ArticleCancer medicine2023
Hypoxic lung adenocarcinoma-derived exosomal miR-1290 induces M2 macrophage polarization by targeting SOCS3.
Article in Cancer medicine, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed.
- MicroRNA regulation of macrophage polarization in lung cancer: Regulatory networks and therapeutic potential (Review).International journal of oncology · 2026Review
- Advances in miRNA-Mediated Bidirectional Crosstalk and Immune Evasion Mechanisms Between Lung Cancer Cells and CD8International journal of molecular sciences · 2026Review
- Breast milk miRNAs and their potential role in the development of atopy in infants.Frontiers in molecular biosciences · 2026Review
- Advances in Tumor-Derived Exosomal Non-Coding RNAs Regulating M2 Macrophage Polarization: Molecular Mechanisms and Signaling Pathway.Cancer medicine · 2025Review
- Exosomes promote pre-metastatic niche formation in lung cancer.Cancer cell international · 2025Review
- SOCS3: An Immunological Biomarker Offering Potential Therapeutic Targets for Malignant Tumors.Biological procedures online · 2025Review
- Exosomal FGD5-AS1 promotes proliferation of lung cancer cells under hypoxia by inhibiting miR-1179 and activating P-cadherin.Human cell · 2025Article
- Identification and evaluation of metabolic mRNAs and key miRNAs in colorectal cancer liver metastasis.Cancer cell international · 2025Article
- Hypoxia studies in non‑small cell lung cancer: Pathogenesis and clinical implications (Review).Oncology reports · 2025Review
- Exosomes and immune modulation: implications for neuroblastoma immunotherapy.Frontiers in immunology · 2025Review
- Extracellular vesicles activated cancer-associated fibroblasts promote lung cancer metastasis through mitophagy and mtDNA transfer.Journal of experimental & clinical cancer research : CR · 2024Article
- Research advances on signaling pathways regulating the polarization of tumor-associated macrophages in lung cancer microenvironment.Frontiers in immunology · 2024Review
- Hypoxia-Driven Changes in Tumor Microenvironment: Insights into Exosome-Mediated Cell Interactions.International journal of nanomedicine · 2024Review
- Tumor-derived extracellular vesicles regulate macrophage polarization: role and therapeutic perspectives.Frontiers in immunology · 2024Article
- Hypoxic lung adenocarcinoma-derived exosomal miR-1290 induces M2 macrophage polarization by targeting SOCS3.Cancer medicine · 2023Article
Corrections and comments
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Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundExosomes are critical mediators of tumor cell-microenvironment cross talk. However, the mechanisms by which hypoxic Lung adenocarcinoma (LUAD)-derived exosomes modulate macrophage polarization remain largely unknown. The aim of this study was to investigate the effects of hypoxic LUAD-derived exosome on macrophage polarization and explore the underlying molecular mechanism. MATERIALS AND
methodsLUAD-derived exosomes were isolated, and then confirmed by transmission electron microscopy, nanoparticle tracking analysis, and Western blot. Internalization of exosomes in macrophages was detected by confocal microscope. Gain- and loss-of-function experiments, rescue experiments, and xenograft models were performed to uncover the underlying mechanisms of exosomal miR-1290 induced macrophage polarization in vitro and in vivo.
resultsmiR-1290 was enriched in hypoxic LUAD cancer cell-derived exosomes and could be transferred to macrophages. Overexpression of miR-1290 in macrophages-induced polarization of M2 phenotype. Luciferase assay verified SOCS3 was the target of miR-1290. Hypoxic LUAD cell-derived exosomal miR-1290 activated the STAT3 signaling pathway by targeting SOCS3 to promote M2 macrophage polarization.
conclusionHypoxic LUAD cells generate miR-1290-rich exosomes that promote M2 polarization of macrophages. Targeting exosomal miR-1290 may provide a potential immunotherapeutic strategy for LUAD.
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