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Coal dust exposure induces proliferation and migration of human bronchial epithelial cells

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Abstract

Background

Coal dust exposure has caused a variety of lung diseases. In addition to genotoxicity and cytotoxicity, other biological changes caused by coal dust (CD) exposure need further study.

Objective

To observe the cellular transformation effects of CD exposure and explore its underlying molecular mechanism, human bronchial epithelial cells (BEAS-2B) were cultured with continuous CD exposure. Methylthiazolyldiphenyl-tetrazolium bromide (MTT) assay, colony formation assay, wound healing assay, next-generation sequencing (NGS) and western blotting were performed to observe the cell proliferation, migration, genomic transcription and pathological signaling pathways.

Results

We demonstrated that BEAS-2B cells with long-term chronic CD exposure show accelerated proliferation rate and enhanced migration ability, and have altered gene expression profiles and aberrant activation of EGFR/Raf/ERK and PI3K/AKT/mTOR pathways.

Conclusions

The results indicate that chronic CD exposure could induce abnormal proliferation and migration of BEAS-2B cells, lead to the transformation potential of human bronchial epithelial cells.

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References

  • Basset G, Crone C, Saumon G (1987) Fluid absorption by rat lung in situ: pathways for sodium entry in the luminal membrane of alveolar epithelium. J Physiol 384:325–345

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  • Bassiouni W, Ali MAM, Schulz R (2021) Multifunctional intracellular matrix metalloproteinases: implications in disease. FEBS J 288:7162–7182

    Article  CAS  PubMed  Google Scholar 

  • Bianchi ME, Mezzapelle R (2020) The chemokine receptor CXCR4 in cell proliferation and tissue regeneration. Front Immunol 11:2109

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  • Blackley DJ, Halldin CN, Laney AS (2018) Continued increase in prevalence of coal workers’ pneumoconiosis in the United States, 1970–2017. Am J Public Health 108:1220–1222

    Article  PubMed  PubMed Central  Google Scholar 

  • Cheng Y, Cheng T, Zhao Y, Qu Y (2019) HMGA1 exacerbates tumor progression by activating miR-222 through PI3K/Akt/MMP-9 signaling pathway in uveal melanoma. Cell Signal 63:109386

    Article  CAS  PubMed  Google Scholar 

  • Di Nardo L et al (2020) Molecular genetics of cutaneous squamous cell carcinoma: perspective for treatment strategies. J Eur Acad Dermatol Venereol 34:932–941

    Article  PubMed  Google Scholar 

  • Doney BC et al (2020) Respirable coal mine dust at surface mines, United States, 1982–2017. Am J Ind Med 63:232–239

    Article  CAS  PubMed  Google Scholar 

  • Gasparotto J et al (2018) Obese rats are more vulnerable to inflammation, genotoxicity and oxidative stress induced by coal dust inhalation than non-obese rats. Ecotoxicol Environ Saf 165:44–51

    Article  CAS  PubMed  Google Scholar 

  • Guo CB et al (2007) Relationship between matrix metalloproteinase 2 and lung cancer progression. Mol Diagn Ther 11:183–192

    Article  CAS  PubMed  Google Scholar 

  • Jhanwar-Uniyal M et al (2019) Diverse signaling mechanisms of mTOR complexes: mTORC1 and mTORC2 in forming a formidable relationship. Adv Biol Regul 72:51–62

    Article  CAS  PubMed  Google Scholar 

  • Jiang W et al (2018) Sulfated polysaccharide of Sepiella Maindroni ink inhibits the migration, invasion and matrix metalloproteinase-2 expression through suppressing EGFR-mediated p38/MAPK and PI3K/Akt/mTOR signaling pathways in SKOV-3 cells. Int J Biol Macromol 107:349–362

    Article  CAS  PubMed  Google Scholar 

  • Kania N et al (2014) Subchronic inhalation of coal dust particulate matter 10 induces bronchoalveolar hyperplasia and decreases MUC5AC expression in male Wistar rats. Exp Toxicol Pathol 66:383–389

    Article  CAS  PubMed  Google Scholar 

  • Kashyap T et al (2018) Crosstalk between Raf-MEK-ERK and PI3K-Akt-GSK3β signaling networks promotes chemoresistance, invasion/migration and stemness via expression of CD44 variants (v4 and v6) in oral cancer. Oral Oncol 86:234–243

    Article  CAS  PubMed  Google Scholar 

  • Kurth LM, McCawley M, Hendryx M, Lusk S (2014) Atmospheric particulate matter size distribution and concentration in west Virginia coal mining and non-mining areas. J Expo Sci Environ Epidemiol 24:405–411

    Article  CAS  PubMed  Google Scholar 

  • León-Mejía G et al (2016) Cytotoxicity and genotoxicity induced by coal and coal fly ash particles samples in V79 cells. Environ Sci Pollut Res Int 23:24019–24031

    Article  PubMed  Google Scholar 

  • Li L, Jiang M, Li X, Zhou B (2021) Association between coalmine dust and mortality risk of lung cancer: a meta-analysis. Biomed Res Int 2021:6624799

    PubMed  PubMed Central  Google Scholar 

  • Lin X, Tan S, Fu L, Dong Q (2020) BCAT1 overexpression promotes proliferation, invasion, and Wnt signaling in non-small cell lung cancers. Onco Targets Ther 13:3583–3594

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  • Liu J, Ping W, Zu Y, Sun W (2014) Correlations of lysyl oxidase with MMP2/MMP9 expression and its prognostic value in non-small cell lung cancer. Int J Clin Exp Pathol 7:6040–6047

    CAS  PubMed  PubMed Central  Google Scholar 

  • Luanpitpong S et al (2014) Appalachian mountaintop mining particulate matter induces neoplastic transformation of human bronchial epithelial cells and promotes tumor formation. Environ Sci Technol 48:12912–12919

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  • Matzenbacher CA et al (2017) DNA damage induced by coal dust, fly and bottom ash from coal combustion evaluated using the micronucleus test and comet assay in vitro. J Hazard Mater 324:781–788

    Article  CAS  PubMed  Google Scholar 

  • Perret JL et al (2020) Respiratory surveillance for coal mine dust and artificial stone exposed workers in Australia and New Zealand: a position statement from the thoracic society of Australia and New Zealand. Respirology 25:1193–1202

    Article  PubMed  PubMed Central  Google Scholar 

  • Rajesh T, Jaya M (2017) Jaya M. In: Gunasekaran P, Noronha S, Pandey A (eds) Current Developments in Biotechnology and Bioengineering: Functional Genomics and Metabolic Engineering. Elsevier, London., pp 143–158

    Chapter  Google Scholar 

  • Rivero DH et al (2005) Acute cardiopulmonary alterations induced by fine particulate matter of Sao Paulo, Brazil. Toxicol Sci 85:898–905

    Article  CAS  PubMed  Google Scholar 

  • Saba E et al (2020) Effects of a herbal formulation, KGC3P, and its individual component, nepetin, on coal fly dust-induced airway inflammation. Sci Rep 10:14036

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  • Tirado-Ballestas IP et al (2022) Oxidative stress and alterations in the expression of genes related to inflammation, DNA damage, and metal exposure in lung cells exposed to a hydroethanolic coal dust extract. Mol Biol Rep. https://doi.org/10.1007/s11033-022-07341-0 (Epub ahead of print. PMID: 35334019)

    Article  PubMed  Google Scholar 

  • U.S. EPA (2011) Inhalation rates Exposure factors handbook 2011 ed. (final). US Environmental Protection Agency, Washington, DC (EPA/600/R-09/052F, 2011)

    Google Scholar 

  • Yu D, Qin Y, Jun-Qiang L, Shun-Lin G (2018) CNPY2 enhances resistance to apoptosis induced by cisplatin via activation of NF-κB pathway in human non-small cell lung cancer. Biomed Pharmacother 103:1658–1663

    Article  CAS  PubMed  Google Scholar 

  • Zhao L et al (2021) Characterization of dissolved organic matter derived from coal gangue packed in underground reservoirs of coal mines using fluorescence and absorbance spectroscopy. Environ Sci Pollut Res 28:17928–17941

    Article  CAS  Google Scholar 

Download references

Acknowledgements

The National Natural Science Foundation of China (NO. 82071862, 81872017, 81572431), Anhui Provincial Science and Technology program (NO. 1604a0802094, 202004j07020053), University Natural Science Research Project of Anhui Province (NO. KJ2018ZD011, KJ2018A0097, KJ2019A0093, KJ2020A0340, KJ2020A0338) and Research Foundation of the Institute of Environment-friendly Materials and Occupational Health (Wuhu), Anhui University of Science and Technology (ALW2020YF11) funded this research.

Author information

Author notes

  1. Amin Li, Yinci Zhang and Ruikai Wang contributed equally to this work.

Authors and Affiliations

  1. Medical School, Anhui University of Science and Technology, 168 Taifeng Street, Tianjiaan District, Huainan, China

    Amin Li, Yinci Zhang, Ruyue Xu, Yongfang Ma, Li Song, Weiya Cao & Xiaolong Tang

  2. First Affiliated Hospital, Anhui University of Science and Technology (Huainan First People’s Hospital), Huainan, China

    Amin Li & Ruikai Wang

  3. Institute of Environment-Friendly Materials and Occupational Health, Anhui University of Science and Technology, Wuhu, China

    Amin Li, Yinci Zhang, Ruyue Xu, Yongfang Ma, Li Song, Weiya Cao & Xiaolong Tang

Authors
  1. Amin Li
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  2. Yinci Zhang
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  3. Ruikai Wang
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  4. Ruyue Xu
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  8. Xiaolong Tang
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Contributions

XT and AL: conceived and designed the study; AL, YZ and RW: performed data analysis; RX, YM, LS and WC: performed the biological methodology and acquisition of data; AL: drafted the manuscript (assign co-first authors order according to workload). All the authors read and approved the final version of the manuscript.

Corresponding author

Correspondence to Xiaolong Tang.

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Conflict of interest

Amin Li declares that she has no conflict of interest. Yinci Zhang declares that she has no conflict of interest. Ruikai Wang declares that he has no conflict of interest. Ruyue Xu declares that she has no conflict of interest. Yongfang Ma declares that she has no conflict of interest. Li Song declares that he has no conflict of interest. Weiya Cao declares that she has no conflict of interest. XiaolongTang declares that he has no conflict of interest.

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This article does not contain any studies with human participants or animals performed by any of the authors.

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Li, A., Zhang, Y., Wang, R. et al. Coal dust exposure induces proliferation and migration of human bronchial epithelial cells. Mol. Cell. Toxicol. 19, 237–245 (2023). https://doi.org/10.1007/s13273-022-00252-y

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  • DOI: https://doi.org/10.1007/s13273-022-00252-y

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