Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Dynamic properties of enhancer and promoter during DNA damage in hepatocellular carcinoma [ATAC-Seq]

ABSTRACT: DNA damage is a critical factor contributing to tumorigenesis, however, the dynamic changes in multi-omics signatures of enhancers and promoters during the DNA damage response (DDR) remain poorly understood. In this study, we discovered that the expression levels, chromatin accessibility, and element activity of distal/proximal enhancers and promoters exhibited obvious dynamic similarity and duality of characteristics at different stages of DNA damage in hepatocellular carcinoma (HCC). Furthermore, we found that the pre-damage accessibility and activity status of enhancers and promoters played an important role in determining their regulatory features following DNA damage in HCC. Finally, we identified transcription factors (TFs) with significantly altered activity in response to DNA damage, with notable differences between p53 activity in enhancers and promoters during the DDR. Overall, these findings reveal the complex dynamic changes within cis-regulatory elements in response to DNA damage.

ORGANISM(S): Homo sapiens

PROVIDER: GSE278055 | GEO | 2025/06/03

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Dynamic properties of enhancer and promoter during DNA damage in hepatocellular carcinoma [ChIP-Seq]

Project description:DNA damage is a critical factor contributing to tumorigenesis, however, the dynamic changes in multi-omics signatures of enhancers and promoters during the DNA damage response (DDR) remain poorly understood. In this study, we discovered that the expression levels, chromatin accessibility, and element activity of distal/proximal enhancers and promoters exhibited obvious dynamic similarity and duality of characteristics at different stages of DNA damage in hepatocellular carcinoma (HCC). Furthermore, we found that the pre-damage accessibility and activity status of enhancers and promoters played an important role in determining their regulatory features following DNA damage in HCC. Finally, we identified transcription factors (TFs) with significantly altered activity in response to DNA damage, with notable differences between p53 activity in enhancers and promoters during the DDR. Overall, these findings reveal the complex dynamic changes within cis-regulatory elements in response to DNA damage.

2025-06-03 | GSE278056 | GEO

Dynamic properties of enhancer and promoter during DNA damage in hepatocellular carcinoma [RNA-Seq]

2025-06-03 | GSE278054 | GEO

Enhancers reside in a unique epigenetic environment during early development

Project description:During development and differentiation, enhancers, and not promoters are most dynamic in their DNA methylation status. However, the causal relationship between enhancer activity and methylation is not clear. Here, we describe that during early zebrafish development, enhancer activity has little influence on DNA methylation, and that hypo-methylation is a unique feature of primed enhancers, whereas active enhancers are hyper-methylated. Hypo-methylated enhancers (hypo-enhancers) are enriched close to important transcription factors (TFs) that act later in development, are specifically de-methylated before the maternal-zygotic transition (MZT), and reside in a unique epigenetic environment. Finally, we demonstrate that hypo-enhancers are functionally active and that they are physically associated with the transcriptional start site (TSS) of target-genes, irrespective of target-gene activity. In conclusion, we demonstrate that early development in zebrafish represents a time-window characterized by non-canonical DNA methylation-enhancer relationships, including global DNA hypo-methylation of inactive enhancers and DNA hyper-methylation of active enhancers. DNA methylation profiles of 4 time points during zebrafish early development.

2015-11-09 | E-GEOD-74789 | biostudies-arrayexpress

Expression data of Schizosaccharomyces pombe deletions involved in DNA damage response

Project description:DNA damage response (DDR) plays pivotal roles in maintaining genome integrity and stability. An effective DDR requires the involvement of hundreds of genes that compose a complicated network. To identify novel genes involved in DDR, we screened a genome-wide Schizosaccharomyces pombe (S. pombe) haploid deletion library against six different DNA damage reagents. We identified 52 genes that were actively involved in DDR. Among the 52 genes, 20 genes were linked to DDR for the first time. For a better understanding of DDR genes function, we performed a DNA microarray assay to analyze the gene expression profiles of eight deletions. Cells of wild type and eight deletions involved in DDR were collected during the expontentially growing stage, and were subjected to RNA extraction and hybridization on Affymetrix microarrays. We tried to understand the role of genes in DDR by comparing the expression profiles of deletions with that of wild type.

2012-09-11 | E-GEOD-40747 | biostudies-arrayexpress

p53 Regulates Enhancer Accessibility and Activity in Response to DNA Damage

Project description:The tumor suppressor p53 is a well-characterized transcription factor that can bind gene promoters and regulate target gene transcription in response to DNA damage. Recent studies, however, have revealed that p53 binding events occur predominantly within regulatory enhancer elements. The effect of p53 binding on enhancer function has not been systematically evaluated. Here, we perform a genome-scale analysis of enhancer activity from p53-bound sequences using a series of massively parallel reporter assays (MPRAs) coupled with the assay for transpose-accessible chromatin (ATAC-Seq). We find that the majority of p53 bound sequences examined are potent regulators of enhancer activity during the DNA damage response. Enhancer regulation requires the presence of the p53 consensus sequence and results in significant induction of target gene transcription. Surprisingly, our analyses revealed that most p53-bound enhancers are located within regions of inaccessible chromatin. Many of these enhancers display significantly increased accessibility in response to DNA damage suggesting that p53 regulates their activity, in part, by altering local chromatin environments. The recognition and activation of inaccessible enhancers may contribute to the ability of the p53 network to function across the diverse chromatin landscapes of different cell and tissue types.

2017-07-21 | GSE83780 | GEO

DNA damage responsive microRNAs misexpressed in human cancer regulate chemotherapy sensitivity (lung cancer cell lines)

Project description:The DNA damage response (DDR) is a cellular process that protects the genetic information against DNA damage and inhibits malignant transformation. Tumor cells are characterized by an aberrant DDR, which is exploited by genotoxic chemotherapy. However, cancer cells are able to develop drug resistance, for example by modulation of the DDR. Although the regulation of the DDR has been extensively studied, not much is known about the role of microRNAs (miRNAs). Here, we describe an approach to specifically identify DDR miRNAs in human primary epithelial cells that also play a role in tumorigenesis and response to cancer therapy in corresponding cancer cells. The miRNA expression profile was determined of 12 lung cancer cell lines.

2013-05-31 | E-GEOD-47524 | biostudies-arrayexpress

Altered levels of MOF and decreased levels of H4K16ac correlate with a defective DNA damage response (DDR).

Project description:Full title: Altered levels of MOF (member of MYST family histone acetyl transferase) and decreased levels of H4K16ac correlate with a defective DNA damage response (DDR). The human MOF gene encodes a protein that specifically acetylates histone H4 at lysine 16 (H4K16ac). Here we show that altered levels of H4K16ac correlate with a defective DNA damage response (DDR) to ionizing radiation (IR). The defect however is not due to altered expression of proteins involved in DDR. Specific inhibition of H4K16ac deacetylation in MOF-depleted cells rescued IR-induced abrogation of DDR. MOF was found associated with DNA-dependent protein kinase catalytic subunit (DNAPKcs), a protein involved in non-homologous end joining (NHEJ) repair, whose ATMdependent IR-induced phosphorylation was abrogated in MOF-depleted cells. Our data indicate that MOF depletion greatly decreased the repair of DNA double-strand breaks (DSBs) by NHEJ and homologous recombination (HR). In addition, the MOF protein activity associates with chromatin upon DNA damage and colocalizes with the synaptonemal complex in male meiocytes. We propose that MOF, through H4K16ac, plays a critical role in the cellular DNA damage response. Keywords: Cell type comparison HEK293 cells were transfected with plasmids encoding hMOF for over-expression of the histone acetyl transferase that leads to elevated levels of acetylation of Lysine 16 of histone H4. siRNA mediated knock-down of hMOF was performed to deplete the H4K16ac levels. Total RNA samples for expression profiling was obtained from wild type (293 cells without any treatment), hMOF over-expressed and hMOF knock-down 293 cell lines. Each sample was analyzed in triplicates using EGPF dsRNA treated samples as control.

2010-03-23 | E-GEOD-20193 | biostudies-arrayexpress

DNA damage responsive microRNAs misexpressed in human cancer regulate chemotherapy sensitivity (lung tumors)

2013-05-31 | E-GEOD-47525 | biostudies-arrayexpress

Human Fibroblast cells immortalised cells: Control vs DNA damage

Project description:Transcriptional profiling of human fibroblast cells after DNA damage with Camptothecin or Etoposide or Neocarzinostatin Upon DNA damage, the DNA damage response (DDR) elicits a complex signaling cascade, which includes the induction of multiple non-coding RNA species. Recently long non-coding RNAs (lncRNAs) have been shown to contribute to DDR by regulating gene expression. However, very little is known about the role that lncRNAs play in regulating DNA Repair. Using a genome-wide microarray screen we identified a novel ubiquitously expressed lncRNA, DDSR1 (DNA damage-sensitive RNA 1), which is induced upon DNA damage by several DNA double-strand break (DSB) agents. Two-condition experiment, Control vs. DNA damage human fibroblast cells. No Replicates, DNA damage was induced with either Camptothecin or Etoposide or Neocarzinostatin, Total RNA or Nuclear RNA was profiled.

2015-09-01 | E-GEOD-67062 | biostudies-arrayexpress

Active DNA damage response signaling initiates and maintains meiotic sex chromosome inactivation

Project description:Meiotic sex chromosome inactivation (MSCI) is an essential process in the male germline. While genetic experiments have established that the DNA damage response (DDR) pathway directs MSCI, due to limitations to the experimental systems available, mechanisms underlying MSCI remain largely unknown. Here we establish a system to study MSCI ex vivo, based on a short-term culture method, and demonstrate that active DDR signaling is required both to initiate and maintain MSCI via a dynamic and reversible process. DDR-directed MSCI follows two layers of modifications: active DDR-dependent reversible processes and irreversible histone post-translational modifications. Further, the DDR initiates MSCI independent of the downstream repressive histone mark H3K9 trimethylation (H3K9me3), thereby demonstrating that active DDR signaling is the primary mechanism of silencing in MSCI. By unveiling the dynamic nature of MSCI, and its governance by active DDR signals, our study highlights the sex chromosomes as an active signaling hub in meiosis.

2022-10-05 | GSE211519 | 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