Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Super-enhancer redistribution as a mechanism of broad gene dysregulation in repeatedly drug-treated cancer cells

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Homo sapiens

PROVIDER: GSE129702 | GEO | 2020/04/01

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Super-enhancer redistribution as a mechanism of broad gene dysregulation in repeatedly drug-treated cancer cells [dataset 2]

Project description:We provide a series of chromatin and transcriptomic profiles to establish the short-term and long-term effects of cisplatin treatment in ovarian cancer A2780 cells.

2020-04-01 | GSE129701 | GEO

Super-enhancer redistribution as a mechanism of broad gene dysregulation in repeatedly drug-treated cancer cells [dataset 3]

Project description:We provide a series of chromatin and transcriptomic profiles to establish the short-term and long-term effects of cisplatin treatment in ovarian cancer A2780 cells.

2020-04-01 | GSE143691 | GEO

Super-enhancer redistribution as a mechanism of broad gene dysregulation in repeatedly drug-treated cancer cells [dataset 1]

Project description:We provide a series of chromatin and transcriptomic profiles to establish the short-term and long-term effects of cisplatin treatment in ovarian cancer A2780 cells.

2020-04-01 | GSE129700 | GEO

Super-enhancer redistribution as a mechanism of broad gene dysregulation in repeatedly drug-treated cancer cells

Project description:Super-enhancer redistribution as a mechanism of broad gene dysregulation in repeatedly drug-treated cancer cells

| PRJNA532526 | ENA

Super-enhancer redistribution as a mechanism of broad gene dysregulation in repeatedly drug-treated cancer cells [dataset 2]

Project description:Super-enhancer redistribution as a mechanism of broad gene dysregulation in repeatedly drug-treated cancer cells [dataset 2]

| PRJNA532532 | ENA

Super-enhancer redistribution as a mechanism of broad gene dysregulation in repeatedly drug-treated cancer cells [dataset 1]

Project description:Super-enhancer redistribution as a mechanism of broad gene dysregulation in repeatedly drug-treated cancer cells [dataset 1]

| PRJNA532531 | ENA

Super-enhancer redistribution as a mechanism of broad gene dysregulation in repeatedly drug-treated cancer cells [dataset 3]

Project description:Super-enhancer redistribution as a mechanism of broad gene dysregulation in repeatedly drug-treated cancer cells [dataset 3]

| PRJNA601312 | ENA

Transcriptional Dysregulation of MYC Reveals Common Enhancer-Docking Mechanism.

Project description:Transcriptional dysregulation of the MYC oncogene is among the most frequent events in aggressive tumor cells, and this is generally accomplished by acquisition of a super-enhancer somewhere within the 2.8 Mb TAD where MYC resides. We find that these diverse cancer-specific super-enhancers, differing in size and location, interact with the MYC gene through a common and conserved CTCF binding site located 2 kb upstream of the MYC promoter. Genetic perturbation of this enhancer-docking site in tumor cells reduces CTCF binding, super-enhancer interaction, MYC gene expression, and cell proliferation. CTCF binding is highly sensitive to DNA methylation, and this enhancer-docking site, which is hypomethylated in diverse cancers, can be inactivated through epigenetic editing with dCas9-DNMT. Similar enhancer-docking sites occur at other genes, including genes with prominent roles in multiple cancers, suggesting a mechanism by which tumor cell oncogenes can generally hijack enhancers. These results provide insights into mechanisms that allow a single target gene to be regulated by diverse enhancer elements in different cell types.

| S-EPMC5929158 | biostudies-literature

Super-Enhancer Dysregulation in Rhabdoid Tumor Cells Is Regulated by the SWI/SNF ATPase BRG1.

Project description:Mutations in the SWI/SNF chromatin remodeling complex occur in ~20% of cancers. In rhabdoid tumors defined by loss of the SWI/SNF subunit SMARCB1, dysregulation of enhancer-mediated gene expression is pivotal in driving oncogenesis. Enhancer dysregulation in this setting is tied to retention of the SWI/SNF ATPase BRG1-which becomes essential in the absence of SMARCB1-but precisely how BRG1 contributes to this process remains unknown. To characterize how BRG1 participates in chromatin remodeling and gene expression in SMARCB1-deficient cells, we performed a genome-wide characterization of the impact of BRG1 depletion in multiple rhabdoid tumor cell lines. We find that although BRG1-regulated open chromatin sites are distinct at the locus level, the biological characteristics of the loci are very similar, converging on a set of thematically related genes and pointing to the involvement of the AP-1 transcription factor. The open chromatin sites regulated by BRG1 colocalize with histone-marked enhancers and intriguingly include almost all super-enhancers, revealing that BRG1 plays a critical role in maintaining super-enhancer function in this setting. These studies can explain the essentiality of BRG1 to rhabdoid tumor cell identity and survival and implicate the involvement of AP-1 as a critical downstream effector of rhabdoid tumor cell transcriptional programs.

| S-EPMC10931202 | biostudies-literature

Noncoding mutations cause super-enhancer retargeting resulting in protein synthesis dysregulation during B cell lymphoma progression.

Project description:Whole-genome sequencing of longitudinal tumor pairs representing transformation of follicular lymphoma to high-grade B cell lymphoma with MYC and BCL2 rearrangements (double-hit lymphoma) identified coding and noncoding genomic alterations acquired during lymphoma progression. Many of these transformation-associated alterations recurrently and focally occur at topologically associating domain resident regulatory DNA elements, including H3K4me3 promoter marks located within H3K27ac super-enhancer clusters in B cell non-Hodgkin lymphoma. One region found to undergo recurrent alteration upon transformation overlaps a super-enhancer affecting the expression of the PAX5/ZCCHC7 gene pair. ZCCHC7 encodes a subunit of the Trf4/5-Air1/2-Mtr4 polyadenylation-like complex and demonstrated copy number gain, chromosomal translocation and enhancer retargeting-mediated transcriptional upregulation upon lymphoma transformation. Consequently, lymphoma cells demonstrate nucleolar dysregulation via altered noncoding 5.8S ribosomal RNA processing. We find that a noncoding mutation acquired during lymphoma progression affects noncoding rRNA processing, thereby rewiring protein synthesis leading to oncogenic changes in the lymphoma proteome.

| S-EPMC10703697 | biostudies-literature

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