{
  "abstract": "Background: Occupational coal dust exposure causes persistent pulmonary inflammation, but the mechanisms by which it may influence thyroid cancer progression remain unclear. Macrophage-derived extracellular vesicles (EVs) may participate in intercellular communication under particulate stress.\n\nObjective: This study investigated whether EVs released by coal dust-stimulated macrophages alter thyroid cancer cell behavior and examined the involvement of miR-205-5p, CAMK1G, and NF-κB-associated signaling.\n\nMethods: Coal dust was physicochemically characterized before use. EVs were isolated from PMA-differentiated THP-1 macrophages following coal dust exposure and characterized by transmission electron microscopy, nanoparticle tracking analysis, and Western blotting. Small-RNA sequencing, bulk RNA sequencing, TCGA-THCA analysis, and the GSE274674 single-cell dataset were integrated with RT-qPCR, nuclear–cytoplasmic fractionation, dual-luciferase reporter assays, and genetic rescue experiments. Coal dust-exposed C57BL/6J mice and PBMC-humanized NSFG mice bearing TPC-1 xenografts were used for in vivo evaluation.\n\nResults: PKH26-labeled EV-associated material was detected in TPC-1 cells, and EV preparations increased cell viability, clonogenic growth, migration, and invasion while reducing apoptosis. miR-205-5p was enriched in these EVs and accumulated predominantly in the nuclear fraction of recipient cells. Inhibition of miR-205-5p attenuated the EV-associated malignant phenotypes. Integrated transcriptomic analyses prioritized CAMK1G and NF-κB-related signaling. EV treatment increased endogenous CAMK1G expression and the phosphorylation of p65 and IκBα. CAMK1G knockdown reduced these changes, whereas CAMK1G re-expression partially restored the effects suppressed by miR-205-5p inhibition. The reporter assay showed sequence-dependent repression of the isolated CAMK1G 3′-UTR construct, whereas endogenous-expression and rescue experiments supported a positive functional association; therefore, these findings are not interpreted as a simple direct positive regulatory relationship. In mice, coal dust exposure was associated with pulmonary abnormalities, altered serum FT4 and TPO-Ab levels, increased thyroid CAMK1G expression, and enhanced pulmonary CD206 immunoreactivity. In PBMC-humanized mice, coal dust exposure or experimentally administered macrophage-derived EVs increased xenograft growth, whereas CAMK1G knockdown attenuated tumor burden.\n\nConclusion: These findings support a functional association between coal dust-stimulated macrophage-derived EV signaling and thyroid cancer progression involving miR-205-5p, CAMK1G, and NF-κB-associated activity. However, direct physiological trafficking of endogenous lung-derived EVs to thyroid or tumor tissue was not demonstrated.",
  "abstract_shown": true,
  "affiliations": [
    "The First Affiliated Hospital of Anhui University of Science and Technology",
    "School of Medicine, Anhui University of Science & Technology",
    "Anhui University of Science and Technology"
  ],
  "article_type": "research article",
  "arxiv": null,
  "author_total": 4,
  "authors": [
    {
      "affs": [
        0
      ],
      "name": "Feng Zhao"
    },
    {
      "affs": [
        0
      ],
      "name": "Tianqing Ma"
    },
    {
      "affs": [
        1
      ],
      "name": "Chi Zhang"
    },
    {
      "affs": [
        2
      ],
      "name": "Hongzhen Zhang"
    }
  ],
  "bibtex": "https://research.draconitic.com/paper/azf2fg7k59gmj.bib",
  "cited_by": 0,
  "doi": "10.3389/fimmu.2026.1856770",
  "fulltext_url": "https://europepmc.org/articles/PMC13713815",
  "id": "azf2fg7k59gmj",
  "issns": [
    "1664-3224"
  ],
  "landing_url": "https://www.frontiersin.org/articles/10.3389/fimmu.2026.1856770/full",
  "language": "eng",
  "licence": "CC-BY-4.0",
  "licence_label": "CC BY 4.0",
  "licence_source": "article",
  "licence_url": "https://creativecommons.org/licenses/by/4.0/",
  "metadata_licence": null,
  "native_subjects": [
    [
      "heading",
      "Original Research"
    ],
    [
      "openalex",
      "1312|Extracellular vesicles in disease"
    ]
  ],
  "openalex": "W7221776163",
  "pdf_url": "https://www.frontiersin.org/journals/immunology/articles/10.3389/fimmu.2026.1856770/pdf",
  "pmcid": "PMC13713815",
  "pmid": "42953190",
  "published": "2026-10-14",
  "publisher": "Frontiers Media SA",
  "ris": "https://research.draconitic.com/paper/azf2fg7k59gmj.ris",
  "sources": [
    {
      "first_seen": "2026-10-30T12:19:17Z",
      "native_id": "10.3389/fimmu.2026.1856770",
      "source": "crossref",
      "url": "https://www.frontiersin.org/articles/10.3389/fimmu.2026.1856770/full"
    },
    {
      "first_seen": "2026-10-31T00:20:41Z",
      "native_id": "MED:42953190",
      "source": "europepmc",
      "url": "https://europepmc.org/article/MED/42953190"
    },
    {
      "first_seen": "2026-11-01T12:21:25Z",
      "native_id": "PMC13713815",
      "source": "pmc",
      "url": "https://doi.org/10.3389/fimmu.2026.1856770"
    }
  ],
  "subjects": [
    {
      "field": "biochemistry",
      "origin": "openalex:1312|Extracellular vesicles in disease",
      "subfield": "molecular-biology"
    }
  ],
  "title": "Coal dust-stimulated macrophage-derived extracellular vesicles promote thyroid cancer cell phenotypes involving miR-205-5p, CAMK1G, and NF-κB-associated signaling",
  "title_text": "Coal dust-stimulated macrophage-derived extracellular vesicles promote thyroid cancer cell phenotypes involving miR-205-5p, CAMK1G, and NF-κB-associated signaling",
  "type": "peer-reviewed",
  "updated_at": "2026-11-01T12:21:25Z",
  "url": "https://research.draconitic.com/paper/azf2fg7k59gmj",
  "venue": "Frontiers in Immunology",
  "versions": []
}