Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1106629 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR28857256_1.fastq.gz | Fastqsanger.gz | |||
| SRR28857256_2.fastq.gz | Fastqsanger.gz | |||
| SRR28857257_1.fastq.gz | Fastqsanger.gz | |||
| SRR28857257_2.fastq.gz | Fastqsanger.gz | |||
| SRR28857258_1.fastq.gz | Fastqsanger.gz |
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Project description:The aim of the present study was to characterize a common and unique signalling pathways associated to two seasonal particulate matter (PM) (winter PM2.5 and summer PM10) in human bronchial BEAS-2B cells by mean of a global transcriptomic profiling (including genes and miRNA) and the investigation of selected pathways at protein level.
2016-05-26 | E-MTAB-3629 | biostudies-arrayexpress
Project description:The aim of the present study was to characterize a common and unique signalling pathways associated to two seasonal particulate matter (PM) (winter PM2.5 and summer PM10) in human bronchial BEAS-2B cells by mean of a global transcriptomic profiling (including genes and miRNA) and the investigation of selected pathways at protein level.
2016-05-26 | E-MTAB-3630 | biostudies-arrayexpress
Project description: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.
2021-07-28 | GSE180932 | GEO
Project description:Gene expression data from BEAS-2B cells upon exposure to particulate matter (PM2.5) from biomass combustion
| PRJNA667085 | ENA
Project description:We report the differential expression of circRNAs between T-BEAS-2B cells (cadmium-transformed BEAS-2B cells) and C-BEAS-2B cells (passage-matched control BEAS-2B cells) by high-throughput sequencing. T-BEAS-2B cells are BEAS-2B cells transformed by cadmium at 2.0 μM for twenty weeks, and C-BEAS-2B cells are their passage-matched control. RNAs were sequenced on Illumina HiSeq Xten platform in triplicates, and expressions of circRNAs were calculated by TPM (transcripts per kilobase of exon model per million mapped reads). Clean data per sample exceeds 10 GB. We find 235 significantly up-regulated circRNAs and 271 significantly down-regulated circRNAs in T-BEAS-2B cells relative to C-BEAS-2B cells. Our work provides clues and evidence for exploring the mechanism of circRNAs in cadmium carcinogenesis.
2024-01-26 | GSE165549 | GEO
Project description:Airborne particulate matter affects gene expression in BEAS-2B bronchial epithelial cells.
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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.
2020-06-26 | GSE153246 | GEO
Project description:Alterations in chromatin modifications, including DNA methylation and histone modification patterns, have been characterized under exposure of several environmental pollutants, including nickel. As with other carcinogenic metals, the mutagenic potential of nickel compounds is low and is not well correlated with its carcinogenic effects. Nickel exposure, however, is associated with alterations in chromatin modifications and related transcriptional programs, suggesting an alternative pathway whereby nickel exposure can lead to disease. To investigate the extent to which nickel exposure disrupts chromatin patterns, we profiled several histone modifications, including H3K4me3, H3K9ac, H3K27me3 and H3K9me2 as well as the insulator binding protein CTCF and the transcriptomes of control BEAS-2B cells and cells treated with nickel for 72 hours. Our results show significant alterations of the repressive histone modification H3K9me2 in nickel-exposed cells with spreading of H3K9me2 into new domains associated with gene silencing. We furthermore show that local regions of active chromatin can protect genes from nickel-induced H3K9me2 spreading. Interestingly, we show that nickel exposure selectively disrupts weaker CTCF sites, leading to spreading of H3K9me2 at these regions. These results have major implications in the understanding of how environmental carcinogens can affect chromatin dynamics and the consequences of chromatin domain disruption in disease progression. Treat BEAS-2B cells with NiCl2 for 72 hours and compare histone modification, CTCF binding to control BEAS-2B cells to see how they regulated gene expression by RNA-seq
2014-09-26 | E-GEOD-56051 | biostudies-arrayexpress
Project description:This study aimed to shed light on the gene regulatory networks underlying plant leaf responses to air particulate matter. Our investigation focused on shrubs of Photinia x fraseri grown in pots located in two contrasting areas: a highly polluted traffic road and rural countryside within the same town (Altopascio, Lucca, Italy). RNA-seq data were related to leaf morphological traitsand air particulate matter, allowing to identify key players in modulating the capabilities of plants to phyllo-remediate high air particulate matter levels in urban environment.
2023-03-23 | E-MTAB-12477 | biostudies-arrayexpress
Project description:This study aimed to shed light on the gene regulatory networks underlying plant leaf responses to air particulate matter. Our investigation focused on autochthonous shrubs of laurel (Laurus nobilis L.) grown in pots located in two contrasting areas: a highly polluted traffic road and rural countryside within the same town (Altopascio, Lucca, Italy). RNA-seq data were related to leaf morphological traits and air particulate matter, allowing to identify key players in modulating the capabilities of plants to phyllo-remediate high air particulate matter levels in urban environment.
2023-03-16 | E-MTAB-12332 | biostudies-arrayexpress