Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

CFL1-induced super enhancer RNA m6A modification promotes local chromatin accessibility and oncogenes transcription in pancreatic cancer [RNA-seq]

ABSTRACT: Herein, we describe the landscape of m6A on super enhancer RNAs (seRNAs) in pancreatic ductal adenocarcinoma (PDAC) and demonstrate a regulatory axis involving m6A-seRNAs, H3K4me3 modification, chromatin accessibility and oncogenic transcription. our study has revealed the CFL1-YTHDC2-MLL1 epigenetic regulatory axis plays critical roles of dynamic m6A deposition in seRNAs and local chromatin state, which may be a novel oncogenic mechanism in PDAC and shed light on the crosstalk between epitranscriptome and epigenome.

ORGANISM(S): Homo sapiens

PROVIDER: GSE211587 | GEO | 2023/09/20

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

CFL1-induced super enhancer RNA m6A modification promotes local chromatin accessibility and oncogenes transcription in pancreatic cancer [m6A-seq]

Project description:Herein, we describe the landscape of m6A on super enhancer RNAs (seRNAs) in pancreatic ductal adenocarcinoma (PDAC) and demonstrate a regulatory axis involving m6A-seRNAs, H3K4me3 modification, chromatin accessibility and oncogenic transcription. our study has revealed the CFL1-YTHDC2-MLL1 epigenetic regulatory axis plays critical roles of dynamic m6A deposition in seRNAs and local chromatin state, which may be a novel oncogenic mechanism in PDAC and shed light on the crosstalk between epitranscriptome and epigenome.

2023-09-20 | GSE211588 | GEO

CFL1-induced super enhancer RNA m6A modification promotes local chromatin accessibility and oncogenes transcription in pancreatic cancer [PAR-CLIP]

2023-09-20 | GSE211585 | GEO

CFL1-induced super enhancer RNA m6A modification promotes local chromatin accessibility and oncogenes transcription in pancreatic cancer [CUT&Tag]

2023-09-20 | GSE211582 | GEO

CFL1-induced super enhancer RNA m6A modification promotes local chromatin accessibility and oncogenes transcription in pancreatic cancer [ATAC-seq]

2023-09-20 | GSE211581 | GEO

Lactobacillus delbrueckii subsp. bulgaricus CFL1

Project description:Draft genome of Lactobacillus delbrueckii subsp. bulgaricus CFL1

| PRJEB11306 | ENA

m6A-RIP-seq of Ascl1-induced neurons.

Project description:We performed m6A-RIPs in Ascl1-induced neurons (iNeurons) to investigate the neuronal m6A epitranscriptome. Immunoprecipitation was done twice using two different antibodies, acquired from Abcam and Synaptic Systems (SySy), allowing for a more robust detection of m6A modification marks. Additionally, RIP-seq was performed separately with intact and fragmented RNA. The former approach allowed to identify proportions of m6A-modified transcripts among the total number, while the latter approach provided the information to identify genomic coordinates of m6A peaks.

2023-07-12 | E-MTAB-9542 | biostudies-arrayexpress

Dynamic N6-methyladenosine Epitranscriptomic Landscape in Lung Adenocarcinoma

Project description:Systematically evaluate the global effect of dysregulated m6A regulators on the m6A epitranscriptome in patient tumors, and identify prognostic m6A markers by linking with patients' clinicopathological and outcome information.

| EGAS00001005524 | EGA

YTHDC2 regulates spermatogenesis through promoting the translation of N6-methyladenosine-modified RNA

Project description:N6-methyladenosine (m6A) is the most common internal modification in eukaryotic mRNA. It is dynamically installed and removed, and acts as an essential layer of mRNA metabolism, regulating biological processes including stem cell pluripotency, cell differentiation, and energy homeostasis. m6A is recognized by selective binding proteins; YTHDF1 and YTHDF3 work in concert to promote the translation of m6A-containing mRNAs, YTHDF2 expedites mRNA decay, and YTHDC1 affects the splicing of its targets. The biological function of YTHDC2, the final member of the YTH protein family, remains unknown. We report that YTHDC2 selectively binds m6A along its consensus motif GGACU. YTHDC2 promotes translation of its targets, and associates with cellular fractions involved in translation initiation. Ythdc2 knockout mice are infertile and have significantly smaller testes compared to those of littermates. In the testes, Ythdc2 is temporally expressed as meiosis begins, and germ cells of Ythdc2 knockout mice do not develop past the spermatogonium stage. Thus, YTHDC2 is an m6A binding protein that plays essential roles in spermatogenesis.

2017-08-01 | GSE98085 | GEO

6487d66b-e640-439a-b525-5746cdd12503 - samples

Project description:Applying a refined m6A RNA immunoprecipitation method, we profiled the m6A epitranscriptome on 10 non-neoplastic lung (NL) tissues and 53 lung adenocarcinoma tumors.

| EGAD00001008026 | EGA

METTL3/MYCN cooperation drives neural crest differentiation and provides therapeutic vulnerability in neuroblastoma

Project description:Neuroblastoma (NB) is a childhood cancer. Improper differentiation of developing trunk neural crest cells (tNCC) cause NB tumor formation in sympathetic nervous system. N6-methyladenosine (m6A) epitranscriptomic modification control post-transcriptional gene expression but the mechanism which recruit m6A methyltransferase complex to specific locus is less characterized. We explored if m6A epitranscriptome could fine tune gene regulation in migrating/differentiating tNCC. We uncovered m6A epitranscriptome based regulation of HOX gene expression in tNCC which contributes in their timely differentiation to sympathetic neurons. Posterior HOX genes are m6A modified in MYCN NB cells and tumors. We provided evidence that sustained overexpression of MYCN oncogene could drive METTL3 recruitment in subset of genes to create an undifferentiated state in tNCC. Our study suggests oncogenic transcription factor mediated modulation of m6A epitranscriptome could be a prevalent mechanism in other cancers. METTL3 depletion/inhibition induces DNA damage and differentiation in MYCN overexpressed cells. METTL3 inhibition increases vulnerability to the chemotherapeutic drug in MYCN-amplified Patient-derived xenografts (PDX) cells, suggesting METTL3 inhibition could be a potential therapeutic approach for NB.

2024-09-30 | GSE244473 | 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