Lung cancer-derived exosomal miR-132-3p contributed to interstitial lung disease development
Abstract Purpose Interstitial 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 m...
| Main Authors: | , , , , , |
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| Format: | Article |
| Language: | English |
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BMC
2023-07-01
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| Series: | World Journal of Surgical Oncology |
| Subjects: | |
| Online Access: | https://doi.org/10.1186/s12957-023-03095-6 |
| _version_ | 1827899893151170560 |
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| author | Sufang Fang Ting Wang Ling Weng Ximei Han Rongshan Zheng Hongying Zhang |
| author_facet | Sufang Fang Ting Wang Ling Weng Ximei Han Rongshan Zheng Hongying Zhang |
| author_sort | Sufang Fang |
| collection | DOAJ |
| description | Abstract Purpose Interstitial 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. Method Characteristics 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. Results Lung 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. Conclusion Exosomal 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. |
| first_indexed | 2024-03-12T23:23:49Z |
| format | Article |
| id | doaj.art-ff244661f36b4fa2a2d2a8278e08fb44 |
| institution | Directory Open Access Journal |
| issn | 1477-7819 |
| language | English |
| last_indexed | 2024-03-12T23:23:49Z |
| publishDate | 2023-07-01 |
| publisher | BMC |
| record_format | Article |
| series | World Journal of Surgical Oncology |
| spelling | doaj.art-ff244661f36b4fa2a2d2a8278e08fb442023-07-16T11:18:46ZengBMCWorld Journal of Surgical Oncology1477-78192023-07-0121111110.1186/s12957-023-03095-6Lung cancer-derived exosomal miR-132-3p contributed to interstitial lung disease developmentSufang Fang0Ting Wang1Ling Weng2Ximei Han3Rongshan Zheng4Hongying Zhang5Respiratory Department, Fuzhou Pulmonary Hospital of Fujian Province, the Teaching Hospital of Fujian Medical UniversityRespiratory Department, Fuzhou Pulmonary Hospital of Fujian Province, the Teaching Hospital of Fujian Medical UniversityRespiratory Department, Fuzhou Pulmonary Hospital of Fujian Province, the Teaching Hospital of Fujian Medical UniversityRespiratory Department, Fuzhou Pulmonary Hospital of Fujian Province, the Teaching Hospital of Fujian Medical UniversityRespiratory Department, Fuzhou Pulmonary Hospital of Fujian Province, the Teaching Hospital of Fujian Medical UniversityRespiratory Department, Fuzhou Pulmonary Hospital of Fujian Province, the Teaching Hospital of Fujian Medical UniversityAbstract Purpose Interstitial 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. Method Characteristics 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. Results Lung 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. Conclusion Exosomal 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.https://doi.org/10.1186/s12957-023-03095-6Interstitial lung diseasesmiR-132-3pExosomeNHLFSPRY1 |
| spellingShingle | Sufang Fang Ting Wang Ling Weng Ximei Han Rongshan Zheng Hongying Zhang Lung cancer-derived exosomal miR-132-3p contributed to interstitial lung disease development World Journal of Surgical Oncology Interstitial lung diseases miR-132-3p Exosome NHLF SPRY1 |
| title | Lung cancer-derived exosomal miR-132-3p contributed to interstitial lung disease development |
| title_full | Lung cancer-derived exosomal miR-132-3p contributed to interstitial lung disease development |
| title_fullStr | Lung cancer-derived exosomal miR-132-3p contributed to interstitial lung disease development |
| title_full_unstemmed | Lung cancer-derived exosomal miR-132-3p contributed to interstitial lung disease development |
| title_short | Lung cancer-derived exosomal miR-132-3p contributed to interstitial lung disease development |
| title_sort | lung cancer derived exosomal mir 132 3p contributed to interstitial lung disease development |
| topic | Interstitial lung diseases miR-132-3p Exosome NHLF SPRY1 |
| url | https://doi.org/10.1186/s12957-023-03095-6 |
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