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Gene expression profiling in BEAS-2B cells treated with organic extracts from particulate matter produced by gasoline (E0) or gasoline-ethanol blend (E15)

ABSTRACT: The aim of this study was to perform comparative analysis of global gene expression changes in lung BEAS-2B cells in response to treatment with extracts of particulate matter produced by conventional gasoline (E0) or biogasoline (E15) differing in the content of organic compounds, particularly PAHs. To examine the toxicity, we monitored genome-wide gene expression changes in human lung BEAS-2B cells, exposed for 4h and 24h to a subtoxic dose of each PM extract. After 4h exposure, numerous dysregulated genes and processes such as oxidative stress, lipid and steroid metabolism, PPARα signaling and immune response, were found to be common for both extract treatments. Twenty four hour exposure resulted in more distinctive gene expression patterns. Although several common modulated processes indicating the metabolism of PAHs and activation of aryl hydrocarbon receptor (AhR) were identified, E15 specifically dysregulated a variety of other genes and pathways related to cancer promotion and progression, possibly due to the increased PAH content in PM organic extract.

ORGANISM(S): Homo sapiens

PROVIDER: GSE180932 | GEO | 2021/07/28

REPOSITORIES: GEO

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Project description:As environmental pollutants and possible carcinogens, carbon nanotubes (CNTs) have recently been found to promote tumorigenesis and tumor metastasis after long-term pulmonary exposure. However, whether CNT-induced carcinogenesis can be inherited and last for generations remains unknown. Here, we establish a post-chronic single-walled carbon nanotubes (SWCNTs) exposed human bronchial epithelium BEAS-2B cell model to investigate SWCNTs-induced carcinogenesis. At a tolerated sublethal dose level, post-chronic SWCNTs exposure significantly increases the migration and colony formation abilities of BEAS-2B cells, leading to cell malignant transformation. Notably, the malignant transformation of BEAS-2B cells is irreversible within 60 days recovery period after SWCNTs exposure, and the malignant transformation activities of cells gradually increase during the recovery period. Mechanism analyses show that post-chronic exposure to SWCNTs causes substantial DNA methylation and transcriptome dysregulation of BEAS-2B cells. Subsequent enrichment and clinical database analyses reveal that differentially expressed/methylated genes of BEAS-2B cells are enriched in cancer-related biological pathways, and several of these genes are validated in lung cancer patients. As environmental pollutants and possible carcinogens, carbon nanotubes (CNTs) have recently been found to promote tumorigenesis and tumor metastasis after long-term pulmonary exposure. However, whether CNT-induced carcinogenesis can be inherited and last for generations remains unknown. Here, we establish a post-chronic single-walled carbon nanotubes (SWCNTs) exposed human bronchial epithelium BEAS-2B cell model to investigate SWCNTs-induced carcinogenesis. At a tolerated sublethal dose level, post-chronic SWCNTs exposure significantly increases the migration and colony formation abilities of BEAS-2B cells, leading to cell malignant transformation. Notably, the malignant transformation of BEAS-2B cells is irreversible within 60 days recovery period after SWCNTs exposure, and the malignant transformation activities of cells gradually increase during the recovery period. Mechanism analyses show that post-chronic exposure to SWCNTs causes substantial DNA methylation and transcriptome dysregulation of BEAS-2B cells. Subsequent enrichment and clinical database analyses reveal that differentially expressed/methylated genes of BEAS-2B cells are enriched in cancer-related biological pathways, and several of these genes are validated in lung cancer patients.

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Gene expression profiling in BEAS-2B cells treated with organic extracts from particulate matter produced by gasoline (E0) or gasoline-ethanol blend (E15)

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