Decreased expression of long non-coding RNA SNHG7 cause recurrent spontaneous abortion through suppression proliferation and invasion of trophoblast cells via miR-34a.

Little is known about the role of long non-coding RNA SNHG7-1 in the development of recurrent spontaneous abortion (RSA). The aim of the present study was to investigate the levels of SNHG7-1 in villi of RSA, and explore its underlying mechanism. The qRT-PCR assay SNHG7-1 showed that the expression level was downregulated in RSA and HTR-8/SVneo cells. In addition, the growth rate of cells transfected with si-SNHG7-1 was significantly decreased compared to that with si-NC, which was reversed by miR-34a targeted with 3'-UTR. Moreover, miR-34a suppressed the expression of WNT1 by binding with the 3'-UTR, which interact with WNT1 to inhibit the proliferation of cells. Furthermore, miR-34a inhibitor rescued the dysregulation of WNT1, p-β-catenin, β-catenin, cyclinD and c-Myc by si-SNHG7A-1. In short, the current study suggests SNHG7-1 plays as an important role in RSA progression targeted by miR-34a via Wnt/β-catenin signaling pathway, providing a novel insight for the pathogenesis and underlying therapeutic target for RSA.