ArticleBMC pulmonary medicine2021
Silencing of long non-coding RNA KCNQ1OT1 alleviates LPS-induced lung injury by regulating the miR-370-3p/FOXM1 axis in childhood pneumonia.
Article in BMC pulmonary medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 26 citations in OpenAlex.
- Article
- MIR210HG promotes the progression of pediatric pneumonia by inducing apoptosis and inflammation through downregulating miR-195-5p and upregulating FGF2.BMC pediatrics · 2026Article
- METTL3 aggravates lung injury in neonatal mice withInfection and immunity · 2025Article
- ARF3 knockdown inhibits influenza a virus and virus-induced pneumonia.Virus genes · 2025Article
- Mesenchymal stem cell-derived exosomal CBLB ameliorates infantile pneumonia progression probably by ubiquitinating MAPK14.Journal of inflammation (London, England) · 2025Article
- Article
- Role of the FOXM1/CMA/ER stress axis in regulating the progression of nonalcoholic steatohepatitis.Clinical and translational medicine · 2025Article
- Clinical value of miR-200b in diagnosis and prognosis of childhood pneumonia.BMC pediatrics · 2025Article
- Mechanism of KLF2 in young mice with pneumonia induced by Streptococcus pneumoniae.Journal of cardiothoracic surgery · 2024Article
- Detection of serum FOXM1 and IGF2 in patients with ARDS and their correlation with disease and prognosis.Open medicine (Warsaw, Poland) · 2024Article
- Long non coding RNAs reveal important pathways in childhood asthma: a future perspective.Journal of molecular histology · 2023Review
- Long noncoding RNA signatures in intrauterine infection/inflammation-induced lung injury: an integrative bioinformatics study.BMC pulmonary medicine · 2023Article
- Circ_0035292 knockdown alleviates lipopolysaccharide (LPS)-induced WI-38 cell apoptosis and inflammatory injury.Immunity, inflammation and disease · 2023Article
- FOXM1: Functional Roles of FOXM1 in Non-Malignant Diseases.Biomolecules · 2023Review
- Protective role of FBXL19 in Streptococcus pneumoniae-induced lung injury in pneumonia immature mice.Journal of cardiothoracic surgery · 2023Article
- Role of M2 macrophages-derived extracellular vesicles in IL-1β-stimulated chondrocyte proliferation and inflammatory responses.Cell and tissue banking · 2023Article
- Combination therapy with budesonide and acetylcysteine alleviates LPS-induced acute lung injury via the miR-381/NLRP3 molecular axis.PloS one · 2023Article
- Abnormal expression of lncRNA CASC9 in pneumonia children with respiratory failure and its feasible value for the clinical diagnosis of patients.Cell cycle (Georgetown, Tex.) · 2022Article
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
purposeLong non-coding RNAs (lncRNAs) play important roles in the development of pneumonia. We aimed to explore the role of the lncRNA KCNQ1OT1 in pneumonia and its underlying mechanisms.
methodsThe expression of KCNQ1OT1, FOXM1, and miR-370-3p was detected in the serum of 24 children with pneumonia and in 24 healthy controls. Normal human embryonic lung-derived diploid fibroblasts (WI-38 cells) were stimulated with LPS (10 μg/mL) to simulate the cellular model of pneumonia, and cell viability, apoptosis, and inflammation were analysed. Dual luciferase reporter and/or RNA binding protein immunoprecipitation assays were performed to test the relationship between miR-370-3p and KCNQ1OT1/FOXM1. Mice were intratracheally administered LPS (5 mg/kg) to induce an in vivo model of pneumonia, and pathological injury and inflammation were analysed.
resultsThe expression of KCNQ1OT1 and FOXM1 was up-regulated, and miR-370-3p was down-regulated in the serum of children with pneumonia, LPS-treated WI-38 cells, and in lung tissues of LPS-treated mice. Silencing of KCNQ1OT1 or overexpression of miR-370-3p suppressed cell apoptosis and inflammation and facilitated cell viability in LPS-treated WI-38 cells. KCNQ1OT1 directly targets miR-370-3p and negatively regulates its expression. FOXM1 was targeted by miR-370-3p and negatively modulated by miR-370-3p. In addition, silencing of KCNQ1OT1 mitigated LPS-induced lung injury and inflammation in mice. The protective effects of KCNQ1OT1 silencing in LPS-treated WI-38 cells and mice were reversed by silencing of miR-370-3p or overexpression of FOXM1.
conclusionSilencing of KCNQ1OT1 alleviates LPS-induced lung injury by regulating the miR-370-3p/FOXM1 axis in pneumonia.
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