ArticleOncology reports2020
NEAT1 knockdown suppresses endothelial cell proliferation and induces apoptosis by regulating miR‑638/AKT/mTOR signaling in atherosclerosis.
Article in Oncology reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed, 43 citations in OpenAlex.
- SerumInternational journal of molecular sciences · 2026Article
- Single-cell and spatial transcriptomics identify immune-stromal interactions in cardiac allograft vasculopathy.Nature cardiovascular research · 2026Article
- USP7 Drives Atherosclerosis by Promoting Ferroptosis in Vascular Endothelial Cells via the KIAA1429/NEAT1/CTCF Axis.Biological procedures online · 2026Article
- Recent advances and emerging perspectives in vascular and cardiovascular research: A 2025 update.Hypertension research : official journal of the Japanese Society of Hypertension · 2026Review
- Long non-coding RNAs as molecular hubs integrating inflammatory and osteogenic pathways in calcific aortic valve disease.Frontiers in cardiovascular medicine · 2026Review
- Single Cell and Spatial Transcriptomics Identify Novel Immune-Stromal Interactions in Cardiac Allograft Vasculopathy.Research square · 2025Article
- NEAT1-mediated regulation of proteostasis and mRNA localization impacts autophagy dysregulation in Rett syndrome.Nucleic acids research · 2025Article
- Downregulation ofBrain communications · 2025Article
- LncRNA NEAT1 Knockdown Alleviates Macrophage Ferroptosis and Atherosclerosis by Suppressing STAT3 Activation.Mediators of inflammation · 2025Article
- The role of 5-methylcytosine regulator-related genes in diagnostic and immune regulatory functions in atherosclerosis.Frontiers in immunology · 2025Article
- Non-Coding RNA-Mediated Gene Regulation in Cardiovascular Disorders: Current Insights and Future Directions.Journal of cardiovascular translational research · 2024Review
- Noncoding RNAs in atherosclerosis: regulation and therapeutic potential.Molecular and cellular biochemistry · 2024Review
- Transcriptomics analysis of long non-coding RNAs in smooth muscle cells from patients with peripheral artery disease and diabetes mellitus.Scientific reports · 2024Article
- The roles of long noncoding RNA NEAT1 in cardiovascular diseases.Hypertension research : official journal of the Japanese Society of Hypertension · 2024Review
- Exploration of ferroptosis and necroptosis-related genes and potential molecular mechanisms in psoriasis and atherosclerosis.Frontiers in immunology · 2024Article
- The role of splicing events in the inflammatory response of atherosclerosis: molecular mechanisms and modulation.Frontiers in immunology · 2024Review
- Transcriptome-wide NBMC genomics · 2023Article
- FUS regulates the alternative splicing of cell proliferation genes related to atherosclerosis.Experimental biology and medicine (Maywood, N.J.) · 2023Article
- Atherosclerosis and Inflammation: Insights from the Theory of General Pathological Processes.International journal of molecular sciences · 2023Review
- Discovery of Transacting Long Noncoding RNAs That Regulate Smooth Muscle Cell Phenotype.Circulation research · 2023Article
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Long non‑coding RNAs (lncRNAs) have been validated to mediate the development of atherosclerosis (AS). In the present study, the molecular mechanisms and functions of lncRNA nuclear paraspeckle assembly transcript 1 (NEAT1) in the advancement of human aortic endothelial cells (HAECs) were investigated. The levels of lncRNA‑NEAT1 and miR‑638 expression in clinical samples and cells were explored via quantitative reverse transcription polymerase chain reaction. Colony formation and CCK‑8 assays were performed to determine the proliferative capacity of cells, and the apoptotic capacity of cells was analyzed on the basis of apoptotic cell proportion and caspase‑3 activity. Then, the proportion of cells and correlations among phosphoglycerate kinase 1 (PGK1), NEAT1, and miR‑638 were determined through RNA immunoprecipitation and luciferase assays and bioinformatics analysis. Moreover, the expression levels of Ki‑67, proliferating cell nuclear antigen, PGK1, Bax, Bcl‑2, (p)‑mTOR, (p)‑AKT, and β‑catenin were analyzed via western blot analysis. In the serum of patients with AS and HAECs induced by oxidized low‑density lipoprotein (ox‑LDL), the expression level of miR‑638 was decreased, whereas that of NEAT1 was increased. After ox‑LDL therapy, NEAT1 knockdown suppressed HAEC proliferation and stimulated HAEC apoptosis, which could be reversed by the miR‑638 inhibitor. NEAT1 inhibited miR‑638 expression through direct mutual action. The following mechanical investigations revealed that PGK1 was a miR‑638 target, whose expression was increased by NEAT1, a competing endogenous RNA of miR‑638. Additionally, the miR‑638 inhibitor contributed to proliferation and suppressed apoptosis through the activation of the AKT/mTOR signaling pathway in ox‑LDL‑induced HAECs. NEAT1 adjusted the AKT/mTOR signaling pathway via miR‑638 in ox‑LDL‑induced HAECs to accelerate their proliferation and impede their apoptosis. This result revealed that NEAT1 may be valuable in the treatment of AS.
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