Unknown,Transcriptomics,Genomics,Proteomics

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Gene expression profiles in human alveolar epithelial cell line exposure to single carbon nanotubes

ABSTRACT: To further development of our gene expression approach to assess the effects of manufactured nanomaterials at the molecular level, we have employed whole genome microarray expression profiling as a discovery platform to identify genes with the potential to distinguish characterization of physico-chemical properties of single-wall carbon nanotubes (SWCNTs). Three kinds of single-wall carbon nanotubes (SWCNTs), CNT-1, CNT-2 or CNT-3 induced gene expression in human alveolar epithelial cell lines were measured at 24 and 48 hours exposure to doses of 90.8Î¼g/mL (CNT-1), 109.0Î¼g/mL (CNT-2), and 77.0Î¼g/mL (CNT-2). Three independent experiments were performed at each time (24 or 48 hours) using different untreated control for each experiment (n=4).

ORGANISM(S): Homo sapiens

SUBMITTER: Katsuhide Fujita

PROVIDER: E-GEOD-41101 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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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 profiles in human alveolar epithelial cell line exposure to single carbon nanotubes

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