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Peer-reviewedCC BYEcotoxicology and Environmental Safety

Carbon nanoparticle exposure promotes the progression of non-small cell lung cancer via the ARNT2/ARL14 axis: Findings from

  • Weiyu Jiang1
  • Chao Lu1
  • Yaru Yang2
  • Bowen Duan1
  • Qiuxue Yang1
  • Yuting Huang1
  • Run Hu1
  • Lihong Xiang1
  • Jun Tao1
  • Yinci Zhang3
  1. 1The First Hospital of Anhui University of Science and Technology, Huainan, Anhui Province, 232000, China
  2. 2The Second Affiliated Hospital of Anhui Medical University, Hefei, Anhui Province, 230071, China
  3. 3The First Hospital of Anhui University of Science and Technology, Huainan, Anhui Province, 232000, China; Corresponding author.
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Abstract

We investigated whether carbon nanoparticles (CNPs), a shared core component of coal dust, ambient PM2.5, and tobacco smoke, drive non-small cell lung cancer (NSCLC) progression. In an experimental mouse model of CNP‑induced pulmonary fibrosis (intranasal instillation, 200 µg/kg every other day for 90 days), we used transcriptomic screening to identify aryl hydrocarbon receptor nuclear translocator 2 (ARNT2) as a key upregulated transcription factor. In an ectopic xenograft model (nude mice pre‑exposed to 15 µg/kg CNPs for 1 week, subsequently inoculated with A549/A427 cells with or without ARNT2 silencing, with CNP administration continued for a total of 40 days), CNP exposure increased tumor volume at day 36 (A549, 194 ± 17–308 ± 22 mm³; A427, 245 ± 31–417 ± 42 mm³), proliferation (Ki‑67/PCNA: A549, 2.93‑/3.33-fold; A427, 1.94‑/3.55-fold), and levels of epithelial–mesenchymal transition markers (N‑cadherin/Vimentin: A549, 1.61‑/3.17-fold; A427, 2.44‑/1.98-fold), while ARNT2 knockdown reversed these effects. In vitro , CNP treatment (2 µg/mL, 48 h) enhanced proliferation (A549, 2.01‑fold; A427, 1.43-fold), migration (A549, 1.83‑fold; A427, 3.61‑fold), invasion (A549, 2.50‑fold; A427, 2.40‑fold), levels of stemness markers (CD133/SOX2/Oct4: A549, 2.38-/1.93-/2.02-fold; A427, 2.44-/1.44-/1.60-fold), and concentrations of inflammatory cytokines (TNF‑α/IL‑1β/IL‑6: A549, 5.39‑/6.41-/13.70-fold; A427, 3.59‑/10.02-/9.66-fold), reduced apoptosis (A549, 0.47‑fold; A427, 0.36-fold) and senescence (A549, 0.61-fold; A427, 0.37-fold), and increased reactive oxygen species levels (A549, 2.32‑fold; A427, 2.01‑fold); all these changes were attenuated by ARNT2 silencing. Transcriptomic and bioinformatic analyses identified ADP-ribosylation factor-like protein 14 (ARL14) as a downstream effector of ARNT2; ARL14 overexpression in ARNT2 ‑silenced cells restored proliferation and invasion and reduced apoptosis. Overall, experimental CNP exposure promotes NSCLC progression in an ARNT2-dependent manner, with ARL14 as a downstream mediator, which suggests potential targets for intervention in particulate-associated lung cancer.

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Cite

BibTeXRIS
BibTeX
@article{jiang2026carbon,
  title = {{Carbon nanoparticle exposure promotes the progression of non-small cell lung cancer via the ARNT2/ARL14 axis: Findings from}},
  author = {Weiyu Jiang and Chao Lu and Yaru Yang and Bowen Duan and Qiuxue Yang and Yuting Huang and Run Hu and Lihong Xiang and Jun Tao and Yinci Zhang},
  journal = {Ecotoxicology and Environmental Safety},
  year = {2026},
  month = oct,
  doi = {10.1016/j.ecoenv.2026.120951},
  url = {https://doi.org/10.1016/j.ecoenv.2026.120951},
  note = {CC BY},
}
RIS
TY  - JOUR
TI  - Carbon nanoparticle exposure promotes the progression of non-small cell lung cancer via the ARNT2/ARL14 axis: Findings from
AU  - Weiyu Jiang
AU  - Chao Lu
AU  - Yaru Yang
AU  - Bowen Duan
AU  - Qiuxue Yang
AU  - Yuting Huang
AU  - Run Hu
AU  - Lihong Xiang
AU  - Jun Tao
AU  - Yinci Zhang
PY  - 2026
DA  - 2026/10/23
JO  - Ecotoxicology and Environmental Safety
DO  - 10.1016/j.ecoenv.2026.120951
UR  - https://doi.org/10.1016/j.ecoenv.2026.120951
AB  - We investigated whether carbon nanoparticles (CNPs), a shared core component of coal dust, ambient PM2.5, and tobacco smoke, drive non-small cell lung cancer (NSCLC) progression. In an experimental mouse model of CNP‑induced pulmonary fibrosis (intranasal instillation, 200 µg/kg every other day for 90 days), we used transcriptomic screening to identify aryl hydrocarbon receptor nuclear translocator 2 (ARNT2) as a key upregulated transcription factor. In an ectopic xenograft model (nude mice pre‑exposed to 15 µg/kg CNPs for 1 week, subsequently inoculated with A549/A427 cells with or without ARNT2 silencing, with CNP administration continued for a total of 40 days), CNP exposure increased tumor volume at day 36 (A549, 194 ± 17–308 ± 22 mm³; A427, 245 ± 31–417 ± 42 mm³), proliferation (Ki‑67/PCNA: A549, 2.93‑/3.33-fold; A427, 1.94‑/3.55-fold), and levels of epithelial–mesenchymal transition markers (N‑cadherin/Vimentin: A549, 1.61‑/3.17-fold; A427, 2.44‑/1.98-fold), while ARNT2 knockdown reversed these effects. In vitro , CNP treatment (2 µg/mL, 48 h) enhanced proliferation (A549, 2.01‑fold; A427, 1.43-fold), migration (A549, 1.83‑fold; A427, 3.61‑fold), invasion (A549, 2.50‑fold; A427, 2.40‑fold), levels of stemness markers (CD133/SOX2/Oct4: A549, 2.38-/1.93-/2.02-fold; A427, 2.44-/1.44-/1.60-fold), and concentrations of inflammatory cytokines (TNF‑α/IL‑1β/IL‑6: A549, 5.39‑/6.41-/13.70-fold; A427, 3.59‑/10.02-/9.66-fold), reduced apoptosis (A549, 0.47‑fold; A427, 0.36-fold) and senescence (A549, 0.61-fold; A427, 0.37-fold), and increased reactive oxygen species levels (A549, 2.32‑fold; A427, 2.01‑fold); all these changes were attenuated by ARNT2 silencing. Transcriptomic and bioinformatic analyses identified ADP-ribosylation factor-like protein 14 (ARL14) as a downstream effector of ARNT2; ARL14 overexpression in ARNT2 ‑silenced cells restored proliferation and invasion and reduced apoptosis. Overall, experimental CNP exposure promotes NSCLC progression in an ARNT2-dependent manner, with ARL14 as a downstream mediator, which suggests potential targets for intervention in particulate-associated lung cancer.
SN  - 0147-6513
SN  - 1090-2414
ER  -