Promotion of trophoblast invasion by lnc<scp>RNA MVIH</scp> through inducing Jun‐B

Zou, Yanfen; Li, Qian; Xu, Yetao; Yu, Xiang; Zuo, Qiang; Huang, Shiyun; Chu, Yongli; Jiang, Ziyan; Sun, Lichao

doi:10.1111/jcmm.13400

Cited by 21 publications

(18 citation statements)

References 30 publications

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“…The lncRNAs are localized in the nucleus and are enriched in the chromatin or specific subnuclear compartments, where they can act as structural scaffolds of nuclear domains and influence chromatin organization, 33 as well as transcriptional and posttranscriptional regulation of gene expression. 34 , 35 In our previous studies, we have shown the involvement of several lncRNAs (MEG3, TUG1, PVT1, and MVIH) 36 , 37 , 38 , 39 in the occurrence and development of PE. Thus, exploration and identification of PE-associated lncRNAs and their functions may provide a new angle in the understanding of PE pathogenesis and define novel therapeutic targets and diagnostic and prognostic markers for PE.…”

Section: Discussionmentioning

confidence: 92%

Long Noncoding RNA 00473 Is Involved in Preeclampsia by LSD1 Binding-Regulated TFPI2 Transcription in Trophoblast Cells

Zou

et al. 2018

Molecular Therapy - Nucleic Acids

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Preeclampsia (PE) is a syndrome manifested by high blood pressure that could develop in the latter half of pregnancy; however, the underlying mechanisms are not understood. Recent evidence points to the function of noncoding RNAs (ncRNAs) as novel regulators of the invasion, migration, proliferation, and apoptosis of trophoblasts involved in the development of placental vasculature. Here, we investigated the role of long intergenic ncRNA 00473 (linc00473) in PE and the associated molecular mechanisms. The expression of linc00473 was downregulated in the placenta of patients with severe PE as revealed by qRT-PCR analysis. In vitro, linc00473 knockdown in trophoblast cell lines HTR-8/SVneo, JAR, and JEG3 significantly inhibited cell proliferation and promoted apoptosis, whereas linc00473 overexpression stimulated trophoblast proliferation. The mechanistic insights were provided by RNA-seq and qRT-PCR, which revealed that linc00473 could regulate the transcription of genes relevant to cell growth, migration, and apoptosis. In particular, linc00473 inhibited the expression of tissue factor pathway inhibitor 2 (TFPI2) through binding to lysine-specific demethylase 1 (LSD1). These results indicate that linc00473 could be involved in the pathogenesis and development of PE and may be a candidate biomarker as well as therapeutic target for this disease.

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Section: Discussionmentioning

confidence: 92%

Long Noncoding RNA 00473 Is Involved in Preeclampsia by LSD1 Binding-Regulated TFPI2 Transcription in Trophoblast Cells

Zou

et al. 2018

Molecular Therapy - Nucleic Acids

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“…The lncRNA plasmacytoma variant translocation 1 knockdown significantly suppressed cell proliferation, invasion, and migration and stimulated cell cycle accumulation and apoptosis [22]. The silencing of lncRNA microvascular invasion in hepatocellular carcinoma inhibited cell proliferation, invasion, migration, and angiogenesis in various trophoblast cell lines [23]. Inhibition of endogenous lncRNA activated by TGF- β suppressed HTR-8/SVneo cell proliferation, migration, and tube formation [24].…”

Section: Discussionmentioning

confidence: 99%

The Increased lncRNA MIR503HG in Preeclampsia Modulated Trophoblast Cell Proliferation, Invasion, and Migration via Regulating Matrix Metalloproteinases and NF-κB Signaling

et al. 2019

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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.

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“…LncRNA PVT1 downregulation substantially decreased cell proliferation; besides inducing the cell cycle as well as cell apoptosis, the mechanism of PVT1 was through the regulation of angiopoietin-like 4 (ANGPTL4) as well as Ezh2 [59]. The downregulation of MVIH in PE decreased not only cell proliferation, but also cell migration, invasion and angiogenesis in trophoblast cell lines by targeting Jun-B protein [60].…”

Section: Lncrnas Affect Cellular Functions Of Trophoblast Cellsmentioning

confidence: 99%

Long Noncoding RNA in Preeclampsia: Transcriptional Noise or Innovative Indicators?

Yang

Meng

2019

BioMed Research International

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Preeclampsia (PE) is termed as an obstetric issue that is characterized by hypertension (≧140/90 mm Hg), together with proteinuria following 20 weeks of pregnancy. Until today, PE still constitutes a severe threat to the lives of both the mothers and fetuses. In the past, long noncoding RNAs (lncRNAs) were considered as the transcriptional noise. However, some investigations have indicated that lncRNAs could be used as innovative indicators in PE. The current review aims to discuss the relationship between lncRNAs and PE in recent years. According to the retrieved data, we concluded that lncRNAs can exert an impact on both the occurrence and development of PE through the changes in the biological functions of trophoblasts, immune regulation, epigenetic regulation, decidualization, and energy metabolism. The mechanisms of lncRNAs in PE will help us to better understand the pathogenesis of PE and help us to find targets for predicting and diagnosing PE in the future.

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Promotion of trophoblast invasion by lncRNA MVIH through inducing Jun‐B

Cited by 21 publications

References 30 publications

Long Noncoding RNA 00473 Is Involved in Preeclampsia by LSD1 Binding-Regulated TFPI2 Transcription in Trophoblast Cells

Long Noncoding RNA 00473 Is Involved in Preeclampsia by LSD1 Binding-Regulated TFPI2 Transcription in Trophoblast Cells

The Increased lncRNA MIR503HG in Preeclampsia Modulated Trophoblast Cell Proliferation, Invasion, and Migration via Regulating Matrix Metalloproteinases and NF-κB Signaling

Long Noncoding RNA in Preeclampsia: Transcriptional Noise or Innovative Indicators?

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