Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

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

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

PROVIDER: PRJNA421345 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR6355770.fastq.gz	Fastqsanger.gz
	SRR6355771.fastq.gz	Fastqsanger.gz
	SRR6355772.fastq.gz	Fastqsanger.gz
	SRR6355763.fastq.gz	Fastqsanger.gz
	SRR6355773.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 11

Similar Datasets

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.

2020-02-28 | GSE107774 | GEO

RNA-sequencing of lung tissues from Gprc5a-/- and Gprc5a-/-/Lcn2-/- mice at baseline and seven months post-NNK

Project description:We have shown that Gprc5a-/- mice form Kras-mutant lung tumors spontaneously which is accelerated by tobacco carcinogen (NNK) exposure. We found in these mice that Lcn2 was distinctively up-regulated along the spectrum of Kras-mutant lung cancer development. To understand the role of Lcn2 in lung cancer pathogenesis, we generated Gprc5a-/-/Lcn2-/- mice and found that these animals have increased lung tumor devleopment following NNK compared to Gprc5a-/- animals with intact Lcn2. To understand these effects, we performed RNA-sequencing (RNA-Seq) of lung tissues from Gprc5a-/-/Lcn2-/- and Gprc5a-/- mice at baseline (prior to NNK exposure) and of tumor-bearing lungs from both groups at seven months post-NNK exposure.

2021-03-19 | GSE147148 | GEO

Differential gene expression patterns in lung carcinogenesis mediated by loss of mouse tumor supressor Gprc5a

Project description:Increasing the understanding of the impact of changes in oncogenes and tumor suppressor genes is essential for improving the management of lung cancer. Recently, we identified a new mouse lung-specific tumor suppressor - the G-protein coupled receptor 5A (Gprc5a). We sought to understand the molecular consequences of Gprc5a loss and towards this we performed microarray analysis of the transcriptomes of lung epithelial cells cultured from normal tracheas of Gprc5a knockout and wild-type mice to define a loss-of-Gprc5a gene signature. Moreover, we analyzed differential gene expression patterns between Gprc5a knockout normal lung epithelial cells as well as lung adenocarcinoma cells isolated and cultured from tumors of NNK-exposed Gprc5a knockout mice.

2010-04-13 | GSE21309 | GEO

RNA-sequencing of lung tissues from Gprc5a-/- mice at baseline, end of NNK exposure, three months and seven months post-NNK

Project description:We have previously shown that Gprc5a-KO mice develop lung tumors that are accelerated by exposure to the tobacco-specific carcinogen NNK. In this study we sought to understand the temporal evolution of gene expression changes in tumors and normal-appearing tissues.

2021-03-31 | GSE147187 | GEO

RNA-sequencing of lung tissues from Gprc5a-/- and Gprc5a-/-/Lcn2-/- mice at baseline and seven months post-NNK

Project description:RNA-sequencing of lung tissues from Gprc5a-/- and Gprc5a-/-/Lcn2-/- mice at baseline and seven months post-NNK

| PRJNA613199 | ENA

Differential gene expression patterns signifying loss of the mouse tumor supressor Gprc5a in lung epithelial cells

Project description:Increasing the understanding of the impact of changes in oncogenes and tumor suppressor genes is essential for improving the management of lung cancer. Recently, we identified a new mouse lung-specific tumor suppressor - the G-protein coupled receptor 5A (Gprc5a). We sought to understand the molecular consequences of Gprc5a loss and towards this we performed microarray analysis of the transcriptomes of lung epithelial cells cultured from normal tracheas of Gprc5a knockout and wild-type mice to define a loss-of-Gprc5a gene signature. Gprc5a wild type cells (WT-NLE) and Gprc5a knockout cells (NULL-NLE) were isolated and cultured from trachea of three week old Gprc5a wild type and knockout mice, respectively. Following RNA extraction and purification, the transcriptome of the Gprc5a wild type and knockout cells were analyzed by microarray analysis using the Affymetrix MG-430 2.0 murine array platform.

2010-04-13 | E-GEOD-21309 | biostudies-arrayexpress

Expression data from Gprc5a wild type or knockout mouse tracheal epithelial cells (MTECs)

Project description:Gprc5a is a lung tumor suppressor gene. Gprc5a-knockout (ko) mice can develop spontaneous lung cancer and Gprc5a-ko mouse model is relevant to human lung cancer. Thus, exploration of the mechanisms underlying lung tumorigenesis in Gprc5a-ko mice would be very helpful for revealing those in human lung cancer. We used microarrays to detail the global gene expression profile that underlies oncogenesis by Gprc5a-knockout gene deletion in mouse tracheal epithelial cells. Wild type and gene-knockout mouse tracheal epithelial cells that were divided into two groups were used for RNA extraction.

2013-10-29 | E-GEOD-51777 | biostudies-arrayexpress

Gene expression analysis of mouse Kras-mutant lung adenocarcinoma cells and cancer stem cells

Project description:Mechanisms underlying cancer stemness in Kras-mutant lung adenocarcinoma (KM-LUAD) are poorly understood. We previously found that mice with knockout of Gprc5a develop LUADs with somatic Kras mutations. We also previously derived Gprc5a-/- KM-LUAD cells (MDA-F471 cells) from a mouse exposed to the tobacco-specific carcinogen NNK. We also derived cancer stem cells (CSCs; grown and cultured as spheres in 3D cultures) from MDA-F471 cells. To better understand the biology of these CSCs, we compared the transcriptomes of MDA-F471 cells and their CSC counterparts by bulk RNA-sequencing.

2022-11-30 | GSE219124 | GEO

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

Expression data from Gprc5a wild type or knockout mouse tracheal epithelial cells (MTECs)

2013-10-29 | GSE51777 | GEO