Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA382636 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR5444680.fastq.gz | Fastqsanger.gz | |||
| SRR5444681.fastq.gz | Fastqsanger.gz | |||
| SRR5444682.fastq.gz | Fastqsanger.gz | |||
| SRR5444683.fastq.gz | Fastqsanger.gz | |||
| SRR5444684.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 12 |
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Project description:A systematic RNA-seq study comparing the transcriptional response to three independent bulky DNA damage inducing agents: UV, the chemotherapy cisplatin and benzo[a]pyrene, a component of cigarette smoke. It was performed in 2 different cell lines - GM12878 immortalized lymphoblast cell line and A549 lung cancer cell line.
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Project description:Benzo[a]pyrene (BaP) is a known human carcinogen (IARC Group 1) found in food, coal tar, as well as cigarettes and other smoke. Its diol-epoxide metabolites (Benzo[a]pyrene diol-epoxide [BPDE]) react with DNA forming DNA adducts, predominantly N2-BPDE-deoxyguanosine (N2-BPDE-dG). While the capacity of BPDEs to alkylate DNA and induce mutations is well known, little is known about how the genomic features influence the accumulation of DNA damage at a genome-wide level. To bridge this gap, we developed a single-nucleotide resolution damage sequencing method to map N2-BPDE-dG in a BPDE exposed human lung cell line, and combined this analysis with mass spectrometry to quantify the total absolute levels of the adduct in the genome. Comparing damage abundance with DNase hypersensitive sites, transcription levels, and other genome annotation data showed that although the overall adduct levels increased with increasing concentration of BPDE, the genomic distribution patterns of N2-BPDE-dG were stable and correlated with the genomic features related to chromatin state and transcriptional activities. In addition, we extracted the preferred local DNA sequence contexts for N2-BPDE-dG, i.e., its DNA damage signature, and found that it was highly similar to the mutational signatures identified from smoking-related lung cancers. These results suggest that genomic features and sequence contexts are important in shaping the landscape of DNA damage arising from chemical exposures and provide an effective strategy for linking single-nucleotide resolution damage sequencing data with cancer mutations.
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Project description:Benzo[a]pyrene is a Group 1 carcinogen. It undergoes metabolism in the liver through CYP1A1 and CYP1B1 enzymes. This study was conducted to investigate the response to benzo[a]pyrene in the liver when these enzymes are knocked down.
2024-01-03 | GSE252339 | GEO
Project description:Benzo(a)pyrene is a well-established human carcinogen in humans and rodents. In the present study, we sought to determine the dose- and time-dependent changes in gene expression upon oral exposure to benzo(a)pyrene. Adult male B6C3F1 mice were exposed to four doses of benzo(a)pyrene or vehicle control for three days and sacrificed 4 or 24 hours after the final exposure.
2015-07-01 | GSE43633 | GEO
Project description:Benzo(a)pyrene is a well-established human carcinogen in humans and rodents. In the present study, we sought to determine the dose- and time-dependent changes in gene expression upon oral exposure to benzo(a)pyrene. Adult male MutaTMMouse were exposed to three doses of benzo(a)pyrene or vehicle control (olive oil) for 28 days and sacrificed three days after the final exposure.
2013-09-27 | GSE43438 | GEO
Project description:DNA damage induced by benzo(a)pyrene may lead to the formation of mutations and as a consequence to the development of diseases. However, it is uncertain whether benzo(a)pyrene causes heritable mutations in male germ cells, which would increase health risks in offspring. In a previous study, benzo(a)pyrene induced DNA damage was observed at all stages of spermatogenesis and in testis. In addition, we observed that spermatogonial stem cells and testis rely, at least in part, on nucleotide excision repair for the removal of this damage, because removal was less efficient in Xpc-/- than in wild type mice. Efficient removal will protect the germ cells against the formation of heritable mutations. By using microarray technology, we investigated in this study the consequences of this difference in DNA adduct removal at the level of gene expression in testis 4 days after a single exposure to benzo(a)pyrene.
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Project description:DNA damage induced by benzo(a)pyrene may lead to the formation of mutations and as a consequence to the development of diseases. However, it is uncertain whether benzo(a)pyrene causes heritable mutations in male germ cells, which would increase health risks in offspring. In a previous study, benzo(a)pyrene induced DNA damage was observed at all stages of spermatogenesis and in testis. In addition, we observed that spermatogonial stem cells and testis rely, at least in part, on nucleotide excision repair for the removal of this damage, because removal was less efficient in Xpc-/- than in wild type mice. Efficient removal will protect the germ cells against the formation of heritable mutations. By using microarray technology, we investigated in this study the consequences of this difference in DNA adduct removal at the level of gene expression in testis 4 days after a single exposure to benzo(a)pyrene. We analyzed 20 testis samples of mice divided into 4 groups (5 mice per group): C57BL/6 control mice, C57BL/6 mice exposed to B[a}P, Xpc-/- control mice, Xpc-/- mice exposed to B[a]P. We used a pool of 3 C57BL/6 control mice as a reference.
2010-08-23 | E-GEOD-17979 | biostudies-arrayexpress
Project description:Global loss of DNA methylation and locus/gene-specific gain of DNA methylation are two distinct hallmarks of carcinogenesis. Aberrant DNA methylation is implicated in smoking-related lung cancer. In this study, we have comprehensively investigated the modulation of DNA methylation consequent to chronic exposure to a prototype smoke-derived carcinogen, benzo[a]pyrene diol epoxide (B[a]PDE), in genomic regions of significance in lung cancer, in normal human cells. We have used a pulldown assay for enrichment of the CpG methylated fraction of cellular DNA combined with microarray platforms, followed by extensive validation through conventional bisulfite-based analysis. Here, we demonstrate strikingly similar patterns of DNA methylation in non-transformed B[a]PDE-treated cells vs control using high-throughput microarray-based DNA methylation profiling confirmed by conventional bisulfite-based DNA methylation analysis. The absence of aberrant DNA methylation in our model system within a timeframe that precedes cellular transformation suggests that following carcinogen exposure, other as yet unknown factors (secondary to carcinogen treatment) may help initiate global loss of DNA methylation and region-specific gain of DNA methylation, which can, in turn, contribute to lung cancer development. Unveiling the initiating events that cause aberrant DNA methylation in lung cancer has tremendous public health relevance, as it can help define future strategies for early detection and prevention of this highly lethal disease. Methylated fragments in genomic DNA extracted from benzo[a]pyrene diol epoxide (B[a]PDE)-treated normal human fibroblasts versus control (solvent [dimethylsulfoxide (DMSO)-treated counterpart cells] were enriched with the MIRA assay and hybridized together with input genomic DNA to NimbleGen's whole genome tiling array.
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Project description:Benzo(a)pyrene is a well-established human carcinogen in humans and rodents. In the present study, we sought to determine the dose- and time-dependent changes in gene expression upon oral exposure to benzo(a)pyrene. Adult male MutaTMMouse were exposed to three doses of benzo(a)pyrene or vehicle control (olive oil) for 28 days and sacrificed three days after the final exposure. This experiment examined the forestomach transcriptional response of male mice exposed to BaP for 28 days at three different doses, including D1 (25 mg/kg BW/day), D2 (50 mg/kg BW/day), and D3 (75 mg/kg BW/day) and vehicle control. Each dose group was examined 72 hours following the final exposure. Each dose group and time point had 4-5 biological replicates. There were a total 17 samples (arrays) included in the final analysis using a two-colour reference design.
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Project description:Benzo(a)pyrene (Bap), a key component of cigarette smoke (CS), is a pollutant and widely present in our daily life. The roles of Bap on viral replication have been amply discussed and controversial. In our present study, we investigated the effect and mechanism of Bap on the replication of vesicular stomatitis virus (VSV) and respiratory syncytial virus (RSV) in vitro. HeLa cells were pre-exposed to Bap at 10 μM for 48 h and then infected with VSV (MOI=1) for 24 h. RNA sequencing analysis was conducted to identify Bap-dysregulated genes and qPCR analysis was used to identify the result. Chronic exposed to Bap significantly inhibited the replication of VSV and RSV in vitro and in vivo.
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