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Transcriptome Profiling of PanIN Cells Exposed to Tobacco Carcinogen

ABSTRACT: Transcriptome Profiling of PanIN Cells Exposed to Tobacco Carcinogen

PROVIDER: PRJNA489448 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR7789350.fastq.gz	Fastqsanger.gz
	SRR7789351.fastq.gz	Fastqsanger.gz
	SRR7789352.fastq.gz	Fastqsanger.gz
	SRR7789343.fastq.gz	Fastqsanger.gz
	SRR7789353.fastq.gz	Fastqsanger.gz

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Transcriptome Profiling of PanIN Cells Exposed to Tobacco Carcinogen

Project description:Purpose: The goals of this study are to compare transcriptome profiling (RNA-seq) in pancreatic intraepithelial neoplasm (PanIN) cells exposed to tobacco-specific nitrosamine 4-(methyl nitrosamino)-1-(3-pyridyl)-1-butanone (NNK) and to examine the upregulated pathways.

2018-09-06 | GSE119517 | GEO

Lipopolysaccharide-mediated chronic inflammation promotes tobacco carcinogen-induced lung tumorigenesis

Project description:We developed a two-staged lung cancer mouse model, which mimics the smoking carcinogen-induced, and chronic obstructive pulmonary disease (COPD)-related airway inflammation promoted lung cancers. We used the carcinogen 4-(methylnitrosamino)-1-(3- pyridyl)-1-butanone (NNK) to induce lung cancer and in parallel to repeated Lipopolysaccharide (LPS) installation to induce chronic lung inflammation. To identify genes associated with chronic inflammation promoting lung tumorigenesis, we have performed whole genome microarray expression profiling of mice exposed to Phosphate-Buffered Saline (PBS), NNK, LPS, and combined NNK and LPS.

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Lipopolysaccharide-mediated chronic inflammation promotes tobacco carcinogen-induced lung tumorigenesis

Project description:Lipopolysaccharide-mediated chronic inflammation promotes tobacco carcinogen-induced lung tumorigenesis

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RNA-sequencing of NNK-exposed Gprc5a-/- lung tumors

Project description:We have previously found that tobacco carcinogen exposed Gprc5a-/- develop lung tumors including adenocarcinoma. We sought to understand the molecular pathology of these lung tumors by whole-transcriptome sequence (RNA-Seq) analysis.

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Temporal RNA-sequencing of cytologically-normal mouse airway epithelia during tobacco carcinogen-associated lung tumorigenesis

Project description:Smoking perpetuates in cytologically-normal airways a molecular “field of injury” that is pertinent to lung cancer and early detection. The evolution of airway field changes prior to lung cancer onset is poorly understood largely due to the long latency of lung malignancy in smokers. Here we studied airway expression changes prior to lung cancer onset in mice with knockout of the Gprc5a gene and tobacco carcinogen (nicotine-specific nitrosamine ketone; NNK) exposure and that develop the most common type of lung cancer, lung adenocarcinoma (LUAD). Cytologically-normal airway epithelial brushings were collected before exposure and at multiple times following NNK exposure until time of LUAD development and then analyzed by RNA-sequencing (RNA-Seq).

2020-02-28 | GSE102707 | GEO

Genome-wide Methylation in Cordblood CD4+ Cells from Newborns Exposed vs. Unexposed to Maternal Tobacco Smoke During Pregnancy

Project description:We generated genome-wide methylation levels, using whole-genome bisulfite sequencing, for sorted CD4+ cells from cordblood of newborns exposed vs. unexposed to tobacco smoke in utero

2019-03-13 | GSE109212 | GEO

Dek overexpression under the environment exposed to carcinogen in oral squamous cell.

Project description:Oral squamous cell carcinoma (OSCC) develop multi-step carcinogenesis, including the concept of the field cancerization. DEK gene is considered to be a proto-oncogene, has multifaceted functions, such as replication, transcription, and chromatin remodeling, and also affects oncogenic process, such as cellular proliferation, differentiation, senescence, and apoptosis. DEK overexpression has proposed to be closely associated with many malignancies, however, functional mechanisms and crucial roles are still unclear. DEK-expressing cells significantly increased in human oral squamous cell carcinogenesis. We generated ubiquitous and squamous cell-specific Doxycycline (DOX)- inducible Dek mice (iDek and iDek-e mice, respectively). DOX administrated (DOX+) iDek mice promoted field cancerization and the development of OSCC in the environment exposed to carcinogen. By the microarray expression profiling analysis, the promotion of the filed cancerization by Dek overexpression was mediated by the upregulation of DNA replication- and cell cycle (G1 to S phase transition)-related genes. Further, Dek-overexpressed tongue tumors were progressed by proliferating cell nuclear antigen (Pcna) and the elongator complex protein 3 (Elp3). Our data suggest that, by DEK overexpression enhances the carcinogenesis, including field cancerization, of OSCC stimulating the G1-to-S phase transition in the cell-cycle and DNA replication, even after carcinogen-exposed environment, and offers a fascinating target for treatment and prevention of OSCC.

2016-10-05 | GSE87587 | GEO

Endothelial cells and exposure to enviromental tobacco

Project description:Endothelial cells from mice exposed to enviromental tobacco smoke for 1 or 6 weeks. Keywords: parallel sample

2005-01-20 | GSE2090 | GEO

Transcriptome of senescent and non-senescent cells within PanIN pancreatic premalignant lesions in a KRas-driven mouse model

Project description:Cellular senescence is a central barrier to tumorigenesis, acting to block the proliferation of premalignant cells. However, senescent cells residing within tumor lesions can also exert paracrine effects influencing tumor growth and progression. Premalignant pancreatic intraepithelial neoplasia (PanIN) lesions contain senescent cells, yet whether these influence disease progression is unknown. Here we report that senescent cells in PanINs that develop in a Kras-driven mouse model express a pro-inflammatory gene signature, which includes high Cox2 levels. Pharmacologic Cox2 inhibition caused a dramatic reduction in PanIN growth. Senolytic treatment with the Bcl2-family inhibitor ABT-737 reduced the numbers of Cox2-expressing PanIN cells and blocked PanIN formation and progression to carcinoma. These findings indicate that senescent PanIN cells support tumor growth and progression through Cox2 activity, representing crosstalk between interspersed senescent and dividing premalignant cells. Targeted elimination of senescent cells may thus be effective in limiting progression of precancerous lesions.

2021-02-17 | GSE128319 | GEO

DNA methylation patterns in newborns exposed to tobacco in utero

Project description:Background: Maternal smoking during pregnancy is a major risk factor for adverse health outcomes. The main objective of the study was to assess the impact of in utero tobacco exposure on DNA methylation in children born at term with appropriate weight at birth. Methods: Twenty mother-newborn dyads, after uncomplicated pregnancies, in the absence of perinatal illness were included. All mothers were healthy with no cardiovascular risk factors, except for the associated risks among those mothers who smoked. Umbilical cord blood (for methylation arrays) and maternal peripheral venous blood (for cotine level measurement) were collected and an epigenome-wide association study was performed using a 450K epigenome-wide scan (Illumina Infinium HumanMethylation 450BeadChip) with adjustment to normalize the DNA methylation for data cell variability in whole blood. Results: The maternal plasmatic cotinine levels ranged from 10.70-115.40 ng/ml in the exposed group to 0-0.59 ng/ml in the non-exposed group. After adjusting for multiple comparisons in 427102 probes, statistically significant differences for 31 CpG sites, associated to 25 genes were observed. There was a greater than expected proportion of statistically-significant loci located in CpG islands (Fisher’s exact test, p=0.029) and of those CpG islands, 90.3% exhibit higher methylation levels in the exposed group. The most striking and significant CpG site, cg05727225, is located in the chromosome 11p15.4, within the adrenomedullin gene. Conclusions: In utero tobacco exposure, even in the absence of fetal growth restriction, may alter the epigenome, contributing to global DNA hypomethylation. Therefore, DNA status can be used as a biomarker of prenatal insults. Considering the possibility to reverse epigenetic modifications, a window of opportunity exists to change the programmed chronic disease.

2015-02-16 | GSE64316 | GEO

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