Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

ABSTRACT: Targeting of Super-Enhancer-Associated Oncogenic Transcription in MYCN-driven tumor cells by CDK7 inhibition

PROVIDER: PRJNA264968 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR1631230.fastq.gz	Fastqsanger.gz
	SRR1631240.fastq.gz	Fastqsanger.gz
	SRR1631231.fastq.gz	Fastqsanger.gz
	SRR1631241.fastq.gz	Fastqsanger.gz
	SRR1631232.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 18

Similar Datasets

Homo sapiens

Project description:Targeting of Super-Enhancer-Associated Oncogenic Transcription in MYCN-driven tumor cells by CDK7 inhibition [ChIP-Seq]

| PRJNA264969 | ENA

Homo sapiens

Project description:Targeting of Super-Enhancer-Associated Oncogenic Transcription in MYCN-driven tumor cells by CDK7 inhibition [Gene Expression]

| PRJNA264970 | ENA

Targeting super-enhancer-driven oncogenic transcription by CDK7 inhibition in anaplastic thyroid cancer

Project description:Targeting super-enhancer-driven oncogenic transcription by CDK7 inhibition in anaplastic thyroid cancer

| PRJNA491858 | ENA

Targeting super-enhancer-driven oncogenic transcription by CDK7 inhibition in anaplastic thyroid cancer [RNA-Seq]

Project description:Targeting super-enhancer-driven oncogenic transcription by CDK7 inhibition in anaplastic thyroid cancer [RNA-Seq]

| PRJNA491864 | ENA

Targeting super-enhancer-driven oncogenic transcription by CDK7 inhibition in anaplastic thyroid cancer [ChIP-Seq]

Project description:Targeting super-enhancer-driven oncogenic transcription by CDK7 inhibition in anaplastic thyroid cancer [ChIP-Seq]

| PRJNA491865 | ENA

Targeting super-enhancer induced gene expression using novel BRD4 inhibitor OTX015 in preclinical models of MYCN-amplified neuroblastoma

Project description:Bromodomain-containing protein 4 (BRD4) functions as an epigenetic reader and binds to so-called super-enhancer regions of driving oncogenes such as MYC in cancer. We investigated the possibility to target super-enhancer regulated genes in neuroblastoma and in MYCN amplified disease in particular. We used OTX015, the first small-molecule BRD4 inhibitor to enter clinical phase I/II trials in adults, to test the feasibility to specifically target super-enhancer regulated gene-expression in neuroblastoma. BRD4 inhibition lead to significant transcriptional down-regulation of genes that were associated with super-enhancers, supporting the notion that BRD4 preferentially acts at these chromatin sites. BRD4 inhibition not only attenuated MYCN transcription but most significantly affected MYCN-regulated transcriptional programs.

2016-07-03 | E-MTAB-3672 | biostudies-arrayexpress

Dissecting Super-enhancer driven Transcriptional Dependencies Reveals Novel Oncogenes and Therapeutic Strategies of Group 3 Subtype Medulloblastoma [RNA-seq]

Project description:Medulloblastoma (MB) is the most common malignant pediatric brain tumor and group 3 subtype (G3-MB) exhibits the worst prognosis. Dissecting super-enhancer (SE) driven transcriptional dependencies of cancer has been shown to facilitate identifying novel oncogenic mechanisms and therapeutic targets or strategies. In this study, our integrative SE analyses of primary tissues and patient-derived tumor cell lines of G3-MB revealed their partially conserved SE-associated transcripts were enriched of subtype-specific tumor-dependent genes and MB patients harboring enrichment of those transcripts exhibited worse prognosis. Fourteen such conserved SE-associated genes were identified to be members of SE-driven core transcriptional regulatory network of G3-MB, including three well-recognized master TFs and eleven newly identified effector oncogenes. ARL4D, one of the effector oncogenes, was further demonstrated to exert its oncogenic role via maintaining cell-cycle progression and stemness of G3-MB cells. Moreover, BET inhibition with CDK7 inhibition or proteasome inhibition, two combinatory strategies of targeting SE complex components (BRD4, CDK7) or SE-associated effector oncogene (PSMB5), were shown to exhibit synergistic therapeutic effects against G3-MB. Taken together, our study verifies the oncogenic role and therapeutic potential of SE-driven transcriptional dependencies of G3-MB, resulting in better understanding of its tumor biology and identification of novel SE-associated therapeutic targets or strategies.

2021-10-04 | GSE185024 | GEO

Dissecting Super-enhancer driven Transcriptional Dependencies Reveals Novel Oncogenes and Therapeutic Strategies of Group 3 Subtype Medulloblastoma [ChIP-seq]

2021-10-04 | GSE185003 | GEO

CDK7 Inhibition Suppresses Melanoma Growth By Depleting A Super-enhancer Associated "Achilles" Lineage Cluster [ChIP-Seq]

Project description:Cutaneous malignant melanoma (CMM) lacks targeted therapies beyond the oft-circumvented BRAF inhibitors. Part of the difficulty in treating melanomas has been attributed to a strong survival program controlled by melanocyte transcription factors such as MITF - a phenomenon first described in melanoma as “lineage dependency.” Recently, a highly selective covalent CDK7 inhibitor (THZ1) has been shown to potently suppress the growth of various cancers through the depletion of master transcription-regulating oncogenes and the disruption of their attendant super-enhancers. We now show that melanoma cells are highly sensitive to CDK7 inhibition and that a melanocyte “lineage cluster,” whose members are transcriptionally driven by super-enhancers, is also strongly suppressed by THZ1. These results point to CDK7 inhibition as a viable strategy to deprive oncogenic transcription and suppress tumor growth in melanoma.

2017-10-23 | GSE75814 | GEO

CDK7 Inhibition Suppresses Melanoma Growth By Depleting A Super-enhancer Associated Achilles Lineage Cluster [Array]

2017-10-23 | GSE75810 | GEO