Long-term faecal incubations
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ABSTRACT:
PROVIDER: PRJNA574256 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Short-term celecoxib supplementation impacts compositional and functional features of in vitro gut microbial ecosystem
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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:Decreased diversity of butyrate-producing bacteria followed by functional adjustment occurs in the microbiome of the simulated proximal colon upon long-term treatment with aspirin
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Project description:Cancer cells metastatic to the leptomeninges encounter a metabolically-challenging extreme microenvironment. To understand adaptations to this space, we subjected leptomeningeal-metastatic (LeptoM) mouse breast and lung cancers isolated from either the leptomeninges or orthotopic primary sites to ATAC- and RNA-sequencing. When inhabiting the leptomeninges, the LeptoM cells demonstrated transcription downstream of retinoid-X-receptors (RXRs). We found evidence of local retinoic acid (RA) generation in both human leptomeningeal metastasis and mouse models in the form of elevated spinal fluid retinol and expression of RA-generating dehydrogenases within the leptomeningeal microenvironment. Stimulating LeptoM cells with 9-cis RA induced expression of transcripts encoding de novo fatty acid synthesis pathway enzymes in vitro. In vivo, whereas knockout of Stra6 did not alter cancer cell leptomeningeal growth, knockout of Rxra/b/g interrupted cancer cell lipid biosynthesis and arrested cancer growth. These observations illustrate a mechanism whereby locally-generated developmental cues metabolically reprogram metastatic cancer cells and suggest novel therapeutic approaches.
2024-10-13 | GSE278624 | GEO
Project description:Cancer cells metastatic to the leptomeninges encounter a metabolically-challenging extreme microenvironment. To understand adaptations to this space, we subjected leptomeningeal-metastatic (LeptoM) mouse breast and lung cancers isolated from either the leptomeninges or orthotopic primary sites to ATAC- and RNA-sequencing. When inhabiting the leptomeninges, the LeptoM cells demonstrated transcription downstream of retinoid-X-receptors (RXRs). We found evidence of local retinoic acid (RA) generation in both human leptomeningeal metastasis and mouse models in the form of elevated spinal fluid retinol and expression of RA-generating dehydrogenases within the leptomeningeal microenvironment. Stimulating LeptoM cells with 9-cis RA induced expression of transcripts encoding de novo fatty acid synthesis pathway enzymes in vitro. In vivo, whereas knockout of Stra6 did not alter cancer cell leptomeningeal growth, knockout of Rxra/b/g interrupted cancer cell lipid biosynthesis and arrested cancer growth. These observations illustrate a mechanism whereby locally-generated developmental cues metabolically reprogram metastatic cancer cells and suggest novel therapeutic approaches.
2024-10-13 | GSE277504 | GEO
Project description:The coxibs are a subset of non-steroidal anti-inflammatory drugs (NSAIDs) that selectively target cyclooxygenase-2 (COX-2) to inhibit prostaglandin signaling and reduce inflammation. However, only celecoxib remains in use, necessitating exploration of broader mechanisms of the coxibs. Here, we report a novel binding site for celecoxib on prostaglandin E synthase (PTGES), an enzyme downstream of COX-2 in the prostaglandin signaling pathway using an isotopically-coded cleavable chelation-assisted biotin probe. Evaluation of the multi-functional probe revealed significantly improved tagging efficiencies attributable to promotion of CuAAC chemistry by the embedded picolyl functional group. Application of the probe within the small molecule interactome mapping by photo-affinity labeling (SIM-PAL) platform using photo-celecoxib as a reporter for celecoxib identified known targets (e.g., carbonic anhydrase 12) and the significant enrichment of PTGES, along with six additional membrane proteins and 15 subunits of the cytochrome complex. In addition, four binding sites to celecoxib were mapped by the probe, including a direct interaction with PTGES. The interaction between celecoxib and PTGES was validated by competitive displacement and thermal shift assay. The binding site between celecoxib and PTGES enabled the development of a structural model of the interaction and will inform the further development of new selective inhibitors of the prostaglandin signaling pathway.
2024-01-04 | PXD014299 | Pride
Project description:Microarray analysis is a useful methodology to identify target genes modulated by anticancer drugs. Here, celecoxib effect on gene expression profiles was evaluated in the modified resistant hepatocyte model. Animals subjected to carcinogenic treatment were fed with diet containing 1500 ppm of celecoxib. Two schemes of celecoxib administration were designed. In the progression protocol, celecoxib was administrated between days 18 and 25 post-cancer initiation, a total of 8 celecoxib treatment days, when well established preneoplastic lesions starts to appear. In the initiation protocol, celecoxib was administrated from one week before until 25 days after of cancer initiation, a total of 32 celecoxib treatment days. A rat group was subjected only to the carcinogenic treatment as cancer positive control. Gene expression profiles of all groups were compared to a negative untreated control. The evaluation of gene expression profiles permitted us to identify new target genes that are modulated by celecoxib treatment. A possible mechanism of celecoxib chemoprevention of hepatocarcinogenesis is proposed. 9 weeks old Sprague Dawley rats, 4 rats per group, were subjected to Semple-Roberts' modified hepatocarcinogenesis protocol and sacrificed 25 days post-initiation. In celecoxib-treated groups, celecoxib was administrated mixed in diet at 1500 ppm. Negative and positive cancer progression controls were included to compare gene expression profiles. Microarray analysis was performed on liver samples, one replicate per rat, using dye swap.
2009-07-10 | E-GEOD-12112 | biostudies-arrayexpress
Project description:Microarray analysis is a useful methodology to identify target genes modulated by anticancer drugs. Here, celecoxib effect on gene expression profiles was evaluated in the modified resistant hepatocyte model. Animals subjected to carcinogenic treatment were fed with diet containing 1500 ppm of celecoxib. Two schemes of celecoxib administration were designed. In the progression protocol, celecoxib was administrated between days 18 and 25 post-cancer initiation, a total of 8 celecoxib treatment days, when well established preneoplastic lesions starts to appear. In the initiation protocol, celecoxib was administrated from one week before until 25 days after of cancer initiation, a total of 32 celecoxib treatment days. A rat group was subjected only to the carcinogenic treatment as cancer positive control. Gene expression profiles of all groups were compared to a negative untreated control. The evaluation of gene expression profiles permitted us to identify new target genes that are modulated by celecoxib treatment. A possible mechanism of celecoxib chemoprevention of hepatocarcinogenesis is proposed.
2009-07-10 | GSE12112 | GEO
Project description:To test the utility of iPSC-derived OC tissue chip in drug screening, Celecoxib, a selective cyclooxygenase 2 (COX-2) inhibitor commonly used to treat OA, was administered to the system. Celecoxib was administered at 10 µM concentration, and showed no noticeable adverse effect on the health of normal chondral tissue. Administration of Celecoxib to both OC-C and OC-B were used to simulate the typically systemic action of Celecoxib, represented by the “SY” group. In addition, we also examined the potential effect of intraarticular (IA) application of Celecoxib in treating OA, by delivery only to OC-C, namely the “IA” group. Normal OC tissues without any treatments served as the control (CL).
2019-11-14 | GSE140336 | GEO