ArticleHeliyon2024
Long non-coding RNA (LncRNA) non-coding RNA activated by DNA damage (NORAD) knockdown alleviates airway remodeling in asthma via regulating miR-410-3p/RCC2 and inhibiting Wnt/β-catenin pathway.
Article in Heliyon, 2024. 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.
- Anticancer Bioactive Peptides from Plants: Sources, Action Mechanisms, and Potential Superiority to Conventional Chemotherapy.Probiotics and antimicrobial proteins · 2026Review
- Photobiomodulation in orthodontics: an overview of systematic reviews with meta-regression and evidence map.Odontology · 2026Review
- Childhood Asthma Biomarkers Derived from Plasma and Saliva Exosomal miRNAs.International journal of molecular sciences · 2025Article
- Non-Coding RNAs in Asthma: Regulators of Eosinophil Biology and Airway Inflammation.Diagnostics (Basel, Switzerland) · 2025Review
- circUQCRC2 promotes asthma progression in children by activating the VEGFA/NF-κB pathway by targeting miR-381-3p.The Kaohsiung journal of medical sciences · 2024Article
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Authors and funding
5 authors.
Funding
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Abstract
Background: Asthma is a chronic inflammatory disorder with high prevalence in childhood. Airway remodeling, an important structural change of the airways, is resulted from epithelial-mesenchymal transition. Long non-coding RNA non-coding RNA activated by DNA damage (NORAD) has been found to promote epithelial-mesenchymal transition in multiple cancers. This study aimed to analyze the role of NORAD in asthma, mainly focusing on epithelial-mesenchymal transition-mediated airway remodeling, and further explored the NORAD-miRNA-mRNA network. Methods: NORAD expression was analyzed in transforming growth factor-β1-induced BEAS-2B human bronchial epithelial cells and ovalbumin-challenged asthmatic mice. The influences of NORAD on the epithelial-mesenchymal transition characteristics and Wnt/β-catenin pathway activation were analyzed Results: NORAD expression was elevated in both asthmatic models. Knockdown of NORAD impeded spindle-like morphology changes, elevated E-cadherin expression, decreased N-cadherin expression, suppressed cell migration, and inactivated the Wnt/β-catenin pathway in transforming growth factor-β1-stimulated BEAS-2B cells. NORAD acted as a sponge of miR-410-3p to regulate chromosome condensation 2 expression. Rescue assays demonstrated that silencing of NORAD ameliorated transforming growth factor-β1-induced EMT via miR-410-3p/chromosome condensation 2/Wnt/β-catenin axis. Conclusions: Silencing of NORAD alleviated epithelial-mesenchymal transition-mediated airway remodeling in asthma via mediating miR-410-3p/chromosome condensation 2/Wnt/β-catenin pathway.
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