Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Epigenetic enhancer changes during oncogenic transformation [ChIP-seq]

ABSTRACT: Identification of differential enhancers active during oncogenic transformation, using FAIRE-seq and ChIP-seq for H3K4me1 and H3K27ac

ORGANISM(S): Homo sapiens

PROVIDER: GSE101170 | GEO | 2020/07/11

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Epigenetic enhancer changes during oncogenic transformation [RNA-seq]

Project description:Identification of differential enhancers active during oncogenic transformation, using RNA-seq with FAIRE-seq and ChIP-seq for H3K4me1 and H3K27ac.

2020-07-11 | GSE101241 | GEO

Epigenetic enhancer changes during oncogenic transformation

Project description:Epigenetic enhancer changes during oncogenic transformation

| PRJNA393898 | ENA

Deregulation of the Ras-Erk Signaling Axis Modulates the Enhancer Landscape [ChIP-seq]

Project description:Unrestrained receptor tyrosine kinase (RTK) signaling and epigenetic deregulation are root causes of tumorigenesis. We establish linkage between these processes by demonstrating that aberrant RTK signaling unleashed by oncogenic HRasG12V or loss of negative feedback through Sprouty gene deletion remodels histone modifications associated with active typical and super-enhancers. However, while both lesions disrupt the Ras-Erk axis, the expression programs, enhancer signatures, and transcription factor networks modulated upon HRasG12V-transformation or Sprouty deletion are largely distinct. Oncogenic HRasG12V elevates histone 3 lysine 27 acetylation (H3K27ac) levels at enhancers near the transcription factor Gata4 and the kinase Prkcb, as well as their expression levels. We show that Gata4 is necessary for the aberrant gene expression and H3K27ac marking at enhancers, and Prkcb is required for the oncogenic effects of HRasG12V-driven cells. Taken together, our findings demonstrate that dynamic reprogramming of the cellular enhancer landscape is a major effect of oncogenic RTK signaling. We performed ChIP-seq to assess the global changes in the histone modifications H3K27ac (AC), H3K4me1 (me1), and H3K4me3 (me3) upon loss of feedback regulation through Sprouty (Spry) deletion, and upon unrestrained signaling driven by oncogenic HRasG12V. ChIP-seq was performed in biological duplicate; replicate2 is indicated in the sample name. Spry124fl/fl (VEC) and Spry124-/- (CRE) MEFs were profiled in three conditions: unsynchronized (U), serum starved (S), and serum starved and FGF treated (F). Spry124fl/fl (VEC) MEFs transduced with empty vector (EV) control or HRasG12V (HRas) were profiled in the unsynchronized state.

2015-08-22 | E-GEOD-64190 | biostudies-arrayexpress

Kim et al. STRIPAK directs PP2A activity towards MAP4K4 to promote oncogenic transformation

Project description:STRIPAK directs PP2A activity towards MAP4K4 to promote oncogenic transformation

2019-10-04 | MSV000084422 | MassIVE

Enhancer chromatin signatures predict Smad2/3 binding in Xenopus

Project description:In this study we have examine the deposition of H3K4me1,H3K4Me3 and H3K27Ac and the Nodal transcription factor, Smad2/3, immediately following zygotic transcription and continuing through gastrulation. We profiled 4 histone modifications (H3K4Me3, H3K27Me3, H3K27AC, H3K4Me1) and one transcription factor smad2/3 (+ chromatin input) using ChIP-Seq, and expression profiles (3' RNA-Seq) for Xenopus tropicalis embryos stage8, stage9 and stage10.5. Furthermore, we have profile two histone modifications (H3K4Me1 and H3K27Ac) in absance of nodal signaling in stage9 Xenopus tropicalis embryos using ChIP-seq and 3-seq

2014-09-17 | E-GEOD-56000 | biostudies-arrayexpress

A novel oncogenic enhancer of estrogen receptor positive breast cancer

Project description:To understand the regulatory landscape of oncogene c-Myc in breast cancer, two epigenetic hallmarks of open chromatin, consisting of H3K4me1 and H3K27ac, were investigated by ChIP-seq in distinct types of human breast cancer cells (estrogen receptor positive MCF-7 and triple-negative MDA-MB-231), respectively. By visualizing the ChIP-seq at c-Myc locus, we noticed that the H3K4me1 and H3K27ac signals were enriched remarkably upstream ~65 kb of c-Myc in MCF-7 cells but not in MDA-MB-231 cells. The results indicated that c-Myc may be regulted by an enhancer located upstream ~65 kb.

2022-10-04 | GSE180080 | GEO

Enhancer engagement sustains oncogenic transformation and progression of B-cell precursor acute lymphoblastic leukemia

Project description:Numerous evidence report that non-genetic-driven events such as enhancer reprogramming promotes neoplastic transformation and strongly contribute to the phenotypical heterogeneity of cancers as much as genetic variation. In this study, we investigated the role of enhancers in sustaining oncogenic transformation in Paediatric B-cell Acute Lymphoblastic Leukemia (ALL-B), a type of cancer caused by the accumulation of lymphoid progenitor cells in the bone marrow.

2024-06-27 | GSE214916 | GEO

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

Project description:ChIP-seq for Pol II, H3K27ac and H3K4me1 in neuroblastoma

2014-11-21 | GSE62725 | GEO

Epigenetic antagonism between Snf5 and Ezh2 during oncogenic transformation

Project description:Epigenetic alterations have been increasingly implicated in oncogenesis. Analysis of Drosophila mutants suggests that Polycomb and SWI/SNF complexes can serve antagonistic developmental roles. However, the relevance of this relationship to human disease is unclear. Here we have investigated functional relationships between these epigenetic regulators in oncogenic transformation. Mechanistically, we show that loss of the SNF5 tumor suppressor leads to elevated expression of the Polycomb gene EZH2 and that Polycomb targets are broadly H3K27-trimethylated and repressed in SNF5-deficient fibroblasts and cancers. Further, we show antagonism between SNF5 and EZH2 in the regulation of stem cell-associated programs and that Snf5 loss activates those programs. Finally, using conditional mouse models, we show that inactivation of Ezh2 blocks tumor formation driven by Snf5 loss. Mouse Embryonic Fibroblasts (MEFs) conditionally inactivated for Ezh2, Snf5 and Ezh2, or from control WT MEFs were used to evaluated epigenetic antagonism between Snf5 and Ezh2 in the control of gene expression programs. Snf5-deficient lymphoma samples and control CD8+ WT T-cells were used to evaluate genetic programs misregulated by Snf5 inactivation during tumorigenesis. RNA was isolated from each of these samples and used for gene expression profiling on Affymetrix arrays.

2010-10-19 | E-GEOD-23656 | biostudies-arrayexpress

STRIPAK directs PP2A activity to promote oncogenic transformation

Project description:STRIPAK directs PP2A activity to promote oncogenic transformation

| PRJNA485011 | ENA