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

• Published in: Molecular & cellular toxicology Vol. 19; no. 2; pp. 237 - 245
• Main Authors: Li, Amin, Zhang, Yinci, Wang, Ruikai, Xu, Ruyue, Ma, Yongfang, Song, Li, Cao, Weiya, Tang, Xiaolong
• Format: Journal Article
• Language: English
• Published: Singapore Springer Nature Singapore 01-04-2023; Springer Nature B.V
• Subjects: 1-Phosphatidylinositol 3-kinase; AKT protein; Biomedical and Life Sciences; Cell Biology; Cell migration; Cell proliferation; Coal; Coal dust; Cytotoxicity; Dust; Epithelial cells; Gene expression; Genetic transformation; Genotoxicity; Life Sciences; Lung diseases; Next-generation sequencing; Original Article; Pharmacology/Toxicology; Raf protein; TOR protein; Western blotting; Wound healing; EGFR/Raf/ERK; PI3K/AKT/mTOR; Proliferation; Human bronchial epithelial cells; Migration; Coal dust
• ISSN: 1738-642X; 2092-8467
• DOI: 10.1007/s13273-022-00252-y

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.