ArticleCell death & disease2022
Syntenin-1-mediated small extracellular vesicles promotes cell growth, migration, and angiogenesis by increasing onco-miRNAs secretion in lung cancer cells.
Article in Cell death & disease, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers, 1 of them a synthesis that pooled it.
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Who cites it
28 citing papers in PubMed, 1 synthesis or guideline pooled it, 45 citations in OpenAlex.
- MicroRNAs in Tumor Endothelial Cells: Regulation, Function and Therapeutic Applications.Cells · 2023Pooled it
- Targeting MDA-9/syntenin-1 (SDCBP) as a strategy to eliminate head and neck squamous cell carcinoma stem cells.Cancer letters · 2026Article
- The role of extracellular vesicles-associated proteins markers in prostate cancer: a review.Discover oncology · 2026Review
- Expression of PSTPIP1 in Renal Cell Carcinoma and Its Prognostic Value.Biochemical genetics · 2026Article
- Exosome profile and composite indices reflect immune exhaustion in periodontitis.Scientific reports · 2025Article
- Identification of multicohort-based predictive signature for NMIBC recurrence reveals SDCBP as a novel oncogene in bladder cancer.Annals of medicine · 2025Article
- Extracellular Vesicles for Clinical Diagnostics: From Bulk Measurements to Single-Vesicle Analysis.ACS nano · 2025Review
- Syntenin inhibition impairs stroma-tumor communication in multiple myeloma and improves bortezomib treatment efficiency.HemaSphere · 2025Article
- Mir-494-3p enhances aggressive phenotype of non-small cell lung cancer cells by regulating SET/I2PP2A.Scientific reports · 2025Article
- Mapping Small Extracellular Vesicle Secretion Potential in Healthy Human Gingiva Using Spatial Transcriptomics.Current issues in molecular biology · 2025Article
- Extracellular vesicles in tumor immunity: mechanisms and novel insights.Molecular cancer · 2025Review
- MiR-425-5p intervenes in autoimmune myocarditis by regulating Treg cell differentiation through NRAS.Frontiers in cell and developmental biology · 2025Article
- Biological disturbance of MiR-425 and its application prospects in cardiovascular diseases.Frontiers in cell and developmental biology · 2025Review
- Study on the Mechanism of Competing Endogenous Network of 'Current computer-aided drug design · 2025Article
- Harnessing EVs-ncRNA for Lung Cancer: From Oncogenic Pathways to Novel Diagnostic and Therapeutic Strategies.International journal of nanomedicine · 2025Review
- Neuroendocrine gene subsets are uniquely dysregulated in prostate adenocarcinoma.Cancer biology & therapy · 2024Article
- GCC2 promotes non-small cell lung cancer progression by maintaining Golgi apparatus integrity and stimulating EGFR signaling pathways.Scientific reports · 2024Article
- Research on the TSPAN6 regulating the secretion of ADSCs-Exos through syntenin-1 and promoting wound healing.Stem cell research & therapy · 2024Article
- Extracellular vesicles as tools and targets in therapy for diseases.Signal transduction and targeted therapy · 2024Review
- RAS‑stimulated release of exosomalInternational journal of molecular medicine · 2023Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Small extracellular vesicles (sEVs) play a pivotal role in tumor progression by mediating intercellular communication in the tumor microenvironment (TME). Syntenin-1 induces malignant tumor progression in various types of human cancers, including human lung cancer and regulates biogenesis of sEVs. However, the function of syntenin-1-regulated sEVs and miRNAs in sEVs remains to be elucidated. In the present study, we aimed to demonstrate the role of oncogenic Ras/syntenin-1 axis in the release of sEVs and elucidate the function of syntenin-1-mediated miRNAs in sEVs in lung cancer progression. The results revealed that oncogenic Ras promoted the release of sEVs by inducing syntenin-1 expression; disruption of syntenin-1 expression impaired the release of sEVs as well as sEV-mediated cancer cell migration and angiogenesis. Moreover, we identified three miRNAs, namely miR-181a, miR-425-5p, and miR-494-3p, as onco-miRNAs loaded into syntenin-1-dependent sEVs. Remarkably, miR-494-3p was highly abundant in sEVs and its release was triggered by syntenin-1 expression and oncogenic Ras. Ectopic expression of the miR-494-3p mimic enhanced the migration and proliferation of lung cancer cells as well as tube formation in endothelial cells; however, the miR-494-3p inhibitor blocked sEV-mediated effects by targeting tyrosine-protein phosphatase nonreceptor type 12 (PTPN12), a tumor suppressor. sEVs promoted tumor growth and angiogenesis by downregulating PTPN12 expression; however, the miR-494-3p inhibitor significantly suppressed these effects in vivo, confirming that miR-494-3p acts as a major onco-miRNA loaded into lung cancer cell-derived sEVs. Eventually, the oncogenic Ras/syntenin-1 axis may induce cancer progression by increasing miR-494-3p loading into sEVs in lung cancer cells in the TME.
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