Ontology highlight
ABSTRACT:
PROVIDER: PRJNA872330 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR21169159_1.fastq.gz | Fastqsanger.gz | |||
| SRR21169159_2.fastq.gz | Fastqsanger.gz | |||
| SRR21169160_1.fastq.gz | Fastqsanger.gz | |||
| SRR21169160_2.fastq.gz | Fastqsanger.gz | |||
| SRR21169161_1.fastq.gz | Fastqsanger.gz |
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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:To study modulators of inflammatory airway disease, we developed an in vitro bronchial epithelial cell model system based on the BEAS-2B cell line exposed to lipopolysaccharide (LPS) and diesel exhaust particles (DEP). Combined LPS and DEP exposure triggered a molecular inflammatory phenotype, including elevated TSLP and IL-8 mRNA expression, similar to that observed in airway epithelial cells from asthma patients. In this model, we performed high-throughput perturbation of 24 mRNA and long non-coding (lncRNA) target genes through an arrayed CRISPR-interference screen, followed by shallow RNA-sequencing to identify modulators of inflammation. Perturbation of individual targets had a significant impact on the BEAS-2B DEP/LPS transcriptome. Some mRNA targets reversed the DEP/LPS gene expression signature upon knockdown and could serve as candidate therapeutic targets. Perturbation of other target genes however further amplified the pro-inflammatory signature and thus may have an anti-inflammatory role in these cells. In conclusion, we present a novel in vitro model system for airway inflammation that exhibited an inflammatory profile relevant for asthmatic patients, and demonstrate the feasibility to perform high-throughput target perturbation and molecular phenotyping by integrating CRISPR-interference and shallow RNA-sequencing.
2024-09-15 | GSE271359 | GEO
Project description:Sepsis-induced acute lung injury (ALI) poses a significant threat to human health, necessitating further investigation into its underlying mechanisms. Long noncoding RNAs (lncRNAs) have emerged as key regulators in various diseases, including sepsis. In our prior research, we observed significant downregulation of lncRNA RP11-284N8.3 in the blood samples of sepsis patients. Herein, we elucidate the functional role and regulatory molecular targets of RP11-284N8.3 in lipopolysaccharide (LPS)-exposed BEAS-2B cells. Initially, we found that LPS treatment notably repressed RP11-284N8.3 expression. However, overexpression of RP11-284N8.3 significantly promoted cell proliferation, inhibited apoptosis, and attenuated IL-1β expression in response to LPS stimulation, indicative of its anti-inflammatory properties. Further RNA-seq analysis revealed that RP11-284N8.3 might have contributed to the significant down-regulation of genes associated with the inflammatory response, while genes related to cell cycle/division and apoptosis underwent alternative splicing (AS) deregulation. Finally, RT-qPCR was used to validate differentially expressed genes (DEGs) (ICAM5, GDF15, NECTIN4, SERPINB2) and AS genes (IL24, APEX1, PVT1, HNRNPUL1) regulated by RP11-284N8.3, consistent with transcriptome changes. In summary, RP11-284N8.3 has a significant global regulatory effect in LPS-treated BEAS-2B cells and its possible protective role against sepsis-induced ALI. We propose RP11-284N8.3 and its downstream targets as potential therapeutic targets for sepsis management in the future.
2025-06-12 | GSE299503 | GEO
Project description:In order to identify H3K27ac enhancer marks influenced by FOXA2 and/or KRAS.G12V, BEAS-2B cells were infected with lentivirus carrying rat FOXA2 and/or retrovirus carrying human KRAS.G12V. FOXA2 and/or KRAS.G12V-expressing BEAS-2B cells were used for chromatin immunoprecipitation-sequencing (ChIP-seq) to detect genome-wide H3K27ac positive regions.
2025-07-01 | GSE210081 | GEO
Project description:Total RNA samples from human bronchial epithelial BEAS-2B passage-matched control cells and Cr(VI)-transofmred BEAS-2B cells were submitted to ArraySatr for total RNA m6A epitranscriptomic microarray analysis
2022-06-29 | GSE186605 | GEO
Project description:MicroRNA levels in non-transformed BEAS-2B bronchial epithelial cells, two lines of mycoplasma transformed BEAS-2B cells, and A549 lung adenocarcinoma cells were measured. Microarray analyses of 1145 microRNAs in A549 lung adenocarcinoma cells and two other transformed lung cell types relative to BEAS-2B bronchial epithelial cells were performed. 106 miRNAs were down-regulated and 69 miRNAs were up-regulated in all three transformed lines
2014-03-11 | GSE55748 | GEO
Project description:The objective of this study was to determine binding patterns for GR, 65 and RNAP2 in Beas-2B airway epithelial cells after treatment with dexamethasone (100 nm), TNF (20 ng/ml) or both for one hour. This study utilized duplicate samples for each treatment condition and immunoprecipitation except for p65 immunoprcipitation of TNF treated samples, which was analyzed as a single sample. Input from vehicle treated cells was used a control. Experimental comparisons were made between the following samples/ treatment conditions. Duplicate samples of Beas-2B cells treated with ethanol (vehicle) were used for ChIP of GR, p65, and RNAP2 (2 samples each antibody). Duplicate samples of Beas-2B cells treated with dexamethasone were used for ChIP of GR and RNAP2 (2 samples each antibody). Duplicate samples of Beas-2B cells treated with TNF were used for ChIP of p65 and RNAP2 (1 sample p65, 2 samples RNAP2). Duplicate samples of Beas-2B cells treated with dexamethasone + TNF were used for ChIP of GR, p65 and RNAP2 (2 samples each antibody).
2016-04-01 | E-GEOD-79803 | biostudies-arrayexpress
Project description:We reported the application of next generation sequencing technology for high-throughput profiling of miRNA expression in bronchile epithelial cell line Beas-2b with epithelial or mesenchymal mophology. By comparation the expression aboundence of known miRNAs between epithelial type and mesenchymal type Beas-2b cells, we found both upregulated and downregulated miRNAs in bronchial epithelial cells during EMT. This study provides a basic condition for further investigation of the roles of the regulated miRNAs during EMT in bronchial epithelial cells.
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Project description:We report the RNA sequencig results for the constitutive and IFN inducible gene expression in respiratory epithelial cell line (BEAS-2B). We generated IRF1 KO BEAS-2B cells using CRISPR method. Parent and IRF1 KO cells were treated with IFNβ or IFNλ1 for 24h and subjected for RNA isolation and sequencing in Illumina platform. Three independent biological experiments were used for RNA sequenccing.
2019-06-10 | GSE114284 | GEO