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Epigenetic reprogramming of intestinal stemness by dietary arachidonic acid [CutnRun 1]

ABSTRACT: We evaluated tthe necessity of PGE2-Ptger4 signaling in regulating stemness enhancing effects of arachidonic acid (AA) via CutnRun and found that Ptger4 KO organoids failed to cause global methylation changes in signature genes that are associated with stem cell reprogramming in response to AA or PGE2.

ORGANISM(S): Mus musculus

PROVIDER: GSE246875 | GEO | 2025/11/01

REPOSITORIES: GEO

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Epigenetic reprogramming of intestinal stemness by dietary arachidonic acid [CutnRun 2]

Project description:We performed epigenomic profiling to evaluate the effects of arachidonic acid (AA) on intestinal stem cell regeneration via CutnRun and found that AA treatment led to global changes in methylation status of genes that are associated with stem cell reprogramming.

2025-11-01 | GSE246876 | GEO

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

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

Project description: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.

2023-03-01 | GSE188213 | GEO

Epigenetic reprogramming of intestinal stemness by dietary arachidonic acid [ATAC-Seq]

Project description:We performed epigenetic profiling to assess the effects of arachidonic acid (AA) on intestinal stem cell regeneration via ATAC-seq and found that AA treatment led to global changes in chromatin accessibility of genes that are associated with stem cell reprogramming.

2025-11-01 | GSE246873 | GEO

Omega-6 fatty acids, arachidonic acid (AA) activates PI3K signaling and induces gene expression in prostate cancer

Project description:Essential fatty acids (FA) are not only energy-rich molecules; they are also an important component of the membrane bilayer and recently have been implicated in induction of fatty acid synthase (FAS) and other genes. Using gene chip analysis, we have found that arachidonic acid (AA), an omega-6 fatty acid, induced 11 genes that are regulated by NFkappaB. We verified gene induction by omega-6 fatty acids including COX2, IKBA, NFKB, GMCSF, IL1B, CXCL1, TNFA, IL6, LTA, IL8, PPARG, and ICAM1 using qRTPCR. PGE2 synthesis was increased within 5min of addition of AA. Analysis of upstream signal transduction showed that within 5min of FA addition, phophatidylinositol 3-kinase (PI3K) was significantly activated followed by activation of Akt at 30min. ERK1 and 2, p38, and SAPK/JNK were not phosphorylated after omega-6 FA addition. Thirty minutes after FA addition, we found a significant 3-fold increase in translocation of NFkappaB transcription factor to the nucleus. Addition of non-steroidal anti-inflammatory drug (NSAID) caused a decrease in cox-2 protein synthesis, PGE2 synthesis as well as inhibition of PI3K activation. We have previously shown that AA induced proliferation is also blocked (P<0.001) by PI3K inhibitor LY294002. LY294002 also significantly inhibited the AA induced gene expression of COX2, IL1B, GMCSF, and ICAM1. Taken together, the data suggests that AA via conversion to PGE2 plays an important role in stimulation of growth related genes and proliferation via PI3K signaling and NFkappaB translocation to the nucleus. Keywords: Time course of Prostate Cancer Activation by Arachidonic Acid

2006-01-01 | GSE3737 | GEO

Transcription profiling of human prostate cancer cells with arachidonic acid reveals induction of 11 genes that are regulated by NFkappaB

2007-07-03 | E-GEOD-3737 | biostudies-arrayexpress

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

Epigenetic reprogramming of intestinal stemness by dietary arachidonic acid

Project description:Epigenetic reprogramming of intestinal stemness by dietary arachidonic acid

| PRJNA867320 | ENA

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

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