LncRNA-NEAT1 blocks the Wnt/β-catenin signaling pathway by targeting miR-217 to inhibit trophoblast cell migration and invasion

Author:

Jiang Ling-lingORCID,Yang Dan-lin,Han Qing,Zhang Hua-le,Pan Mian,Yan Jian-ying

Abstract

Abstract Objective This study aimed to study the correlation between preeclampsia (PE) and lncRNA nuclear paraspeckle assembly transcript 1 (NEAT1), and to examine the molecular mechanisms behind the development of PE. Methods 30 PE and 30 normal pregnant women placental samples were assessed the levels of NEAT1 and miR-217 by quantitative real-time PCR (qRT-PCR). The trophoblast cell line HTR8/SVneo was used for silencing NEAT1 or miR-217 inhibitor in the absence or presence of an inhibitor and H2O2. Cell counting Kit 8 (CCK-8), flow cytometry, and Transwell were used to detect cell proliferation, apoptosis, migration, and invasion. Luciferase reporter gene assay was utilized to verify the binding between miR-217 and Wnt family member 3 (Wnt3), and between the miR-217 and NEAT1. Proteins related to the Wnt/β-catenin signaling pathway were detected using western blotting. Results The PE group exhibited a significantly downregulated expression of miR-217 and a significantly upregulated expression of NEAT1. NEAT1 targeted miR-217, and Wnt is a miR-217 target gene. siRNA-NEAT1 inhibited the apoptosis of trophoblast cells, but promoted their invasion, migration, and proliferation. MiR-217 inhibitor could partially reverse the effects of siRNA-NEAT1. The expression of the Wnt/β-catenin signaling pathway-related proteins, WNT signaling pathway inhibitor 1 (DKK1), cyclin-D1 and β-catenin, was significantly increased after siRNA-NEAT1. Conclusions NEAT1 could reduce trophoblast cell invasion and migration by suppressing miR-217/Wnt signaling pathway, leading to PE.

Funder

Startup Fund for scientific research, Fujian Medical University

Joint Funds for the innovation of science and Technology, Fujian province

Technology Project of Fujian Maternity and Child Health Hospital, Affiliated Hospital of Fujian Medical University

Fujian Province Natural Science Foundation

Publisher

Springer Science and Business Media LLC

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