Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

RNA mis-splicing sensitizes SETD2-mutant kidney cancer cells to DNMTi (ChiP-Seq and RNA-Seq)

ABSTRACT: RNA mis-splicing sensitizes SETD2-mutant kidney cancer cells to DNMTi (ChiP-Seq and RNA-Seq)

PROVIDER: PRJNA816437 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR18331700_1.fastq.gz	Fastqsanger.gz
	SRR18331700_2.fastq.gz	Fastqsanger.gz
	SRR18331701_1.fastq.gz	Fastqsanger.gz
	SRR18331701_2.fastq.gz	Fastqsanger.gz
	SRR18331702_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 240

Similar Datasets

RNA mis-splicing sensitizes SETD2-mutant kidney cancer cells to DNMTi

Project description:RNA mis-splicing sensitizes SETD2-mutant kidney cancer cells to DNMTi

| PRJNA816424 | ENA

RNA mis-splicing sensitizes SETD2-mutant kidney cancer cells to DNMTi (Methylation)

Project description:The dysregulation of the histone H3 lysine 36 (H3K36) methyltransferase, SETD2, is associated with worse clinical outcomes and metastasis in clear cell Renal Cell Carcinoma (ccRCC). Here, we reveal that kidney cancer cells displaying diminished H3K36me3 levels (SETD2 deficiency) show increased sensitivity to the anti-tumor effects of the DNA hypomethylating agent 5-aza-2’-deoxycytidine (Decitabine/DAC). DAC treatment induced stronger viral mimicry activation and immunostimulatory signals by higher transposable element (TE) expression in SETD2-mutant cancer cells. Surprisingly, we demonstrate that the increased TE abundance in SETD2-knockout (SETD2-KO) kidney cancer cells is substantially derived from mis-spliced products induced by DAC treatment. Epigenetic profiling suggests that differential DNA methylation, H3K36me3, and H3K9me3 marks across exons and intronic TEs might contribute to elevated mis-splicing rates specifically in the SETD2 loss context. Finally, SETD2 dysregulation also sensitized tumors in vivo to combinatorial therapy of DAC and immune checkpoint inhibitors highlighting the translational potential for this precision medicine.

2023-01-27 | GSE198673 | GEO

RNA mis-splicing sensitizes SETD2-mutant kidney cancer cells to DNMTi (ChiP-Seq and RNA-Seq)

2023-01-27 | GSE198670 | GEO

RNA mis-splicing sensitizes SETD2-mutant kidney cancer cells to DNMTi (Methylation)

Project description:RNA mis-splicing sensitizes SETD2-mutant kidney cancer cells to DNMTi (Methylation)

| PRJNA816438 | ENA

Mis-splicing of mitotic regulators sensitizes SF3B1-mutated human HSCs to CHK1 inhibition [RNA-seq]

Project description:Mis-splicing of mitotic regulators sensitizes SF3B1-mutated human HSCs to CHK1 inhibition [RNA-seq]

| PRJNA1096661 | ENA

Quantitative Analysis of Wild Type(wt) and Setd2 knockout(ko) mESCs Transcriptomes [RNA-Seq]

Project description:Purpose: This study aimed at exploring the deregulated genes in setd2 knockout mESCs compared with wt, more particularly to find the mechanism controlled by setd2,which was required for endoderm differentiation. Methods: Setd2 wt and ko mESCs were generated by deep sequencing, using Illumina GAIIx. Using Avadis NGS (version:1.3) software to analyze the sequence reads that passed quality filter to acquire the expression level of all genes. qRT–PCR validation was performed usingSYBR Green assays. Results: Using an optimized data analysis workflow, we mapped about 80 million sequence reads per sample to the mouse genome (build mm9) and identified 17,827 transcripts in the sted2 wt and ko mESCs. About 2,516 genes were deregulated in setd2 ko mESCs, more than 10 genes were validated using qRT-PCR. Conclusions: Through RNA-seq,we noticed that a subset of genes that related to MAPK signaling pathways were down-regulated in ko mESCs. This provided a bridge to connect setd2 and mESCs endoderm differentiation. One wt and one ko mESCs were generated by deep sequencing, using Illumina GAIIx.

2014-10-14 | E-GEOD-54932 | biostudies-arrayexpress

Setd2 inactivation sensitizes lung adenocarcinoma to inhibitors of oxidative respiration and mTORC1 signaling [KPY RNAseq]

Project description:RNA-sequencing analysis of murine KPY lung adenocarcinoma tumors in the presence and absence of Setd2. Tumors were harvested from KPY-Ctrl and KPY-SetdKO mice and were then subject to RNA-Seq to identify gene expression differences following loss of Setd2 expression.

2023-02-08 | GSE224269 | GEO

Setd2 inactivation sensitizes lung adenocarcinoma to inhibitors of oxidative respiration and mTORC1 signaling [K RNAseq]

Project description:RNA-sequencing analysis of murine K lung adenocarcinoma tumors in the presence and absence of Setd2. Tumors were harvested from K-Ctrl and K-Setd2KO mice. Tumors were then subject to RNA-Seq to identify gene expression differences following loss of Setd2 expression.

2023-02-08 | GSE224267 | GEO

SETD2 loss sensitizes kidney cancer cells to DNA hypomethylating agents

Project description:SETD2 loss sensitizes kidney cancer cells to DNA hypomethylating agents

| PRJNA927290 | ENA

SETD2 loss sensitizes kidney cancer cells to DNA hypomethylating agents

Project description:Large-scale sequencing efforts in Clear cell renal cell carcinoma (ccRCC) have found a high prevalence of mutations in chromatin-related genes. Prominent within this group is SETD2, which is mutated in 15% of ccRCC and is associated with aggressive disease. SETD2 is a methyltransferase responsible for trimethylating lysine 36 on histone H3 (H3K36me3). Although it is not completely understood how SETD2 loss contributes to ccRCC tumorigenesis, it is thought that it reprograms the epigenetic landscape of the cell. Here we explore the impact that SETD2/H3K36me3 loss has on the DNA methylome in ccRCC cells. DNA methylation was measured using the EPIC DNA methylation assay in 786-O ccRCC cells and non-cancerous transformed proximal tubule kidney cells (HKC) with and without SETD2. Sensitivity to DNA hypomethylating agents was assessed by dose-response assay using 5-aza-2'-deoxycytidine. Apoptosis was measured via Annexin-V/PI staining by flow cytometry. Mitochondrial fitness was evaluated by electron microscopy and flow cytometry. Moreover, activity of 5-aza-2'-deoxycytidine, a DNA hypomethylating agent, in was assessed in SETD2 WT/KO xenografts in NOD-Scid mice. SETD2 loss resulted in DNA hypermethylation in HKC cells and to a greater extent in 786-O. Dose-response assays showed that SETD2-null ccRCC cells are sensitive to 5-aza-2'-deoxycytidine. Furthermore, Annexin-V/PI staining revealed more apoptotic and necrotic cells in SETD2-null cells following 5-aza-2'-deoxycytidine treatment, which was rescued using a Caspase inhibitor. In addition, 5-aza-2'-deoxycytidine induced profound changes in mitochondria in SETD2-null cells, including loss of membrane potential and size reduction. Indeed, in vivo experiments verified increased SETD2-null xenografts’ sensitivity to 5-aza-2'-deoxycytidine. We show that SETD2 loss in ccRCC cells causes DNA hypermethylation, creating a synthetic lethal dependency with DNA hypomethylating agents.

2024-07-01 | GSE223688 | 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