ArticleWorld journal of surgical oncology2023
Lung cancer-derived exosomal miR-132-3p contributed to interstitial lung disease development.
Article in World journal of surgical oncology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 8 citations in OpenAlex.
- Exosomes Derived from Non-small Cell Lung Cancer Cells Transfer LINC00467 to Induce the Proliferation of Cancer-associated Fibroblasts.Cell biochemistry and biophysics · 2026Article
- Association of Plasma miRNA-7-5p and miRNA-214-5p With Rheumatoid Arthritis Associated Interstitial Lung Disease.International journal of rheumatic diseases · 2026Article
- Urinary exosomal miR-132-3p as a novel non‑invasive biomarker for kidney scarring in pediatric vesicoureteral reflux patients.BMC pediatrics · 2026Article
- LY86-AS1 predicts poor prognosis and inhibits progression in non-small cell lung cancer by targeting the miR-132-3p/RB1CC1 axis.World journal of surgical oncology · 2026Article
- RpaA Overexpression Enhances Bioluminescence Intensity and Elevates Rhythmic Extracellular Vesicle Yield inLife (Basel, Switzerland) · 2026Article
- microRNA-132 attenuates inflammation in induced pluripotent stem cell-derived microglia from Alzheimer's disease patients.Acta neuropathologica communications · 2026Article
- From Gut to Lung: The Role of Bile Acids in Rheumatoid Arthritis-Associated Interstitial Lung Disease (RA-ILD).Journal of inflammation research · 2025Review
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
purposeInterstitial lung diseases (ILDs) have high morbidity and mortality and poor prognosis. The significance of microRNAs (miRNAs) was highlighted in ILDs development. Currently, we attempted to confirm the functions of lung cancer-derived exosomal miR-132-3p and reveal the underlying mechanism.
methodCharacteristics of exosomes were verified by transmission electron microscope (TEM), nanoparticle tracking analysis, and Western blot assay. Exosome uptake for the normal human lung fibroblasts (NHLF) was assessed using a PKH67 staining assay. MTT and colony formation assays were applied to examine the proliferation abilities of NHLF. The interaction between miR-132-3p and sprouty1 (SPRY1) was confirmed by a luciferase reporter assay.
resultsLung cancer-derived exosomes promoted normal human lung fibroblast activation. Exosome inhibitor GW4869 reversed the effects of Exo on NHLF. Subsequently, miR-132-3p in lung cancer-derived exosomes activated the normal human lung fibroblast and promoted interstitial lung disease development ex vivo. Next, SPRY1 was verified to be the binding protein of miR-132-3p, and sh-SPRY1 abrogated the effects of the miR-132-3p inhibitor on NHLF.
conclusionExosomal miR-132-3p from A549 cells accelerated the development of interstitial lung disease through binding to SPRY1, which might serve as an important target for ILDs.
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