Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

The cooperation among the core regulatory circuitry transcription factors and MYCN on DNA binding [HAND2-MYCN-CRC-knockdown_ChIPseq]

ABSTRACT: MYCN and the core regulatory circuitry transcription factors HAND2, PHOX2B and GATA3 cooperate to bind to DNA.

ORGANISM(S): Homo sapiens

PROVIDER: GSE184057 | GEO | 2023/03/29

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

The cooperation between HAND2 and MYCN on DNA binding [HAND2-overexpression_ChIPseq]

Project description:HAND2 assists MYCN bind to DNA.

2023-03-29 | GSE184059 | GEO

The cooperation among the core regulatory circuitry transcription factors and MYCN on DNA binding [HAND2-MYCN-CRC-knockdown_ChIPseq]

Project description:The cooperation among the core regulatory circuitry transcription factors and MYCN on DNA binding [HAND2-MYCN-CRC-knockdown_ChIPseq]

| PRJNA762917 | ENA

The cooperation between HAND2 and MYCN on DNA binding [HAND2-overexpression_ChIPseq]

Project description:The cooperation between HAND2 and MYCN on DNA binding [HAND2-overexpression_ChIPseq]

| PRJNA762920 | ENA

KDM4 inhibition disrupts the core regulatory transcriptional circuitry in MYCN-driven neuroblastoma [RNA-seq]

Project description:A small set of interconnected lineage-specific transcription factors (TFs) form a core regulatory circuitry (CRC) that establishes and maintains cell identity and grants selective dependencies of distinct cancer types. However, effective therapies to targeting CRC TFs remain lacking. Here, we show that the best-in-class KDM4 inhibitor QC6352 has a potent anticancer activity in MYCN-driven high-risk neuroblastoma and significantly represses the CRC TFs including MYCN, HAND2, ASCL1, PHOX2B by disrupting the super-enhancers that dominate the expression of CRC TFs. Furthermore, we have developed a combination therapy by integrating QC6352 into cytotoxic chemotherapy, which leads to a complete response of MYCN amplified tumors and a better animal survival. This study reveals that targeting histone lysine demethylase 4 family may transform into a therapeutic strategy in clinic for cancers driven by CRC TFs.

2024-03-04 | GSE164455 | GEO

KDM4 inhibition disrupts the core regulatory transcriptional circuitry in MYCN-driven neuroblastoma [Cut&Tag]

2024-03-04 | GSE164454 | GEO

KDM4 inhibition disrupts the core regulatory transcriptional circuitry in MYCN-driven neuroblastoma [ChIP-seq]

2024-03-04 | GSE164451 | GEO

KDM4 inhibition disrupts the core regulatory transcriptional circuitry in MYCN-driven neuroblastoma [ATAC-seq]

2024-03-04 | GSE164450 | GEO

Investigate the effect of loss of HAND2, MYCN, PHOX2B and GATA3 on chromatin accessibility.

Project description:Investigate the effect of loss of HAND2, MYCN, PHOX2B and GATA3 on chromatin accessibility.

| PRJNA763610 | ENA

Super-enhancer Driven Core Regulatory Circuitry in MYCN-amplified Neuroblastoma [array]

Project description:Transcriptional dysregulation plays a major role in the development and progression of human tumors such as pediatric neuroblastoma. Therefore, we sought to elucidate the relationship between genes required for neuroblastoma cell growth and survival and the transcriptional core regulatory circuitry (CRC) that controls the gene expression program. A genome-scale CRISPR-Cas9 screen for oncogenic dependencies revealed that 143 genes are essential for cell survival and growth in neuroblastoma relative to other cancers, including many super-enhancer (SE) regulated transcription factors. Genome-wide occupancy analysis of transcription factor binding demonstrated that at least six of these transcription factors were both dependency genes and components of the CRC in MYCN-amplified neuroblastoma including: HAND2, ISL1, PHOX2B, GATA3, TBX2, and MEIS2. Binding sites for these transcription factors were clustered within a few hundred base pairs in their own enhancers and the enhancers of downstream target genes, which surprisingly included 40% of the independently determined neuroblastoma dependency genes. This profound level of transcriptional control of oncogenesis through self-reinforcing transcriptional circuits led us to test combinatorial pharmacological inhibition of transcriptional initiation and elongation, which synergistically induced tumor cell death, supporting drugging transcription as a means to advance the treatment of high risk neuroblastoma.

2018-05-22 | GSE108914 | GEO

Super-enhancer Driven Core Regulatory Circuitry in MYCN-amplified Neuroblastoma [ATAC-Seq]

Project description:Transcriptional dysregulation plays a major role in the development and progression of human tumors such as pediatric neuroblastoma. Therefore, we sought to elucidate the relationship between genes required for neuroblastoma cell growth and survival and the transcriptional core regulatory circuitry (CRC) that controls the gene expression program. A genome-scale CRISPR-Cas9 screen for oncogenic dependencies revealed that 143 genes are essential for cell survival and growth in neuroblastoma relative to other cancers, including many super-enhancer (SE) regulated transcription factors. Genome-wide occupancy analysis of transcription factor binding demonstrated that at least six of these transcription factors were both dependency genes and components of the CRC in MYCN-amplified neuroblastoma including: HAND2, ISL1, PHOX2B, GATA3, TBX2, and MEIS2. Binding sites for these transcription factors were clustered within a few hundred base pairs in their own enhancers and the enhancers of downstream target genes, which surprisingly included 40% of the independently determined neuroblastoma dependency genes. This profound level of transcriptional control of oncogenesis through self-reinforcing transcriptional circuits led us to test combinatorial pharmacological inhibition of transcriptional initiation and elongation, which synergistically induced tumor cell death, supporting Òdrugging transcriptionÓ as a means to advance the treatment of high risk neuroblastoma.

2018-05-22 | GSE94823 | 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