Faecal incubations
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ABSTRACT:
PROVIDER: PRJNA574261 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Community metrics and functionality from the simulated colon microbiome rebound following sulindac supplementation.
| PRJNA574262 | ENA
Project description:1. Fermentative activities of colon microbiota pre-exposed to celecoxib oscillate and endure irreversible modifications following continuous NSAID supplementation in a simulated model of the gut microbial ecosystem
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Project description:Temporal analysis of colon carcinoma cell line CC531 response to 4.5 mM butyrate or 3 mM aspirin. Samples taken at 2, 6, 12, 16 and 24 hours. The CC531 cell line has been widely used to study different aspects of tumor growth and metastasis and provides an excellent experimental platform to develop novel antitumor strategies. To characterize the CC531 model at the molecular level, we screened for mutations in genes covering important signal-transduction pathways that are known to play major roles during colon carcinogenesis, the wnt and the ki-ras signaling pathways. We found both a prototypic beta-catenin (Ctnnb1) mutation (Thr(41)Ile) and a ki-ras (G12D) mutation, providing unambiguous evidence for the constitutive activation of these pathways in CC531 cells. We further established comprehensive gene expression profiles of CC531 cells and investigated the molecular response to 2 antitumor drugs, butyrate and aspirin. Using oligonucleotide microarrays, we screened the expression levels of 7,700 genes and identified a total of 398 genes whose expression was significantly changed upon treatment with butyrate. When using aspirin, 121 genes were significantly altered. Interestingly, 36 genes were regulated by both butyrate and aspirin and 35 of them were regulated in the same direction. We found 7 differentially expressed genes, cyclin D1, cyclin E, c-myc, Fosl1, c-fos, Cd44 and follistatin, which are known targets of the beta-catenin and/or the ras pathway. In all cases, butyrate and aspirin reversed the changes in expression normally found in response to active signaling of these oncogenic pathways.
2007-10-10 | E-GEOD-424 | biostudies-arrayexpress
Project description:Temporal analysis of colon carcinoma cell line CC531 response to 4.5 mM butyrate or 3 mM aspirin. Samples taken at 2, 6, 12, 16 and 24 hours. The CC531 cell line has been widely used to study different aspects of tumor growth and metastasis and provides an excellent experimental platform to develop novel antitumor strategies. To characterize the CC531 model at the molecular level, we screened for mutations in genes covering important signal-transduction pathways that are known to play major roles during colon carcinogenesis, the wnt and the ki-ras signaling pathways. We found both a prototypic beta-catenin (Ctnnb1) mutation (Thr(41)Ile) and a ki-ras (G12D) mutation, providing unambiguous evidence for the constitutive activation of these pathways in CC531 cells. We further established comprehensive gene expression profiles of CC531 cells and investigated the molecular response to 2 antitumor drugs, butyrate and aspirin. Using oligonucleotide microarrays, we screened the expression levels of 7,700 genes and identified a total of 398 genes whose expression was significantly changed upon treatment with butyrate. When using aspirin, 121 genes were significantly altered. Interestingly, 36 genes were regulated by both butyrate and aspirin and 35 of them were regulated in the same direction. We found 7 differentially expressed genes, cyclin D1, cyclin E, c-myc, Fosl1, c-fos, Cd44 and follistatin, which are known targets of the beta-catenin and/or the ras pathway. In all cases, butyrate and aspirin reversed the changes in expression normally found in response to active signaling of these oncogenic pathways. Keywords: other
2003-05-19 | GSE424 | GEO
Project description:Obesity is a leading cause of primary hypertension in children, and a high-fat intake and the gut microbiota may be involved in the pathogenesis of obesity-related hypertension (OrHTN), but the underlying mechanisms are not fully understood. Here, we show that high-fat diet (HFD) feeding alters the gut microbiota composition in OrHTN rats, resulting in a reduced abundance of the butyrate-producing bacteria Ruminococcus and a subsequent decrease in plasma butyrate levels. Histone 3 lysine 9 butyrylation (H3K9bu) levels decreased in the kidneys of OrHTN rats, which downregulates the expression of the hypertension-related MAS1 gene. Furthermore, sodium butyrate affected H3K9bu modification levels in a concentration-dependent manner, with decreased H3K9bu and downregulated MAS1 expression at low concentrations in human proximal tubular epithelial cells. Our results suggest that a HFD contributes to the development of OrHTN by altering the gut microbiota and its metabolites, leading to the downregulation of H3K9bu and hypertension-related gene expression.
2024-06-27 | GSE235898 | GEO
Project description:Here we report the change in gene expression in placenta-derived MSCs followed exposure to aspirin.
2023-03-28 | GSE181638 | GEO
Project description:Colon carcinoma cell line CC531 response to butyrate and aspirin
| PRJNA84989 | ENA
Project description:Purpose: The aim of this study is to dissect if the microbiota-derived metabolite butyrate alters the transcriptome of antigen-activated CD8+ T cells. Methods: mRNA profiles from Ctrl and Butyrate-treated gBT-I were generated by deep sequencing, in triplicates, using Illumina GAIIx. The sequence reads that passed quality filters were analyzed at the transcript isoform level with two methods: Burrows–Wheeler Aligner (BWA) followed by ANOVA (ANOVA) and TopHat followed by Cufflinks. Results: The analysis of RNAseq data of Ctrl and Butyrate-treated gBT-I lead to ~2,000 differentially expressed genes (FDR < 0.05; fold change>2). GSEA enrichment analysis revealed enrichment of memory T cells signatures in gBT-I following butyrate-treatment (Sarkar et al., 2008). Conclusions: Our data shows that butyrate alters the transcriptome of effector CD8+ T cells, in particular their memory signature.
2019-06-07 | GSE132285 | GEO