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Combustion-derived particles from biomass sources differently promote epithelial-to-mesenchymal transition on A549 cells.

ABSTRACT: Combustion-derived particles (CDPs), due to the presence in their composition of several toxic and carcinogenic chemical compounds, such as polycyclic aromatic hydrocarbons (PAHs) and metals, are linked to several respiratory diseases, including lung cancer. Epithelial-to-mesenchymal transition (EMT) is a crucial step in lung cancer progression, involving several morphological and phenotypical changes. The study aims to investigate how exposure to CDPs from different biomass sources might be involved in cancer development, focusing mainly on the effects linked to EMT and invasion on human A549 lung cells. Biomass combustion-derived particles (BCDPs) were collected from a stove fuelled with pellet, charcoal or wood, respectively. A time course and dose response evaluation on cell viability and pro-inflammatory response was performed to select the optimal conditions for EMT-related studies. A significant release of IL-8 was found after 72 h of exposure to 2.5 μg/cm² BCDPs. The EMT activation was then examined by evaluating the expression of some typical markers, such as E-cadherin and N-cadherin, and the possible enhanced migration and invasiveness. Sub-acute exposure revealed that BCDPs differentially modulated cell viability, migration and invasion, as well as the expression of proteins linked to EMT. Results showed a reduction in the epithelial marker E-cadherin and a parallel increase in the mesenchymal markers N-cadherin, mainly after exposure to charcoal and wood. Migration and invasion were also increased. In conclusion, our results suggest that BCDPs with a higher content of organic compounds (e.g. PAHs) in their chemical composition might play a crucial role in inducing pro-carcinogenic effects on epithelial cells.

SUBMITTER: Marchetti S

PROVIDER: S-EPMC8032642 | biostudies-literature |

REPOSITORIES: biostudies-literature

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Project description:BackgroundExposure to indoor air pollution from solid fuel combustion is associated with lung diseases and cancer. This study investigated the cytotoxicity and molecular mechanisms of biomass combustion-derived particles in human pulmonary alveolar epithelial cells (HPAEpiC) using a platform that combines air-liquid interface (ALI) and dynamic culture (DC) systems.MethodsHPAEpiC were cultured on the surface of polycarbonate (PC) membranes on the ALI-DC platform. The cells were sprayed with an aerosolized solution of biomass combustion soluble constituents (BCSCs) and simultaneously nourished with culture medium flowing beneath the permeable PC membranes. The ALI-DC method was compared with the traditional submerged culture approach. BCSC particle morphology and dosages deposited on the chip were determined for particle characterization. Flow cytometry, scanning electron microscopy, and transmission electron microscopy were used to investigate the apoptosis rate of HPAEpiC and changes in the cell ultrastructure induced by BCSCs. Additionally, the underlying apoptotic pathway was examined by determining the protein expression levels by western blotting.ResultsScanning electron microscope images demonstrated that the sample processing and delivering approach of the ALI-DC platform were suitable for pollutant exposure. Compared with the submerged culture method, a significant decline in cell viability and increase in apoptosis rate was observed after BCSC exposure on the ALI-DC platform, indicating that the ALI-DC platform is a more sensitive system for investigating cytotoxicity of indoor air pollutants in lung cells. The morphology and ultrastructure of the cells were damaged after exposure to BCSCs, and the p53 pathway was activated. The Bcl-2/Bax ratio was reduced, upregulating caspase-9 and caspase-3 expression and subsequently inducing apoptosis of HPAEpiC. The addition of N-acetyl cysteine antioxidant significantly alleviated the cytotoxicity induced by BCSCs.ConclusionA novel ALI-DC platform was developed to study the cytotoxicity of air pollutants on lung cells. Using the platform, we demonstrated that BCSCs could damage the mitochondria, produce reactive oxygen species, and activate p53 in HPAEpiC, ultimately inducing apoptosis.

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Combustion-derived particles from biomass sources differently promote epithelial-to-mesenchymal transition on A549 cells.

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