Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

A Systemic and Integrated Analysis of p63-Driven Regulatory Networks in Mouse Oral Squamous Cell Carcinoma

ABSTRACT: A Systemic and Integrated Analysis of p63-Driven Regulatory Networks in Mouse Oral Squamous Cell Carcinoma

PROVIDER: PRJNA899916 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR22248560.fastq.gz	Fastqsanger.gz
	SRR22248561.fastq.gz	Fastqsanger.gz
	SRR22248562.fastq.gz	Fastqsanger.gz

Items per page:

1 - 3 of 3

Similar Datasets

A Systemic and Integrated Analysis of p63-Driven Regulatory Networks in Mouse Oral Squamous Cell Carcinoma

Project description:Oral squamous cell carcinoma (OSCC) is the most common malignancy of the oral cavity and despite therapeutic advances, late-stage diagnoses continue to negatively affect survival, presenting a continuing challenge for clinicians. Detailed molecular characterization by recent bulk and single-cell RNA-sequencing datasets from OSCC suggest that identification of prognostic biomarkers may lead to more targeted therapies, improving patient outcomes. Development of OSCC is associated with exposure to tobacco, alcohol consumption, and infection with human papillomavirus. The mouse model of 4-Nitroquinoline 1-oxide (4NQO) carcinogenesis produces a spectrum of neoplastic lesions that are a robust model of tobacco-induced OSCC. Specifically, studies have shown that similar to human OSCC, mouse OSCC shows upregulation of the oncogenic master transcription factor p63. We performed complementary loss- and gain-of-function experiments of p63 in mouse 4NQO-transformed OSCC cell lines and utilized RNA-sequencing and ChIP-sequencing to uncover the p63 oncogenic network. By combining our signature with publicly available bulk and scRNA-seq data, we generated a murine p63 signature that we have utilized to better understand the role of p63 in mOSCC. Our analyses have identified several potential biomarkers and conserved pathways that are relevant to hOSCC, as well as highlighted the dynamic role of p63 in migration and invasion.

2023-01-10 | GSE217668 | GEO

A Systemic and Integrated Analysis of p63-Driven Regulatory Networks in Mouse Oral Squamous Cell Carcinoma

2023-01-10 | GSE217669 | GEO

A Systemic and Integrated Analysis of p63-Driven Regulatory Networks in Mouse Oral Squamous Cell Carcinoma

Project description:A Systemic and Integrated Analysis of p63-Driven Regulatory Networks in Mouse Oral Squamous Cell Carcinoma

| PRJNA899917 | ENA

A Systemic and Integrated Analysis of p63-Driven Regulatory Networks in Mouse Oral Squamous Cell Carcinoma

Project description:A Systemic and Integrated Analysis of p63-Driven Regulatory Networks in Mouse Oral Squamous Cell Carcinoma

| PRJNA899918 | ENA

A Systemic and Integrated Analysis of p63-Driven Regulatory Networks in Mouse Oral Squamous Cell Carcinoma.

Project description:Oral squamous cell carcinoma (OSCC) is the most common malignancy of the oral cavity and is linked to tobacco exposure, alcohol consumption, and human papillomavirus infection. Despite therapeutic advances, a lack of molecular understanding of disease etiology, and delayed diagnoses continue to negatively affect survival. The identification of oncogenic drivers and prognostic biomarkers by leveraging bulk and single-cell RNA-sequencing datasets of OSCC can lead to more targeted therapies and improved patient outcomes. However, the generation, analysis, and continued utilization of additional genetic and genomic tools are warranted. Tobacco-induced OSCC can be modeled in mice via 4-nitroquinoline 1-oxide (4NQO), which generates a spectrum of neoplastic lesions mimicking human OSCC and upregulates the oncogenic master transcription factor p63. Here, we molecularly characterized established mouse 4NQO treatment-derived OSCC cell lines and utilized RNA and chromatin immunoprecipitation-sequencing to uncover the global p63 gene regulatory and signaling network. We integrated our p63 datasets with published bulk and single-cell RNA-sequencing of mouse 4NQO-treated tongue and esophageal tumors, respectively, to generate a p63-driven gene signature that sheds new light on the role of p63 in murine OSCC. Our analyses reveal known and novel players, such as COTL1, that are regulated by p63 and influence various oncogenic processes, including metastasis. The identification of new sets of potential biomarkers and pathways, some of which are functionally conserved in human OSCC and can prognosticate patient survival, offers new avenues for future mechanistic studies.

| S-EPMC9856320 | biostudies-literature

FGFR2 Signaling Underlies p63 Oncogenic Function in Squamous Cell Carcinoma

Project description:This study was designed to examine the requirement for the p63 transcription factor in Squamous Cell Carcinoma (SCC) tumor maintenance in an in vivo murine system. A tamoxifen-inducible Keratin 14-driven Cre recombinase transgene was used to conditionally excise p63 in advanced murine SCC tumors. These data show the context-dependent regulation of p63 target genes in cancer. Total RNA from murine Squamous Cell Carcinoma tumors was examined 1-3 days following genomic excision of TP63 in Keratin 14-expressing tumor cells.

2013-08-06 | E-GEOD-45929 | biostudies-arrayexpress

FGFR2 Signaling Underlies p63 Oncogenic Function in Squamous Cell Carcinoma

2013-08-06 | GSE45929 | GEO

Expression data from p63 siRNA in squamous cell lines

Project description:p63, a homologue of the tumor suppressor p53, is critical for the development and maintenance of squamous epithelia. p63 is specifically expressed in the basal layers of stratified epithelial tissues, and is considered to be a specific marker for cells of this type. The role of p63 in tumorigenesis remains poorly defined. Numerous studies have highlighted the oncogenic potential of the predominant p63 isoform, ΔNp63α; however, data suggests that other p63 proteins can act as tumor suppressors or alter the metastatic potential of tumors. ΔNp63α can act as a transcriptional repressor, but the link between the transcriptional functions of p63 and its biological role is still unclear. In this study, we used a loss-of-function approach to investigate the transcriptional programs controlled by p63. Keywords: cell line panel

2006-06-06 | GSE4975 | GEO

A Systemic and Integrated Analysis of p63-Driven Regulatory Networks in Mouse Oral Squamous Cell Carcinoma

Project description:This SuperSeries is composed of the SubSeries listed below.

2023-01-10 | GSE217670 | GEO

SOX2 and p63 occupancy in human squamous carcinoma cell lines and embryonic stem cells.

Project description:SOX2 is a transcription factor essential for pluripotent stem cells, and development and maintenance of squamous epithelium. We previously reported SOX2 an oncogene subject to highly recurrent genomic amplification in squamous cell carcinomas (SCCs). Here we demonstrate in SCCs that SOX2 interacts with another master squamous transcription factor p63, and through ChIP-seq show that genomic occupancy of SOX2 overlaps with that of p63 at a large number of loci and that they cooperatively regulate gene expression including ETV4, which we find essential for SOX2-amplified SCC cell survival. Furthermore, SOX2 binds to distinct genomic loci in SCCs than in embryonic stem cells and the SOX2-p63 coordinate binding is unique to SCC. In addition, a subset of SOX2 genomic binding sites in SCC that lack p63 co-occupancy are co-occupied by the AP-1 transcriptional complex. These demonstrate that SOX2’s actions in SCC differ substantially from its role in pluripotency and identify novel SOX2 interactions that will enable deeper characterization of SOX2’s function in SCC. SOX2 and p63 ChIP-seq from three lung and esophageal squamous carcinoma cell lines with amplification of SOX2 as well as SOX2 ChIP-seq from an ES cells.

2014-03-12 | E-GEOD-46837 | biostudies-arrayexpress

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data