Pelotomaculum
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA454509 | ENA |
REPOSITORIES: ENA
Similar Datasets
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Project description:Tumours contain heterogeneous cell populations. A population enriched in tumour-initiating potential has been identified in soft-tissue sarcoma (STS) by the isolation of side population (SP) cells. In this study, we compared the gene expression profiles of SP and non-SP cells in STS and identified Hedgehog (Hh) and Notch pathways as potential candidates for the targeting of SP cells. Upon verification of the activation of these pathways in SP cells, using primary tumor xenografts in NOD-SCID mice as our experimental model, we used the Hh blocker Triparanol and the Notch blocker DAPT to demonstrate that the suppression of these pathways effectively depleted the abundance of SP cells, reduced tumour growth, and inhibited the tumour-initiating potential of the treated sarcoma cells upon secondary transplantation. The data provide additional evidence that SP cells act as tumour initiating cells and points to Hh and Notch pathways as enticing targets for developing potential cancer therapies. We used microarrays to detail the difference in gene expressions between the side population cells in soft-tissue sarcoma in comparison to the bulk non-side-population cells.
2012-01-17 | GSE24199 | GEO
Project description:Hydrocarbon sludge reactor syntrophic bacterial communities from University of Wageningen, Netherlands that are anaerobic - Co-culture containing Pelotomaculum schinkii HH metagenome
| PRJNA336642 | ENA
Project description:Alishewanella sp. HH-ZS Genome sequencing and assembly
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Project description:Macellibacteroides sp. HH-ZS Genome sequencing and assembly
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Project description:Tumours contain heterogeneous cell populations. A population enriched in tumour-initiating potential has been identified in soft-tissue sarcoma (STS) by the isolation of side population (SP) cells. In this study, we compared the gene expression profiles of SP and non-SP cells in STS and identified Hedgehog (Hh) and Notch pathways as potential candidates for the targeting of SP cells. Upon verification of the activation of these pathways in SP cells, using primary tumor xenografts in NOD-SCID mice as our experimental model, we used the Hh blocker Triparanol and the Notch blocker DAPT to demonstrate that the suppression of these pathways effectively depleted the abundance of SP cells, reduced tumour growth, and inhibited the tumour-initiating potential of the treated sarcoma cells upon secondary transplantation. The data provide additional evidence that SP cells act as tumour initiating cells and points to Hh and Notch pathways as enticing targets for developing potential cancer therapies. We used microarrays to detail the difference in gene expressions between the side population cells in soft-tissue sarcoma in comparison to the bulk non-side-population cells. To examine whether certain pathways may be differentially regulated in SP cells versus non-SP cells, which represent the bulk of tumour cells, we compared the gene expression profiles of SP and non-SP cells in four primary STS tumours each from different patient. Upon surgical excision, these tumours were dissociated mechanically and enzymatically into individual cells. Via Hoechst dye staining and flow-cytometry, these primary tumour cells were sorted into distinct side population and non-side population fractions. Total RNA is extracted from an equal number of SP and NSP cell from each primary tumour. cDNA from each sample was generated from the isolated total RNA and hybridized onto Affymetrix Human Genome EukGE-WS2v4 gene chips against the same reference cDNA library. After initial processing of the raw data, using the Genespring® GX software, the expression of SP cells from each tumour was normalized against the expression of the corresponding non-SP cells. A gene list was constructed by selecting genes that were regulated in the same direction (SP vs. NSP) in all sample pairs with a fold change greater than 1.25. This list was examined using Genespring® GX significant pathway function to identify differentially regulated pathways.
2012-01-17 | E-GEOD-24199 | biostudies-arrayexpress
Project description:<p><strong>BACKGROUND:</strong> Studies have reported clinical heterogeneity between right-sided colon cancer (RCC) and left-sided colon cancer (LCC). However, none of these studies used multi-omics analysis combining genetic regulation, microbiota and metabolites to explain the site-specific difference.</p><p><strong>METHODS:</strong> Here, 494 participants from a 16S rRNA gene sequencing cohort (50 RCC, 114 LCC and 100 healthy controls) and a multi-omics cohort (63 RCC, 79 LCC and 88 healthy controls) were analyzed. 16S rRNA gene, metagenomic sequencing and metabolomics analyses of fecal samples were evaluated to identify tumor location-related bacteria and metabolites. Whole-exome sequencing (WES) and transcriptome sequencing (RNA-seq) were conducted to obtain the mutation burden and genomic expression pattern.</p><p><strong>RESULTS:</strong> We found unique profiles of the intestinal microbiome, metabolome, and host genome between RCC and LCC. The bacteria Flavonifractor plautii (Fp) and Fusobacterium nucleatum, the metabolites L-phenylalanine, and the host genes PHLDA1 and WBP1 were the key omics features of RCC; whereas the bacteria Bacteroides sp. A1C1 (B.A1C1) and Parvimonas micra, the metabolites L-citrulline and D-ornithine, and the host genes TCF25 and HLA-DRB5 were considered the dominant omics features in LCC. Multi-omics correlation analysis indicated that RCC-enriched Fp was related to the accumulation of the metabolite L-phenylalanine and the suppressed WBP1 signal in RCC patients. In addition, LCC-enriched B.A1C1 was associated with accumulation of the metabolites D-ornithine and L-citrulline as well as activation of the genes TCF25, HLA-DRB5 and AC079354.1.</p><p><strong>CONCLUSION:</strong> Our findings identify previously unknown links between intestinal microbiota alterations, metabolites and host genomics in RCC vs. LCC, suggesting that it may be possible to treat colorectal cancer (CRC) by targeting the gut microbiota-host interaction.</p>
2024-12-16 | MTBLS10232 | MetaboLights
Project description:Blautia schinkii DSM 10518 Genome sequencing and assembly
| PRJNA223460 | ENA