The Increased lncRNA MIR503HG in Preeclampsia Modulated Trophoblast Cell Proliferation, Invasion, and Migration via Regulating Matrix Metalloproteinases and NF-κB Signaling
Joint Authors
Cheng, Dan
Jiang, Shan
Chen, Jiao
Li, Jie
Ao, Liangfei
Zhang, Ying
Source
Issue
Vol. 2019, Issue 2019 (31 Dec. 2019), pp.1-12, 12 p.
Publisher
Hindawi Publishing Corporation
Publication Date
2019-07-30
Country of Publication
Egypt
No. of Pages
12
Main Subjects
Abstract EN
Background.
Preeclampsia (PE) is a pregnancy-related syndrome characterized by hypertension and proteinuria after the 20th week of gestation.
The long noncoding RNAs (lncRNAs) have been recently discovered for their roles in the pathogenesis of PE.
This study is aimed at determining the expression of lncRNA MIR503 host gene (MIR503HG) in PE placental tissues and exploring the molecular mechanism underlying MIR503HG-mediated trophoblast cell proliferation, invasion, and migration.
Methods.
The expression level of MIR503HG in placental tissues, HTR-8/SVneo, and JEG3 cells was determined by quantitative real-time PCR; western blot detected the relevant protein expression levels in HTR-8/SVneo and JEG3 cells; flow cytometry determined cell apoptosis and cell cycle of HTR-8/SVneo and JEG3 cells; trophoblast cell proliferation, invasion, and migration of HTR-8/SVneo and JEG3 cells were measured by CCK-8, transwell invasion, and wound healing assays, respectively.
Results.
The highly expressed MIR503HG was detected in PE placental tissues compared to normal placental tissues.
MIR503HG overexpression suppressed cell proliferation, invasion, and migration of HTR-8/SVneo and JEG3 cells, while knockdown of MIR503HG increased trophoblast cell proliferation, invasion, and migration.
Flow cytometry results showed that MIR503HG overexpression induced apoptosis and caused cell cycle arrest at the G0/G1 phase, while MIR503HG knockdown had the opposite actions in HTR-8/SVneo and JEG3 cells.
Western blot assay results showed that MIR503HG overexpression suppressed the matrix metalloproteinase-2/-9 and the snail protein expression and increased the E-cadherin expression in trophoblast cells.
In addition, MIR503HG overexpression suppressed the NF-κB signaling pathway by inhibiting the phosphorylation of IκBα and the nuclear translocation of NF-κB signaling subunit p65.
On the other hand, MIR503HG knockdown played an opposite role in these protein expression levels.
Conclusion.
Our results showed that MIR503HG inhibited the proliferation, invasion, and migration of HTR-8/SVneo and JEG3 cells, which may be related to the pathogenesis of PE.
American Psychological Association (APA)
Cheng, Dan& Jiang, Shan& Chen, Jiao& Li, Jie& Ao, Liangfei& Zhang, Ying. 2019. The Increased lncRNA MIR503HG in Preeclampsia Modulated Trophoblast Cell Proliferation, Invasion, and Migration via Regulating Matrix Metalloproteinases and NF-κB Signaling. Disease Markers،Vol. 2019, no. 2019, pp.1-12.
https://search.emarefa.net/detail/BIM-1147290
Modern Language Association (MLA)
Cheng, Dan…[et al.]. The Increased lncRNA MIR503HG in Preeclampsia Modulated Trophoblast Cell Proliferation, Invasion, and Migration via Regulating Matrix Metalloproteinases and NF-κB Signaling. Disease Markers No. 2019 (2019), pp.1-12.
https://search.emarefa.net/detail/BIM-1147290
American Medical Association (AMA)
Cheng, Dan& Jiang, Shan& Chen, Jiao& Li, Jie& Ao, Liangfei& Zhang, Ying. The Increased lncRNA MIR503HG in Preeclampsia Modulated Trophoblast Cell Proliferation, Invasion, and Migration via Regulating Matrix Metalloproteinases and NF-κB Signaling. Disease Markers. 2019. Vol. 2019, no. 2019, pp.1-12.
https://search.emarefa.net/detail/BIM-1147290
Data Type
Journal Articles
Language
English
Notes
Includes bibliographical references
Record ID
BIM-1147290