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Expression data from MCF-7 breast cancer cells treated with CNTs, ginsenosides (Rb1 and Rg1) and conjugates (Rb-CNTs and Rg-CNTs)

ABSTRACT: To investigate the effects of ginsenosides-CNTs conjugtaes on total expression profile of MCF-7 breast cancer cells, we conjugated ginsenoides Rb1 and Rg1 with multi-walled carbon nanotubes in a 5:1 ratio. Objectives for this study included the identification of genes that were up or down-regulated at the transcriptional level in MCF-7 cells treated with ginsenoside-CNTs conjugates and compare it to the ginsenosides alone (Rb1 and Rg1)

ORGANISM(S): Homo sapiens

PROVIDER: GSE75570 | GEO | 2016/12/15

SECONDARY ACCESSION(S): PRJNA304617

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.

Dataset Information

Expression data from MCF-7 breast cancer cells treated with CNTs, ginsenosides (Rb1 and Rg1) and conjugates (Rb-CNTs and Rg-CNTs)

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