Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Epigenetic reprogramming of intestinal stemness by dietary arachidonic acid [intestinal organoids]

ABSTRACT: We evaluated the effects of arachidonic acid (AA) on intestinal stem cell regeneration by RNA-seq and found that AA treatment led to strong upregulation of genes that are associated with stem cell reprogramming across the time points. AA elicits a conserved stem cell regeneration program in mouse intestinal organoids.

ORGANISM(S): Mus musculus

PROVIDER: GSE188213 | GEO | 2023/03/01

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

Epigenetic reprogramming of intestinal stemness by dietary arachidonic acid [Organoid]

Project description:Single cell transcriptomic profiling (sc RNA-seq) of arachidonic acid (AA) induced gene expression pogram associated with regeneration in intestinal organoids.

2023-03-01 | GSE210728 | GEO

Epigenetic reprogramming of intestinal stemness by dietary arachidonic acid [In_vivo]

Project description:Single cell transcriptomic profiling (sc RNA-seq) of diatery arachidonic acid (AA) induced gene expression pogram associated with regeneration in intestinal organoids.

2023-03-01 | GSE210724 | GEO

Arachidonic acid promotes intestinal regeneration by activating Wnt signaling

Project description:We identify arachidonic acid (AA), as a direct proliferation promoter of intestinal epithelial cells, facilitating small intestinal regeneration. In the transcriptomes, it shows that AA treatment upregulated proliferation-related genes including Wnt signaling target genes, while downregulated differentiation-related genes including enterocyte, goblet cell, Paneth cell, enteroendocrine cell, and tuft cell markers. Additionally, AA could also upregulate stem cell-associated genes which have been highly expressed three days after 12Gy IR injury (e.g. Clu, Lamc2, Anxa1, Areg, and Ly6d). The study shows that AA treatment can be considered a potential therapy for irradiation injury repair and tissue regeneration.

2020-07-27 | GSE146871 | GEO

Arachidonic acid promotes intestinal regeneration by activating Wnt signaling

Project description:Arachidonic acid promotes intestinal regeneration by activating Wnt signaling

| PRJNA612250 | ENA

Epigenetic reprogramming of intestinal stemness by dietary arachidonic acid

Project description:This SuperSeries is composed of the SubSeries listed below.

2023-03-01 | GSE210730 | GEO

Arachidonic acid targets pneumococcal fatty acid homeostasis

Project description:Free fatty acids play an important role during infection by modulating immune responses, but also by directly functioning as antimicrobials. Particularly, the host’s long chain polyunsaturated fatty acids, not commonly found in bacterial pathogens, have significant antibacterial potential. Of these arachidonic acid (AA) is in high abundance, and in this study we show that upon infection with the Streptococcus pneumoniae the AA concentration in the blood increases. Hence, we investigated the transcriptmoic effects of AA on this extremely problematic bacterial pathogen.

2018-05-23 | GSE93102 | GEO

Krüppel-like Factor 5 Regulates Stemness, Lineage Specification, and Regeneration of Intestinal Epithelial Stem Cells

Project description:Intestinal stem cells are required for proliferation, differentiation, and regeneration of the intestinal epithelium. Krüppel-like factor 5 regulates intestinal stem cells in both physiologic and pathological conditions and may be a treatment target in certain diseases of the intestine.

2021-10-27 | GSE131265 | GEO

YTHDF1 Amplifies Wnt/β-Catenin Signaling to Promote Intestinal Stemness

Project description:Wnt/β-catenin signaling is essential for intestinal stem cell homeostasis and aberrant activation of this signaling leads to tumorigenesis. Here we report a function of YTHDF1, an mRNA m6A reader, in mediating β-catenin hyperactivation. Wnt signaling promotes YTHDF1 expression at the translational level. YTHDF1 is dispensable for normal intestinal development in mice while essential for intestinal regeneration. Ythdf1 knockout reduces the stemness of intestinal stem cells, which blocks Wnt-driven tumorigenesis. Genome-wide analysis identifies a subset of Wnt signaling components regulated by YTHDF1 in an m6A-dependent manner. Moreover, we demonstrate that YTHDF1 promotes the translation of TCF7L2/TCF4 to augment β-catenin activation. Targeting YTHDF1 in the established tumors leads to tumor shrinkage and prolonged survival. Together, our studies uncover YTHDF1 as an integral regulator of Wnt signaling at the translational level during intestinal tumorigenesis, which might serve as a promising target for colorectal cancer therapy.

2019-08-31 | GSE136664 | GEO

HDAC5 loss in pancreatic cancer induces enhanced arachidonic acid metabolism via overactivated GATA1-cPLA2 axis

Project description:Unlike class I Histone deacetylase (HDAC) members (HDAC1, 2, 3, etc.), HDAC5, a class IIa HDAC member, is downregulated in multiple solid tumors, including pancreatic cancer, and its loss is associated with unfavorable prognosis. Additionally, HDAC5’s expression correlates negatively with arachidonic acid (AA) metabolism, which is highly implicated in inflammatory responses and cancer progression. This study aimed to elucidate the role of HDAC5 in AA metabolism and its prospect in the treatment of pancreatic cancer.

2023-08-01 | GSE207863 | GEO

ENO1 promotes liver carcinogenesis through YAP1-dependent arachidonic acid metabolism

Project description:Enolase 1 (ENO1) is a glycolytic enzyme that plays essential roles in various pathological activities including cancer development. However, the mechanisms underlying ENO1-contributed tumorigenesis are not well explained. Here, we uncover that ENO1, as an RNA-binding protein, binds to the cytosine-uracil-guanine-rich elements of YAP1 messenger RNA to promote its translation. ENO1 and YAP1 positively regulate alternative arachidonic acid (AA) metabolism by inverse regulation of PLCB1 and HPGD (15-hydroxyprostaglandin dehydrogenase). The YAP1/PLCB1/HPGD axis-mediated activation of AA metabolism and subsequent accumulation of prostaglandin E2 (PGE2) are responsible for ENO1-mediated cancer progression, which can be retarded by aspirin. Finally, aberrant activation of ENO1/YAP1/PLCB1 and decreased HPGD expression in clinical hepatocellular carcinoma samples indicate a potential correlation between ENO1-regulated AA metabolism and cancer development. These findings underline a new function of ENO1 in regulating AA metabolism and tumorigenesis, suggesting a therapeutic potential for aspirin in patients with liver cancer with aberrant expression of ENO1 or YAP1.

2023-05-19 | GSE183703 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

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