Overexpression of long non-coding RNA NEAT1 enhances cell viability and inhibits apoptosis in recurrent spontaneous abortion by targeting the miR-125b/BCL-2 axis.

Abstract

The current study aimed to investigate the function of the long non-coding RNA nuclear paraspeckle assembly transcript 1 (NEAT1) in the pathogenesis of recurrent spontaneous abortion (RSA) and to examine its potential mechanism. The expression of NEAT1, microRNA (miR)-125b and Bcl-2 in the villi of patients with RSAs and women with normal pregnancies was measured by reverse transcription-quantitative PCR. Cell viability was detected by the MTT assay and cell apoptosis was evaluated by flow cytometry. A dual-luciferase reporter assay was performed to verify the associations between NEAT1 and miR-125b. The protein expression of Bcl-2 was detected by western blot analysis. In the present study, the expression of NEAT1 and Bcl-2 was reduced and that of miR-125b was increased in clinical samples of villus tissues from patients with RSAs. In vitro, overexpression of NEAT1 enhanced the viability and suppressed the apoptosis of JEG-3 cells. It was demonstrated that miR-125b acts as a molecular sponge of NEAT1 and its expression was negatively regulated by NEAT1. miR-125b overexpression reduced the viability and promoted the apoptosis of JEG-3 cells. The expression of BCL-2, a target gene of miR-125b, was inversely correlated with that of miR-125b. Overexpression of miR-125b and inhibition of BCL-2 partially reversed the effect of NEAT1 overexpression on the viability and apoptosis of JEG-3 cells. Collectively, it was demonstrated that the NEAT1/miR-125b/BCL-2 axis plays a pivotal role in regulating the viability and apoptosis of JEG-3 cells. The findings of the present study offer new insights into the pathogenesis of RSA and may provide information on RSA treatment.