Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

SETD2 loss in renal epithelial cells drives epithelial to mesenchymal transition in a TGFβ-independent manner

ABSTRACT: SETD2 loss in renal epithelial cells drives epithelial to mesenchymal transition in a TGFβ-independent manner

PROVIDER: PRJNA880278 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR21547400_1.fastq.gz	Fastqsanger.gz
	SRR21547400_2.fastq.gz	Fastqsanger.gz
	SRR21547700_1.fastq.gz	Fastqsanger.gz
	SRR21547700_2.fastq.gz	Fastqsanger.gz
	SRR21547401_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 114

Similar Datasets

SETD2 loss in renal epithelial cells drives epithelial to mesenchymal transition in a TGFβ-independent manner [ATAC-Seq]

Project description:SETD2 loss in renal epithelial cells drives epithelial to mesenchymal transition in a TGFβ-independent manner [ATAC-Seq]

| PRJNA880282 | ENA

SETD2 loss in renal epithelial cells drives epithelial to mesenchymal transition in a TGFβ-independent manner [RNA-Seq]

Project description:SETD2 loss in renal epithelial cells drives epithelial to mesenchymal transition in a TGFβ-independent manner [RNA-Seq]

| PRJNA880283 | ENA

SETD2 loss in renal epithelial cells drives epithelial to mesenchymal transition in a TGFβ-independent manner [ChIP-Seq]

Project description:SETD2 loss in renal epithelial cells drives epithelial to mesenchymal transition in a TGFβ-independent manner [ChIP-Seq]

| PRJNA880284 | ENA

SETD2 loss in renal epithelial cells drives epithelial to mesenchymal transition in a TGFβ-independent manner [RNA-Seq]

Project description:SETD2 is one of most frequently mutated genes in renal cell carcinoma. It is generally known as the only histone methyltransferase that catalyze the trimethylation of lysine 36 on histone H3 (H3K36me3). Mutation of this gene and/or loss of its mark have been linked to metastasis and worse patient outcomes in kidney cancer. In this paper, we will examine the mechanism by which SETD2 loss induces epithelial-to-mesenchymal transition (EMT), which is a major pathway that drives invasion and early metastasis in various cancer types. To achieve the goals, we performed several omics analysis including RNA-seq, ChIP-seq and ATAC-seq to characterize how SETD2 deletion alters transcriptome and epigenome.

2023-07-12 | GSE213258 | GEO

SETD2 loss in renal epithelial cells drives epithelial to mesenchymal transition in a TGFβ-independent manner [ChIP-Seq]

2023-07-12 | GSE213257 | GEO

SETD2 loss in renal epithelial cells drives epithelial to mesenchymal transition in a TGFβ-independent manner [ATAC-Seq]

2023-07-12 | GSE213256 | GEO

SETD2 loss in renal epithelial cells drives epithelial to mesenchymal transition in a TGFβ-independent manner

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

2023-07-12 | GSE213260 | GEO

SETD2 loss in renal epithelial cells drives epithelial-to-mesenchymal transition in a TGF-β-independent manner.

Project description:Histone-lysine N-methyltransferase SETD2 (SETD2), the sole histone methyltransferase that catalyzes trimethylation of lysine 36 on histone H3 (H3K36me3), is often mutated in clear cell renal cell carcinoma (ccRCC). SETD2 mutation and/or loss of H3K36me3 is linked to metastasis and poor outcome in ccRCC patients. Epithelial-to-mesenchymal transition (EMT) is a major pathway that drives invasion and metastasis in various cancer types. Here, using novel kidney epithelial cell lines isogenic for SETD2, we discovered that SETD2 inactivation drives EMT and promotes migration, invasion, and stemness in a transforming growth factor-beta-independent manner. This newly identified EMT program is triggered in part through secreted factors, including cytokines and growth factors, and through transcriptional reprogramming. RNA-seq and assay for transposase-accessible chromatin sequencing uncovered key transcription factors upregulated upon SETD2 loss, including SOX2, POU2F2 (OCT2), and PRRX1, that could individually drive EMT and stemness phenotypes in SETD2 wild-type (WT) cells. Public expression data from SETD2 WT/mutant ccRCC support the EMT transcriptional signatures derived from cell line models. In summary, our studies reveal that SETD2 is a key regulator of EMT phenotypes through cell-intrinsic and cell-extrinsic mechanisms that help explain the association between SETD2 loss and ccRCC metastasis.

| S-EPMC10766198 | biostudies-literature

RNA sequencing of SETD2 isogenic renal cell carcinoma cell lines

Project description:RNA sequencing of SETD2 isogenic renal cell carcinoma cell lines. Examination of RNA expression in SETD2 isogenic cell lines

2015-06-17 | E-GEOD-66879 | biostudies-arrayexpress

Gene expression analysis of murine renal tubular epithelial cells upon SETD2 knockout [RNAseq_RTE]

Project description:SETD2, a H3K36 trimethyltransferase, is frequently mutated in human cancers with the highest prevalence (13%) in clear cell renal cell carcinoma (ccRCC). Genomic profiling of primary ccRCC tumors reveals a positive correlation between SETD2 mutations and metastasis. However, whether and how SETD2-loss promotes metastasis remains unclear. Here, we detected SETD2 mutations in 24 of 51 (47%) metastatic ccRCC tumors. Using SETD2-mutant metastatic ccRCC patient-derived cell line and xenograft models, we showed that H3K36me3 restoration greatly reduced distant metastases of ccRCC in mice. An integrated ATAC-seq, ChIP-seq, and transcriptome analysis concluded a tumor suppressor model in which loss of SETD2-mediated H3K36me3 activates enhancers to drive oncogenic transcription through dysregulating histone chaperone recruitment, enhancing histone exchange, and expanding chromatin accessibility. Furthermore, we uncovered mechanism-based therapeutic strategies for SETD2-deficient cancer through inhibition of histone chaperones. Overall, SETD2-loss creates a permissive epigenetic landscape for cooperating oncogenic drivers to amplify transcriptional output, providing unique therapeutic opportunities.

2021-11-15 | GSE146541 | GEO

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