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RNA-Seq analysis of gene expression changes by wildtype and Nlrx1 deficient BEAS-2B airway epithelial cells in response to A. fumigatus viable conidia

ABSTRACT: RNA-Seq analysis of gene expression changes by wildtype and Nlrx1 deficient BEAS-2B airway epithelial cells in response to A. fumigatus viable conidia

PROVIDER: PRJNA604500 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR11003418_1.fastq.gz	Fastqsanger.gz
	SRR11003418_2.fastq.gz	Fastqsanger.gz
	SRR11003419_1.fastq.gz	Fastqsanger.gz
	SRR11003419_2.fastq.gz	Fastqsanger.gz
	SRR11003420_1.fastq.gz	Fastqsanger.gz

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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.

Dataset Information

RNA-Seq analysis of gene expression changes by wildtype and Nlrx1 deficient BEAS-2B airway epithelial cells in response to A. fumigatus viable conidia

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