MicroRNA‑27a inhibits trophoblast cell migration and invasion by targeting SMAD2: Potential role in preeclampsia

Abstract

Preeclampsia (PE) is a severe idiopathic obstetric complication that occurs worldwide. Insufficient tropho-blast invasion is a characteristic of the pathogenesis of PE. MicroRNA-27a (miR-27a) has been reported to be highly expressed in PE placentas. The aim of the present study was to investigate the role and underlying mechanisms of miR-27a in the pathogenesis of PE. The expression level of miR-27a was evaluated in the placenta and serum from patients with PE and healthy pregnant women. Cell Counting Kit-8 and flow cytom-etry assays were performed to detect human HTR-8/SVneo trophoblast proliferation and apoptosis after miR-27a over-expression or inhibition. In addition, Transwell assays were used to measure cell migration and invasion. A luciferase reporter assay was performed to determine the interaction between miR-27a and SMAD2. The present results suggested that miR-27a expression level was significantly increased in PE placentas and serum. In addition, miR-27a overexpression suppressed cell migratory and invasive abilities, impaired proliferation and promoted apoptosis in human trophoblasts. It was demonstrated that miR-27a may target SMAD and contribute to trophoblast invasion. Collectively, the results of the present study suggested that miR-27a inhibited tropho-blast cell migration and invasion by targeting SMAD2, thus presenting a promising therapeutic target for PE.