Abstract
Extensive use of gallium arsenide (GaAs) has led to increased exposure to humans working in the semiconductor industry. This study employed physicochemical characterization of GaAs obtained from a workplace, cytotoxicity analysis of damage induced by GaAs in 16HBE cells, RNA-seq and related bioinformatic analysis, qRT-PCR verification and survival analysis to comprehensively understand the potential mechanism leading to lung toxicity induced by GaAs. We found that GaAs-induced abnormal gene expression was mainly related to the cellular response to chemical stimuli, the regulation of signalling, cell differentiation and the cell cycle, which are involved in transcriptional misregulation in cancer, the MAPK signalling pathway, the TGF-β signalling pathway and pulmonary disease-related pathways. Ten upregulated genes (FOS, JUN, HSP90AA1, CDKN1A, ESR1, MYC, RAC1, CTNNB1, MAPK8 and FOXO1) and 7 downregulated genes (TP53, AKT1, NFKB1, SMAD3, CDK1, E2F1 and PLK1) related to GaAs-induced pulmonary toxicity were identified. High expression of HSP90AA1, RAC1 and CDKN1A was significantly associated with a lower rate of overall survival in lung cancers. The results of this study indicate that GaAs-associated toxicities affected the misregulation of oncogenes and tumour suppressing genes, activation of the TGF-β/MAPK pathway, and regulation of cell differentiation and the cell cycle. These results help to elucidate the molecular mechanism underlying GaAs-induced pulmonary injury.
Highlights
gallium arsenide (GaAs) is a crystalline intermetallic solid composed of arsenic (As) and gallium (Ga)[7]
As the dose increased to 20.0 μg/cm[2], the cell viability lost nearly 15%, as measured with LDH, and cell mortality increased nearly 20%, as measured with Cell Counting Kit-8 (CCK-8), which was significant compared with that in the control group
Because GaAs has a lower solubility than any other arsenic compound and is associated with lung toxicity, even linked to lung neoplasm risk, exploring the toxicogenomic effects of GaAs on human bronchial epithelial cells is critical to understanding the mechanisms of these adverse health effects[7,16]
Summary
GaAs is a crystalline intermetallic solid composed of arsenic (As) and gallium (Ga)[7]. An in vitro model is an important means to study the adverse effects of particulate pollutants on the respiratory tract and the means of action. To assess the effects of particle pollution on the respiratory tract, it is important to develop systems and methods that allow cultured cells to be repeatedly exposed to particles in the mixture. The objective of this study was to evaluate the cytotoxic effects of GaAs particles on 16HBE cells, to obtain differentially expressed genes induced by GaAs particles, and to reveal potential mechanisms of pulmonary injury after exposure. To better understand the potential molecular mechanisms underlying the pulmonary toxicity of the GaAs particles, 16HBE cells were chosen as the in vitro exposure model, and RNA-seq, related bioinformatic analysis, qRT-PCR verified analysis and survival curve analysis using The Cancer Genome Atlas (TCGA) data were conducted
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