ArticleAnnals of translational medicine2020
Downregulated placental expression of linc00468 contributes to trophoblast dysfunction by inducing epithelial-mesenchymal transition.
Article in Annals of translational medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
2 citing papers in PubMed, 7 citations in OpenAlex.
- CD97 expression level and its effect on cell adhesion in Preeclampsia.BMC pregnancy and childbirth · 2022Article
- ceRNA Network and Functional Enrichment Analysis of Preeclampsia by Weighted Gene Coexpression Network Analysis.Computational and mathematical methods in medicine · 2022Article
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Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundPreeclampsia (PE) is a widespread progressive condition that can occur pregnancy and is related to high maternal morbidity and fetal mortality in the perinatal period. However, the exact mechanism responsible has not been specific. Accumulating evidence has highlighted the prominent role of the epithelial-mesenchymal transition (EMT) in the biological behaviors of PE.
methodsWe explored the role of a lincRNA in extravillous trophoblast (EVTs) cell viability, migration, invasion and apoptosis
resultsWe uncovered that linc00468 was downregulated in PE samples compared to in healthy tissues and in trophoblast cells. Functionally, gain and loss-of-function experiments demonstrated that linc00468 inhibited cell proliferation, migration, invasion and linc00468 accelerated apoptosis of the trophoblast phenotype in cell lines. Moreover, we demonstrated that downregulation of linc00468 promoted the expression of E-cadherin and β-catenin but reduced the expression of N-cadherin, Vimentin and Snail, resulting in progression of EMT.
conclusionsIn conclusion, linc00468 promoted EMT and a consequent increase in invasiveness in HTR-8/Svneo and JAR EVT cell lines. Our study provides the first evidence that linc00468 has a pivotal role in cell invasion and promotes intrinsic and extrinsic EMT ability of PE.
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