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BEAS2B cells and A549 cells: control versus nanoparticle exposure

ABSTRACT: Fragmentary knowledge exists on the adverse health effects of CoO- and CeO2-nanoparticles (NP)s. We analyzed toxicogenomic profiles of BEAS-2B versus A549 cells using genome-wide transcriptomics to identify molecules and cellular processes that are triggered by monodispersed noncytotoxic suspensions of 7-nm CoO- and 4-nm CeO2-NPs for 3, 6, 10, and 24 hours. We aimed to investigate 1) whether a cell type responds similarly to two different NPs exposure, 2) whether alveolar versus bronchial epithelial cells respond differently to the same NP, and 3) whether immune processes are influenced. The kinetics of the cell responses induced by the two NPs were different between the two lung epithelial cell models. Both CoO- and CeO2-NP exposure induced mainly downregulation of gene transcription. BEAS-2B cells were found to be more sensitive towards NP exposure, as they showed a higher total number of differentially expressed transcripts (DET) at a 10-fold lower NP-concentration than A549 cells. Hierarchical clustering of all DET indicated that the transcriptional responses were quite heterogeneous among the two cell types and two NPs. Between 1% and 14% DET encoding markers involved in immune system processes were observed in the BEAS-2B and A549 cell lines, with the highest fractions observed in BEAS-2B cells. Most of these genes, i.e. ITGB2, TLR6, PAG1, HLA-DRB3, TIRAP, and HLA-A, are involved in immune signalling. The AKT1 gene, which showed persistently decreased expression levels, was identified as a possible generic marker of lung epithelial cell-NP interaction. Our data suggest that CoO- and CeO2-NPs give rise to distinct responses.

ORGANISM(S): Homo sapiens

PROVIDER: GSE45763 | GEO | 2014/12/01

SECONDARY ACCESSION(S): PRJNA196235

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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BEAS2B cells and A549 cells: control versus nanoparticle exposure

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