ArticleJournal of clinical laboratory analysis2023
LncRNA LINC00534 regulates cell proliferation and migration via the miR-494-3p/PTEN axis in HTR-8/SVneo cells.
Article in Journal of clinical laboratory analysis, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 8 citations in OpenAlex.
- LINC00534 promotes breast cancer progression by targeting the miR-139-5p/HMGB2 axis.Discover oncology · 2025Article
- Polyhedral oligomeric silsesquioxane (POSS)-silicon/carbon quantum dots nanocomposites for cell imaging.RSC advances · 2024Article
- The Role of Placental Non-Coding RNAs in Adverse Pregnancy Outcomes.International journal of molecular sciences · 2023Review
- LncRNA LINC00534 regulates cell proliferation and migration via the miR-494-3p/PTEN axis in HTR-8/SVneo cells.Journal of clinical laboratory analysis · 2023Article
- Biogenesis and function of exosome lncRNAs and their role in female pathological pregnancy.Frontiers in endocrinology · 2023Review
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundLncRNA LINC00534 has been found to be differentially expressed in placental tissue samples of preeclampsia (PE), but the exact mechanism is still unclear.
methodsIn 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.
resultsWe 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.
conclusionOverall, 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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