Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1139135 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR29928419_1.fastq.gz | Fastqsanger.gz | |||
| SRR29928419_2.fastq.gz | Fastqsanger.gz | |||
| SRR29928420_1.fastq.gz | Fastqsanger.gz | |||
| SRR29928420_2.fastq.gz | Fastqsanger.gz | |||
| SRR29928421_1.fastq.gz | Fastqsanger.gz |
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Project description:Pancreatic ductal adenocarcinoma (PDA) is a lethal malignancy characterised by a pathologicalfibroinflammatorymicroenvironment. Dichotomous tumour-promoting and -restrictive roles have been ascribed to the tumour microenvironment, however thedisparate effect of individual stromal subsets remains incompletely characterised. Here, we describe how heterocellular OSM-OSMR signalling instructsfibroblast reprogramming,tumourgrowth and metastasis.Macrophage-secreted OSM stimulatesinflammatory gene expression in cancer-associated fibroblasts (CAFs), which in turn induce a pro-tumorigenic environment and engage tumour cellsurvival and migratory signalling pathways. Tumour cells implanted in Osm-deficient (Osm-/-) mice display an epithelial-dominated morphology, reduced tumour growth and did notmetastasise. Moreover, the tumour microenvironment of Osm-/-animals exhibit increased abundance of αSMAposmyofibroblasts and a shift in myeloid and T cell phenotypes, consistent with a more immunogenic environment. Taken together, these data demonstrate how OSM-OSMR signalling coordinates heterocellular interactions to drive a pro-tumorigenic environment in PDA.
2021-11-29 | PXD022484 | Pride
Project description:It has been well established that (LIF) is essential for maintaining naive pluripotency of ESCs. Oncostatin M (OSM) is a member of the IL-6 family of cytokines which share gp130 as a receptor subunit, and the OSM-gp130 complex can recruit either LIF receptor β or OSM receptor β. Here we show that OSM can completely replace LIF to maintain naive pluripotency of mouse ESCs. Mouse ESCs cultured in the presence of LIF or OSM not only express pluripotency genes at similar levels but also exhibit the same developmental pluripotency as evidenced by generation of germline competent chimeras, supporting previous findings. Moreover, we demonstrate that mESCs cultured in OSM produce viable all-ESC pups by tetraploid embryo complementation (TEC) assay, the most stringent functional test of authentic pluripotency. Furthermore, the telomere length and telomerase activity also are crucial for unlimited self-renewal and genomic stability of mESCs, and these do not differ in mESCs cultured under OSM or LIF. The transcriptome of mESCs cultured in OSM overall is very similar to that of LIF, and OSM activates Stat3 signaling pathway, like LIF. Additionally, OSM upregulates pentose and glucuronate interconversions, ascorbate and aldarate metabolism, steroid and retinol metabolism pathways. Although the significance of these pathways remains to be determined, our data shows that OSM can maintain the naive pluripotent stem cells in the absence of LIF.
2021-01-23 | GSE165292 | GEO
Project description:Pancreatic ductal adenocarcinoma (PDA) is a lethal malignancy characterised by a pathological fibroinflammatory microenvironment. Dichotomous tumour-promoting and -restrictive roles have been ascribed to the tumour microenvironment, however the effects of individual stromal subsets remains incompletely characterised. Here, we describe how heterocellular OSM-OSMR signalling instructs fibroblast reprogramming, tumour growth and metastasis. Macrophage-secreted OSM stimulates inflammatory gene expression in cancer-associated fibroblasts (CAFs), which in turn induce a pro-tumorigenic environment and engage tumour cell survival and migratory signalling pathways. Tumour cells implanted in Osm-deficient (Osm-/-) mice display an epithelial-dominated morphology, reduced tumour growth and did not metastasise. Moreover, the tumour microenvironment of Osm-/- animals exhibit increased abundance of αSMApos myofibroblasts and a shift in myeloid and T cell phenotypes, consistent with a more immunogenic environment. Taken together, these data demonstrate how OSM-OSMR signalling coordinates heterocellular interactions to drive a pro-tumorigenic environment in PDA.
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Project description:Cutaneous squamous cell carcinoma (cSCC) is the second most common skin cancer in caucasian population and it's important to find new therapeutic targets. Cytokines expressed in tumor microenvironment can have strong effects on tumor cell phenotype. We have characterized the effect of Oncostatin M (OSM), a cytokine belonging to the IL-6 familly on the transcriptome of transformed keratinocytes cell line, PDVC57 cells. In this dataset, we have included the expression data obtained from transformed keratinocytes PDVC57 cells stimulated or not with OSM for 6 or 24 hours. These data have shown that 32 genes were differentially expressed in response to OSM stimulation.
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Project description:The microarrays for the three time course experiments described in the publication titled "Gene expression profiling of Helicobacter pylori reveals a growth phase dependent switch in virulence gene expression". TC1 refers to the first time course investigating gene expression changes over the time course of growth while TC2 refers to the second time course. TC Motility_broth refers to the third time course described in the manuscript used to investigate the concurrent changes in motility and the expression of the genes in the flagellar regulon. Detailed description of the growth of H. pylori for these 3 time courses can be found in the Materials and Methods section of the manuscript along with the exact filtering criteria used to download the data from these arrays. Note that in all three time courses the data for each array were transformed after download such that the abundance of each gene's transcript represented by a given spot was relative to the level of that transcript at the 6 h time point. Also duplicate spots for each ORF on the microarray were averaged for analysis after transformation. Groups of assays that are related as part of a time series. Keywords: time_series_design
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