Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

ARID1A Loss Promotes Lung Adenocarcinoma by Remodeling Chromatin Accessibility and Activating Glycolytic Reprogramming

ABSTRACT: ARID1A Loss Promotes Lung Adenocarcinoma by Remodeling Chromatin Accessibility and Activating Glycolytic Reprogramming

PROVIDER: PRJNA692111 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR13435624_1.fastq.gz	Fastqsanger.gz
	SRR13435624_2.fastq.gz	Fastqsanger.gz
	SRR13435625_1.fastq.gz	Fastqsanger.gz
	SRR13435625_2.fastq.gz	Fastqsanger.gz
	SRR13435626_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 20

Similar Datasets

ARID1A Loss Promotes Lung Adenocarcinoma by Remodeling Chromatin Accessibility and Activating Glycolytic Reprogramming

Project description:This study demonstrated that ARID1A loss markedly promotes lung tumorigenesis in genetic mice models. RNA sequencing reveals significant enrichment of the glycolytic pathway in ARID1A-deficient tumors, which is characterized by the upregulation of PGAM1, PKM2, and PGK1. Besides, ARID1A depletion increases chromatin accessibility and enhances the binding ability of Hif-1a to the promoter regions of Pgam1, Pkm, and Pgk1. In patients with lung cancer, ARID1A status is negatively correlated with mRNA level of PGAM1, PKM, and PGK1.

2022-10-01 | GSE164810 | GEO

ARID1A regulates chromatin organization and establishment of epigenetic marks for DSB repair and transcription silencing

Project description:AT-rich interactive domain-containing protein 1A (ARID1A), a SWI/SNF chromatin remodeling complex subunit, is frequently mutated across various cancer entities. ARID1A contributes to DNA damage response pathways, and we previously reported that ARID1A loss is associated with mutational signatures linked to DNA repair defects. Here we show that ARID1A is promoting both DNA double-strand breaks (DSBs) repair pathways, non-homologous end-joining (NHEJ) and homologous recombination (HR). ARID1A is accumulated at DSBs after DNA damage and regulates the chromatin loop formation at DSB sites by interacting with the cohesin subunit RAD21 and CTCF insulator protein promoting their enrichment around the DSBs. Further analysis demonstrates that ARID1A’s involvement in DSB repair is accompanied by alterations of chromatin accessibility and distribution of activating histone marks at DSBs. ARID1A binds to and promotes the recruitment of the HDAC1 to control transcription repression at these DSBs. Altogether, ARID1A simultaneously regulates DSB repair and transcription silencing in transcriptionally active chromatin. ARID1A depletion resulted in defective DSB repair, which subsequently led to accumulation of micronuclei, activation of cGAS-STING pathway and an increased expression of immunomodulatory cytokines and chemokines upon IR treatment. Furthermore, low ARID1A expression in cancer patients receiving radiotherapy was associated with higher infiltration of several immune cells. The high mutation rate of ARID1A in various cancer types highlights its clinical relevance as a promising biomarker that correlates with the level of immune regulatory cytokines and can estimate the levels of tumor-infiltrating immune cells and response to combination of radio- and immunotherapy.

2025-04-08 | PXD046159 | Pride

ARID1A regulates chromatin organization and establishment of epigenetic marks for DSB repair and transcription silencing

2024-06-22 | PXD047225 | Pride

Single-cell ATAC-seq profiling of ARID1A-loss-associated chromatin accessibility heterogeneity in pancreatic cancer cells

Project description:This Series contains single-cell ATAC-seq datasets from clone-resolved and pooled perturbation experiments examining how ARID1A and other epigenetic modifiers influence chromatin-accessibility heterogeneity in pancreatic ductal adenocarcinoma cells. The datasets include the main 28-clone BxPC3 experiment, a large-scale pooled five-shRNA experiment, acute SMARCA4 degradation with AU-15330, and independent experiments in BxPC3, HPAC/HPAFII, SW1990, and SUIT-2 backgrounds. PseuMO-Tag lineage barcodes were used to connect single-cell chromatin profiles to clonal identity.

2026-09-22 | GSE347847 | GEO

SMARCA4 CUT&Tag profiling in parental and ARID1A-knockdown BxPC3 pancreatic cancer clones

Project description:This Series profiles SMARCA4 (BRG1) chromatin occupancy by CUT&Tag in parental BxPC3 pancreatic ductal adenocarcinoma cells and selected control or ARID1A-knockdown clonal populations. The data were generated to examine whether residual SMARCA4 preferentially occupies regulatory regions associated with increased and variable chromatin accessibility after ARID1A loss. Drosophila spike-in nuclei were included for quantitative normalization.

2026-09-22 | GSE348238 | GEO

Analysis of chromatin accessibility in Arid1a-deficient murine primary pancreatic acinar cells using ATAC-seq

Project description:To gain insight into how the loss of SWI/SNF component ARID1A affects the chromatin accessibility, primary acinar cells were isolated from Arid1a-knockout and control mice and subjected to ATAC-sequencing.

2023-05-31 | GSE166332 | GEO

Gene expression data ARID1A knockdown OE33 cells versus mock OE33 cells

Project description:A nonsense mutation in ARID1A was identified by next generation sequencing in non-dysplastic Barrett's esophagus [BE] tissue and esophageal adenocarcinoma [EAC] tissue of a patient diagnosed with EAC. Immunohistochemistry performed on an independent archival cohort demonstrated ARID1A protein loss in 0% (0/76), 4.9% (2/40), 14.3% (4/28), 16.0% (8/50), and 12.2% (12/98) of normal squamous epithelium, BE, low-, high-grade dysplasia, and EAC tissues, respectively. Enhanced cell growth, proliferation and invasion were observed upon ARID1A knockdown in EAC cells. ARID1A was knocked down in OE33 cells (Sample MS_1 and MS_3) using on-TARGET smartpool ARID1A siRNA. At the same time, OE33 cells were transfected with a non-targeting siRNA, and these experiments (Samples MS_2 and MS_4) functioned as mock controls. Cells were harvested after 48 hours and total RNA was extracted using the Rneasy kit (Qiagen) Aim Affymetrix Human PrimeView Gene Expression Array : to determine the downstream effectors of ARID1A that are likely to contribute to the oncogenic phenotype caused by ARID1A down-regulation. Two biological replicates of each condition (2x ARID1A knockdown, and 2x Mock) were used for the microarray experiment.

2012-05-31 | E-GEOD-38380 | biostudies-arrayexpress

Chromatin accessibility and transcriptome changes in injured retinal ganglion cells (RGCs) after Arid1a deletion

Project description:To gain a deeper insight into roles of Arid1a in injured retinal ganglion cells (RGCs), we performed ATAC-seq and RNA-seq to analyze the genome-wide changes of chromatin accessibility and transcriptome changes before and after Arid1a deletion in RGCs of the adult mouse using Cre-lox system.

2020-04-20 | GSE147844 | GEO

Effect of Arid1a deletion on chromatin accessibility in antiviral effector CD8+ T cells. [ATAC-Seq]

Project description:To investigate the role of ARID1A in the regulation of effector CD8+ T cell responses, we crossed GzmB-Cre P14 Thy1.1 mice with Arid1a-fl/fl mice to generate Arid1a Het and KO mice. We then performed chromatin accessibility profiling analysis by ATAC-seq in WT, Het, and KO cells in vivo at d0, 48h in vitro activated, d3, d5, and d8 post-LCMV Armstrong infection.

2023-06-13 | GSE228171 | GEO

ATAC-seq analysis of ARID1A-deficient TOV112D human ovarian cancer cells treated with the G9a inhibitor BIX01294

Project description:Biological relevance: This study aims to evaluate how G9a inhibition via BIX01294 affects the chromatin landscape in the context of ARID1A deficiency. We investigated whether the loss of the SWI/SNF subunit ARID1A alters the cellular response to G9a pharmacological targeting in ovarian cancer. Experimental workflow: Human ovarian cancer cell line TOV112D was transduced with shRNA against ARID1A or a non-targeting control. These cells were subsequently treated with the G9a inhibitor BIX01294 or DMSO. Chromatin accessibility was profiled using ATAC-seq to compare the epigenetic changes across these conditions.

2026-03-20 | E-MTAB-16777 | biostudies-arrayexpress

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