lncRNA SNHG14 involved in trophoblast cell proliferation, migration, invasion and epithelial-mesenchymal transition by targeting miR-330-5p in preeclampsia

Preeclampsia (PE), a pregnancy-specific disease, has become one of the leading causes of maternal and neonatal morbidity and mortality. Pathogenesis of PE has still not been fully addressed and there is a great need to develop early diagnosis markers and effective therapy. This study aimed to determ...

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Bibliographic Details
Published in:Zygote (Cambridge) 2021-04, Vol.29 (2), p.108-117
Main Authors: Zhang, Yulei, Zhang, Muling
Format: Article
Language:English
Subjects:
Apoptosis
Assaying
Binding
Binding sites
Cell cycle
Cell growth
Cell migration
Cell proliferation
Gene expression
Mesenchyme
Morbidity
Neonates
Pathogenesis
Peripheral blood
Placenta
Pre-eclampsia
Preeclampsia
Reagents
Wound healing
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Summary:Preeclampsia (PE), a pregnancy-specific disease, has become one of the leading causes of maternal and neonatal morbidity and mortality. Pathogenesis of PE has still not been fully addressed and there is a great need to develop early diagnosis markers and effective therapy. This study aimed to determine if lncRNA SNHG14 has a protective effect on placental trophoblast and prevents PE. SNHG14 levels in the peripheral blood from patients with PE or from women with healthy pregnancies were detected using RT-qPCR. The relationship between SNHG14 and miR-330-5p was determined using a dual-luciferase reporter assay. In addition, cell proliferation and cell cycle were evaluated by performing CCK8 assays and flow-cytometric analysis, respectively. Wound-healing and transwell assays were performed to assess cell migration and invasion ability. lncRNA SNHG14 was downregulated in PE patients; it was involved in trophoblast proliferation and regulated cell proliferation during G1/S transition. In addition, lncRNA SNHG14 promoted migration, invasion and epithelial-mesenchymal transition (EMT) in HTR-8/SVneo cells. Luciferase reporter assay indicated that lncRNA SNHG14 served as a molecular sponge for miR-330-5p and negatively regulated miR-330-5p expression in PE. Furthermore, the effects of silenced SNHG14 on trophoblast proliferation, migration, invasion and EMT were reversed by addition of miR-330-5p inhibitor, suggesting that in PE lncRNA SNHG14 functions by competitively binding to miR-330-5p. Taken together, the current study demonstrated that in PE lncRNA SNHG14 is a vital regulator by binding to miR-330-5p. SNHG14 might serve as a therapeutic application in PE progression.
ISSN:0967-1994
1469-8730
DOI:10.1017/S0967199420000507