Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA191099 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Transcriptonal profiling of BEAS-2B cells: Control versus skin sensitizers; Control versus respiratory sensitizers; Control versus non-sensitizing irritants Replicates: 3 biological replicates; Exposure: 10 different chemicals versus solvent, 1 exposure concentration (IC20); Exposure time: 3 different exposure time points;
2013-12-01 | E-GEOD-44729 | biostudies-arrayexpress
Project description:Transcriptonal profiling of BEAS-2B cells: Control versus skin sensitizers; Control versus respiratory sensitizers; Control versus non-sensitizing irritants
2013-12-01 | GSE44729 | GEO
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: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:The study seeks to identify the epigenetic changes caused by exposure of to cigarette smoke condensate. To this goal human bronchial epithelial cells, BEAS-2B, were treated with 5-aza-2’deoxycitidine and trychostatin A (5AzaC/TSA) subsequent to a chronic exposure (1 month) to cigarette smoke condensate (CSC). As negative control served BEAS-2B cells that were untreated or treated with CSC/DMSO for one month without the subsequent application of 5Aza/TSA. Keywords: stress response
2009-08-01 | GSE14385 | GEO
Project description:We established chromate transformed cell lines by chronic exposure of normal human bronchial epithelial BEAS-2B cells to low doses of hexavalent chromium followed by anchorage-independent growth. The gene expression profiles were analyzed in the established cell lines. The gene expression profiles from six chromate transformed cell lines were remarkably similar to each other yet differed significantly from that of either control cell line or normal Beas-2B cells. A total of 409 differentially expressed genes were identified in chromate transformed cells compared to control cells.
2010-09-14 | GSE24025 | 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: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.
2014-12-01 | GSE45763 | GEO
Project description:HmiOA4.1 microarrays-BEAS-2B cells treatment with NiCl2
| PRJNA281473 | ENA