Interference with lncRNA NEAT1 promotes the proliferation, migration, and invasion of trophoblasts by upregulating miR-411-5p and inhibiting PTEN expression

Fan, XuFei; Jianyi, Lou; Zheng, Xiaodong; Wáng, Ying; Wang, Jiayue; Luo, Mengmeng; Hu, Min

doi:10.1080/08923973.2021.1910834

Cited by 8 publications

(4 citation statements)

References 18 publications

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“…40 Interfering with the expression of lncRNA NEAT1 can up-regulate miR-411-5p and inhibit the expression of PTEN, and then promote the proliferation, migration, and invasion of trophoblast cells; thus slowing down the development of PE. 41 By predicting the site, we detected that there may be binding sites between LINC00534 and miR-139-5p…”

Section: Discussionmentioning

confidence: 98%

“…For example, lncRNA KCNQ1OT1 can target miR‐146A‐3p functions in HTR‐8/SVneo cells through the CXCL12/CXCR4 pathway 40 . Interfering with the expression of lncRNA NEAT1 can up‐regulate miR‐411‐5p and inhibit the expression of PTEN, and then promote the proliferation, migration, and invasion of trophoblast cells; thus slowing down the development of PE 41 . By predicting the site, we detected that there may be binding sites between LINC00534 and miR‐139‐5p or miR‐494‐3p, and RT–qPCR experiments confirmed the negative correlation between miR‐494‐3p and LINC00534.…”

Section: Discussionmentioning

confidence: 99%

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LncRNA LINC00534 regulates cell proliferation and migration via the miR‐494‐3p/PTEN axis in HTR‐8/SVneo cells

Song

Zhang

Xia

et al. 2022

Clinical Laboratory Analysis

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Background LncRNA LINC00534 has been found to be differentially expressed in placental tissue samples of preeclampsia (PE), but the exact mechanism is still unclear. Methods In vitro assays were carried out in HTR‐8/SVneo cells using various methods, including cell counting kit‐8 (CCK‐8), transwells, flow cytometry, and Western blotting (WB) and quantitative polymerase chain reaction. RNA pull‐down and bioinformatics analysis were applied to examine other potential underlying mechanisms involved. Results We found that there was a high expression of LINC00534 in the placental tissues of patients with PE. LINC00534 overexpression (OE) significantly inhibited cell proliferation and migration as well as accelerated cell apoptosis in HTR8/SVneo cells. The knockdown of LINC00534 produced an opposite trend. Mechanistically, LINC00534 promoted the expressions of PTEN (Phosphatase and tensin homolog) through decreasing miR‐494‐3p. Further rescue studies showed that LINC00534 played a role by targeting mir‐494‐3p, which controlled the growth and migration of HTR‐8/SVneo trophoblast cells via regulating PTEN/PI3K/AKT (Phosphatidylinositol3‐kinase/protein kinase B). Moreover, lncRNA pull‐down assay identified 198 potential bound proteins for LINC00534. Those proteins were mostly involved in RNA processing and modification, posttranslational modification, protein turnover, and chaperones. Conclusion Overall, by suppressing HTR8/SVneo cell growth and migration via the miR‐494‐3p/PTEN axis and other mechanisms, LINC00534 offers new insight into PE pathogenesis.

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Section: Discussionmentioning

confidence: 98%

Section: Discussionmentioning

confidence: 99%

LncRNA LINC00534 regulates cell proliferation and migration via the miR‐494‐3p/PTEN axis in HTR‐8/SVneo cells

Song

Zhang

Xia

et al. 2022

Clinical Laboratory Analysis

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“…For example, upregulation of lncRNA XIST in trophoblast cells HTR8/Sveno can inhibit cell proliferation and invasion and increase apoptosis by interacting with miRNA-340-5p/KCNJ16 during myogenic differentiation ( Guo et al, 2022 ). Overexpression of miRNA-340-5p or lncRNA NEAT1 can mitigate these effects by mediating the upregulation of miRNA-411 ( Fan et al, 2021 ), slowing the progression of PE. Therefore, lncRNAs are also significant contributors to trophoblast cell function, making them essential factors in the development of PE.…”

Section: Discussionmentioning

confidence: 99%

Mechanistic study of pre-eclampsia and macrophage-associated molecular networks: bioinformatics insights from multiple datasets

Cao,

Jiang,

Yin

et al. 2024

Front. Genet.

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BackgroundPre-eclampsia is a pregnancy-related disorder characterized by hypertension and proteinuria, severely affecting the health and quality of life of patients. However, the molecular mechanism of macrophages in pre-eclampsia is not well understood.MethodsIn this study, the key biomarkers during the development of pre-eclampsia were identified using bioinformatics analysis. The GSE75010 and GSE74341 datasets from the GEO database were obtained and merged for differential analysis. A weighted gene co-expression network analysis (WGCNA) was constructed based on macrophage content, and machine learning methods were employed to identify key genes. Immunoinfiltration analysis completed by the CIBERSORT method, R package “ClusterProfiler” to explore functional enrichment of these intersection genes, and potential drug predictions were conducted using the CMap database. Lastly, independent analysis of protein levels, localization, and quantitative analysis was performed on placental tissues collected from both preeclampsia patients and healthy control groups.ResultsWe identified 70 differentially expressed NETs genes and found 367 macrophage-related genes through WGCNA analysis. Machine learning identified three key genes: FNBP1L, NMUR1, and PP14571. These three key genes were significantly associated with immune cell content and enriched in multiple signaling pathways. Specifically, these genes were upregulated in PE patients. These findings establish the expression patterns of three key genes associated with M2 macrophage infiltration, providing potential targets for understanding the pathogenesis and treatment of PE. Additionally, CMap results suggested four potential drugs, including Ttnpb, Doxorubicin, Tyrphostin AG 825, and Tanespimycin, which may have the potential to reverse pre-eclampsia.ConclusionStudying the expression levels of three key genes in pre-eclampsia provides valuable insights into the prevention and treatment of this condition. We propose that these genes play a crucial role in regulating the maternal-fetal immune microenvironment in PE patients, and the pathways associated with these genes offer potential avenues for exploring the molecular mechanisms underlying preeclampsia and identifying therapeutic targets. Additionally, by utilizing the Connectivity Map database, we identified drug targets like Ttnpb, Doxorubicin, Tyrphostin AG 825, and Tanespimycin as potential clinical treatments for preeclampsia.

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“…It has been reported that downregulated lncNEAT1 promotes proliferation, migration, and invasion of trophoblast cells, and alleviates development of preeclampsia. 26 However, the expression pattern and regulatory target of lncNEAT1 in endometrial decidualization have not been reported.…”

Section: Introductionmentioning

confidence: 99%

Elevated high-mannose N-glycans hamper endometrial decidualization

Chen,

Zhang,

et al. 2023

iScience

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Interference with lncRNA NEAT1 promotes the proliferation, migration, and invasion of trophoblasts by upregulating miR-411-5p and inhibiting PTEN expression

Cited by 8 publications

References 18 publications

LncRNA LINC00534 regulates cell proliferation and migration via the miR‐494‐3p/PTEN axis in HTR‐8/SVneo cells

LncRNA LINC00534 regulates cell proliferation and migration via the miR‐494‐3p/PTEN axis in HTR‐8/SVneo cells

Mechanistic study of pre-eclampsia and macrophage-associated molecular networks: bioinformatics insights from multiple datasets

Elevated high-mannose N-glycans hamper endometrial decidualization

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