch assays were employed to determine the effects of miR-27b-3p and HOXA10 on the proliferative, migratory, and invasive abilities of hEM15A cells.Results: In hEM15A cells, miR-27b-3p expression was increased and showed a negative correlation with the expression of HOXA10 (P<0.05). The dual-luciferase reporter experiment confirmed that miR-27b-3p targeted the HOXA10 gene. Furthermore, qPCR and western blotting showed that miR-27b-3p regulated the expression of HOXA10. The proliferation, migration, and invasion abilities of hEM15A cells was significantly inhibited by suppressing miR-27b-3p expression or overexpressing HOXA10 (P<0.05).Meanwhile, concurrent overexpression of miR-27b-3p and HOXA10 did not affect hEM15A cell activity (P>0.05).Conclusions: Upregulation of miR-27b-3p can suppress HOXA10 expression, resulting in the enhancement of hEM15A cell proliferation, migration, and invasion.

Downregulation of DROSHA: Could It Affect miRNA Biogenesis in Endometriotic Menstrual Blood Mesenchymal Stem Cells?

“…Furthermore, we linked these miRNAs to disease ( Table 1 ). The miRNAs miR-128-3p, miR-27a-3p, miR-27b-3p, miR-181a-5p, miR-181b-5p, miR-452-3p, miR-216a-5p, miR-216b-5p, and miR-93-5p are targets for future functional studies as they are related in endometriosis to diagnostic biomarkers [ 42 ], autophagy [ 43 ], and the regulation of inflammation, vascularization, and angiogenesis of the endometrium during the menstrual cycle and decidualization [ 44 ]; fibrosis modulation [ 45 ]; enhancement of cell proliferation, migration, and invasion [ 46 ]; expression influenced by E2 and BPA [ 44 ]; regulation of human endometrial stromal cell decidualization [ 55 ]; expression regulated by the menstrual cycle [ 42 ]; stromal cell invasion and migration [ 48 ]; expression exclusively in ectopic stromal cells [ 48 ]; and sustained cell proliferation, cellular adhesion, and apoptosis [ 52 ].…”