ArticleInternational journal of nanomedicine2019
Exosomal Transfer Of Cisplatin-Induced miR-425-3p Confers Cisplatin Resistance In NSCLC Through Activating Autophagy.
Article in International journal of nanomedicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 73 papers.
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Who cites it
73 citing papers in PubMed, 113 citations in OpenAlex.
- Circulating MicroRNAs in non-small cell lung cancer: Clinical potential, analytic pitfalls, and barriers to implementation.The journal of liquid biopsy · 2026Review
- TLR7 induces autophagy in non-small cell lung cancer tumor cells and influences anti-tumors responses in patients.Translational lung cancer research · 2026Article
- The role of small extracellular vesicles in ovarian cancer drug resistance: from bench clues to clinical implications.Journal of ovarian research · 2026Review
- Controlling Biogenesis and Engineering of Exosomes to Inhibit Growth and Promote Death in Glioblastoma Multiforme.Brain sciences · 2026Review
- Reduced Exosomal miR-22 Promotes Cisplatin Resistance and Migration in Non-Small Cell Lung Cancer Cells Through MDM4 Upregulation.OncoTargets and therapy · 2026Article
- Exosomal biomarkers and therapeutics in lung cancer: a narrative review on their role in early detection and targeted treatment.Translational lung cancer research · 2025Review
- Exosomes, autophagy, and cancer: A complex triad.International journal of cancer · 2025Review
- Prognostic analysis and mechanistic exploration of the autophagy-related exosome genes ITGA3, ITGB4, and PTK6 in pancreatic ductal adenocarcinoma.Discover oncology · 2025Article
- Exosome-Mediated Chemoresistance in Cancers: Mechanisms, Therapeutic Implications, and Future Directions.Biomolecules · 2025Review
- Intratumoral heterogeneity and drug resistance in cancer.Cancer cell international · 2025Review
- Extracellular Vesicles as Mediators and Potential Targets in Combating Cancer Drug Resistance.Molecules (Basel, Switzerland) · 2025Review
- Exosome, an important transmitter in the drug resistance of non-small cell lung cancer.Frontiers in oncology · 2025Review
- Harnessing EVs-ncRNA for Lung Cancer: From Oncogenic Pathways to Novel Diagnostic and Therapeutic Strategies.International journal of nanomedicine · 2025Review
- Recent advances to address challenges in extracellular vesicle-based applications for lung cancer.Acta pharmaceutica Sinica. B · 2024Review
- Extracellular vesicles in anti-tumor drug resistance: Mechanisms and therapeutic prospects.Journal of pharmaceutical analysis · 2024Review
- Exosomal microRNAs in lung cancer: a narrative review.Translational cancer research · 2024Review
- Linc00673-V3 positively regulates autophagy by promoting Smad3-mediatedLife science alliance · 2024Article
- Review
- Autophagy-Dependent Secretion: Crosstalk between Autophagy and Exosome Biogenesis.Current issues in molecular biology · 2024Review
- The Role of TGFBR3 in the Development of Lung Cancer.Protein and peptide letters · 2024Review
13 more citing papers are in PubMed but not listed here.
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Authors and funding
12 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
introductionExosomes are important mediators of intercellular communication. Previously, we characterized circulating exosomal miR-425-3p as a non-invasive prognostic marker for predicting clinical response to platinum-based chemotherapy in patients with non-small cell lung cancer (NSCLC).
methodsCirculating exosomal miR-425-3p was validated by qRT-PCR in paired serum samples from NSCLC patients during the course of platinum-based chemotherapy. Cell coculture was performed to examine the effects of exosomal miR-425-3p on the sensitivity of recipient A549 cells to cisplatin. Using bioinformatics, ChIP and luciferase reporter assays, the transcription factor essential for miR-425-3p expression was identified. Autophagic activity in the recipient cells was determined by Western blot and fluorescence microscopy.
resultsHigher levels of exosomal miR-425-3p were found in serum samples from the patients in tolerance versus those at baseline. An upward trend in the expression of circulating exosomal miR-425-3p was revealed during chemotherapy. Furthermore, the expression of exosomal miR-425-3p could be induced by cisplatin in NSCLC cells. Exosomes isolated from either cisplatin-treated or cisplatin-resistant NSCLC cells conferred chemoresistance to sensitive A549 cells in a miR-425-3p-dependent manner. Cisplatin-induced c-Myc was found to directly bind the miR-425-3p promoter and transactivated its expression. Exosomal miR-425-3p facilitated autophagic activation in the recipient cells by targeting AKT1, eventually leading to chemoresistance. DISCUSSION: Our results suggest that apart from a prognostic marker of treatment response, exosomal miR-425-3p might be a potential dynamic biomarker to tailor cisplatin resistance in NSCLC patients during the treatment and represent a promising therapeutic target for therapy-resistant NSCLC.
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