Plasmacytoma variant translocation 1 (<i><scp>PVT</scp>1</i>) regulates trophoblast viability, proliferation, and migration and is downregulated in spontaneous abortion

Qin, Xiaoli; Chen, Yan; Chen, Shu-Fang; Liu, Xiaorui; Zeng, Weihong; Tian, Fu‐Ju; Lin, Yi; Fan, Cuifang

doi:10.1111/aji.13048

Cited by 23 publications

(19 citation statements)

References 36 publications

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“…It was reported that in prostate cancer, YY1 might regulate the invasion and metastasis of tumor cells by interacting with the lncRNA plasmacytoma variant translocation 1 (PVT1; Meyer et al, 2011). PVT1 is downregulated in cases of spontaneous abortion and can affect trophoblast invasion (Qin et al, 2018;H. Wang et al, 2014).…”

Section: Introductionmentioning

confidence: 99%

YY1‐PVT1 affects trophoblast invasion and adhesion by regulating mTOR pathway‐mediated autophagy

Yang

Ding

Wang

et al. 2020

Journal Cellular Physiology

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Insufficient trophoblast invasion is the key factor for the occurrence of recurrent spontaneous abortions (RSA). Our previous studies identified Yin Yang 1 (YY1) as a transcription factor involved in the regulation of trophoblast invasiveness at the maternal-fetal interface. Long noncoding RNAs (lncRNAs) can regulate gene expression and autophagy in many ways. The purpose of this study was to explore the relationship between YY1 and lncRNAs and the mechanism by which lncRNAs affect the biological behavior of trophoblasts. Bioinformatic analysis predicted that YY1 had three binding sites in the plasmacytoma variant translocation 1 (PVT1) promoter region. Chromatin immunoprecipitation experiments and electrophoretic mobility shift assays verified that YY1 can directly bind to the PVT1 promoter. Compared with its expression levels in human placental villi tissue samples from the normal pregnancy group, the PVT1 expression levels were significantly lower in tissues from the RSA group. PVT1 knockdown significantly reduced adhesion, invasion, autophagy, and mTOR expression in HTR-8/SVneo cells and greatly increased apoptosis in vitro. This study revealed a novel regulatory pathway in which YY1 can act directly on PVT1 promoter to regulate its transcription, which further affects trophoblast invasion and adhesion by regulating autophagy via the mTOR pathway, and these effects might be involved in RSA pathogenesis.

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Section: Introductionmentioning

confidence: 99%

YY1‐PVT1 affects trophoblast invasion and adhesion by regulating mTOR pathway‐mediated autophagy

Yang

Ding

Wang

et al. 2020

Journal Cellular Physiology

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“…In addition, Wang et al reported that down-regulated long non-coding RNA PVT1 contributes to human gestational diabetes mellitus and preeclampsia and the PVT1 expression was lower in the gestational diabetes mellitus and preeclampsia placentas than the normal placentas (19). Another study reported that PVT1 was downregulated in clinical villi samples from spontaneous abortion (20). In contrast to these ndings, an increased expression of PVT1 has also been previously reported.…”

Section: Discussionmentioning

confidence: 88%

Up-regulated lncRNA-PVT1 expression in peripheral blood mononuclear cells of patients with coronary artery disease is correlated with decreased interleukin-10 production

et al. 2022

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Background: Plasmacytoma variant translocation 1 (PVT1) is a newly discovered long non-coding RNA (lncRNA), and it has not been previously studied in the in ammatory responses of peripheral blood mononuclear cells (PBMCs) of patients with coronary artery disease (CAD).Methods: This cross-sectional study was conducted in 15 CAD patients and 15 non-CAD (NCAD) individuals. PVT1 expression in PBMCs of the participants was measured, using real-time PCR.Interleukin (IL)-10, IL-22 and MMP-9 in the plasma and supernatant of the cultured PBMCs in the presence or absence of lipopolysaccharide (LPS) was assessed, using owcytometry and ELISA.Results: An increased expression of PVT1 was observed in untreated PBMCs of CAD patients compared to the NCAD group. There was a signi cant up-regulation of PVT1 after LPS treatment in PBMCs of both groups. Plasma matrix metalloproteinase-9 (MMP-9) levels were found to be higher in CAD patients compared to the controls. The level of IL-10 and IL-22 production from the non-treated PBMCs of CAD was signi cantly lower compared to the NCAD group. In the total examined population, PVT1 expression was negatively correlated with IL-10 secretion. The results also showed a signi cant negative correlation between PVT1 expression and IL-10 produced by untreated cells.Conclusions: PVT1 expression is increased in PBMCs of CAD patients and this increased expression could be associated with decreased IL-10 production from PBMCs of these patients. Background:Coronary artery disease (CAD) is considered as principal cause of death and disability leading to increased health economic burden worldwide (1). The most common form of CAD is atherosclerosis

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“…26,27 For instance, lncRNA plasmacytoma variant translocation 1 facilitated trophoblast cell proliferation and migration by regulating miR-424/eukaryotic translation initiation factor 5A pathway. 28 Hence, miRNAs that had the probability to interact with IGF2-AS were searched by bioinformatics prediction analysis. Among candidate miRNAs, miR-520g was selected by virtue of its potential roles in regulating phenotypes and behaviors of trophoblast cells.…”

Section: Discussionmentioning

confidence: 99%

Long non‐coding RNA IGF2‐AS promotes trophoblast cell proliferation, migration, and invasion by regulating miR‐520g/N‐cadherin axis

Zhang²,

Kong

2021

J of Obstet and Gynaecol

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Background: Recurrent miscarriage (RM) is a distressing reproductive issue worldwide. Dysfunction of trophoblasts can trigger numerous unfavorable pregnant outcomes such as RM, stillbirth, and fetal malformation. Methods: In this text, the roles and molecular basis of long non-coding RNA insulin growth factor 2 antisense (IGF2-AS) in the development of trophoblast cells were further investigated. IGF2-AS, microRNA-520g (miR-520g), and N-cadherin levels were measured by RT-qPCR assay. Cell viability, the number of colonies, cell apoptosis, migration, and invasion were measured by CCK-8 assay, colony formation assay, flow cytometry, transwell migration, and invasion assays, respectively. The relative proteins expression was detected by western blot. Results: The interaction between miR-520g and IGF2-AS or N-cadherin was tested by bioinformatics prediction analysis, and confirmed by dual-luciferase reporter assay, RNA pull-down assay, and RNA immunoprecipitation (RIP) assay. Our data revealed that IGF2-AS and N-cadherin levels were notably decreased, and miR-520g was strikingly increased in the placentas from RM patients. IGF2-AS overexpression promoted cell proliferation, migration, invasion, epithelial-mesenchymal transition (EMT), and hampered cell apoptosis in trophoblast cells, while IGF2-AS deletion exhibited opposite results. Moreover, miR-520g was a target gene of IGF2-AS and negatively regulated by IGF2-AS. MiR-520g inhibitor enhanced the proliferation, migration, and invasion capability of trophoblast cells, suppressed cell apoptosis, and promoted the EMT process. Moreover, the effects of IGF2-AS overexpression on trophoblast cells were reversed by miR-520g upregulation. Conclusions: These findings indicated that IGF2-AS facilitated trophoblast cell proliferation, migration, invasion, EMT, and suppressed cell apoptosis by regulating miR-520g/N-cadherin axis, providing potential biomarkers for RM.

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Plasmacytoma variant translocation 1 (PVT1) regulates trophoblast viability, proliferation, and migration and is downregulated in spontaneous abortion

Cited by 23 publications

References 36 publications

YY1‐PVT1 affects trophoblast invasion and adhesion by regulating mTOR pathway‐mediated autophagy

YY1‐PVT1 affects trophoblast invasion and adhesion by regulating mTOR pathway‐mediated autophagy

Up-regulated lncRNA-PVT1 expression in peripheral blood mononuclear cells of patients with coronary artery disease is correlated with decreased interleukin-10 production

Long non‐coding RNA IGF2‐AS promotes trophoblast cell proliferation, migration, and invasion by regulating miR‐520g/N‐cadherin axis

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