ArticleBioengineered2022
Depression of long non-coding RNA SOX2 overlapping transcript attenuates lipopolysaccharide-induced injury in bronchial epithelial cells via miR-455-3p/phosphatase and tensin homolog axis and phosphatidylinositol 3-kinase/protein kinase B pathway.
Article in Bioengineered, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed, 27 citations in OpenAlex.
- Vitamin D Reprograms Non-Coding RNA Networks to Block Zika Virus in Human Macrophages.Pathophysiology : the official journal of the International Society for Pathophysiology · 2026Article
- Decreased miR-455-3p promotes diabetic retinopathy progression via modulating retinal endothelial proliferation and apoptosis.BMC ophthalmology · 2025Article
- The emerging role of long non-coding RNA SOX2-OT in cancers and non-malignant diseases.Journal of physiology and biochemistry · 2025Review
- Human umbilical cord mesenchymal stromal cell small extracellular vesicle transfer of microRNA-223-3p to lung epithelial cells attenuates inflammation in acute lung injury in mice.Journal of nanobiotechnology · 2023Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Airway inflammation is associated with various respiratory diseases, and previous research has confirmed that long non-coding RNAs (lncRNAs) play imperative roles in inflammatory responses. However, the function of lncRNA SOX2 overlapping transcript (SOX2-OT) in airway inflammation remains enigmatic. This study aimed to investigate the effects of SOX2-OT on lipopolysaccharide (LPS)-induced cell injury in human bronchial epithelial cells, BEAS-2B, and its potential mechanisms. The results showed increased cell apoptotic ratio, production of inflammatory cytokines, higher expression of adhesion molecules and activation of NF-κB in LPS-stimulated BEAS-2B cells. In LPS-stimulated BEAS-2B cells, SOX2-OT up-regulation and miR-455-3p down-regulation emerged simultaneously. SOX2-OT knockdown or miR-455-3p over-expression restrained LPS-induced inflammation and injury. SOX2-OT sponged to miR-455-3p and functioned as a ceRNA. In addition, phosphatase and tensin homolog (PTEN) served as an endogenous target of miR-455-3p to modulate the phosphatidylinositol 3-kinase/protein kinase B (PI3K/AKT) pathway and disturb the alleviated consequence of miR-455-3p over-expression on LPS-induced BEAS-2B cell inflammation and cell injury. Our data demonstrated that SOX2-OT plays a pivotal role in LPS-induced inflammation and injury in BEAS-2B cells and exerts its function through the miR-455-3p/PTEN axis and modulation of the PI3K/AKT pathway.
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