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AHNAK, regulated by the OSM/OSMR signaling, enhances keratinocyte proliferation and differentiation in PLCA patients

ABSTRACT: AHNAK, regulated by the OSM/OSMR signaling, enhances keratinocyte proliferation and differentiation in PLCA patients

PROVIDER: PRJNA883978 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR21697050_1.fastq.gz	Fastqsanger.gz
	SRR21697050_2.fastq.gz	Fastqsanger.gz
	SRR21697051_1.fastq.gz	Fastqsanger.gz
	SRR21697051_2.fastq.gz	Fastqsanger.gz
	SRR21697052_1.fastq.gz	Fastqsanger.gz

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AHNAK, regulated by the OSM/OSMR signaling, enhances keratinocyte proliferation and differentiation in PLCA patients

Project description:AHNAK, regulated by the OSM/OSMR signaling, enhances keratinocyte proliferation and differentiation in PLCA patients

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Heterocellular OSM-OSMR signalling drives pancreatic tumour growth and metastasis through functional fibroblast reprogramming

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.

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Gene-expression analysis of Oncostatin-M (OSM) signalling in cervical squamous cell carcinomas over-expressing the Oncostatin-M receptor (OSMR)

Project description:The type II Oncostatin M receptor (OSMR) serves as the main binding site for the pleiotropic cytokine OSM. We have previously demonstrated a positive correlation between copy number driven OSMR over-expression and adverse clinical outcome in cervical tumours and have also established enhanced angiogenic, migratory and invasive potential as major consequences of OSMR over-expression using cell-line models of cervical cancer. By analysis of gene expression patterns in cell lines and tumours, this study now systematically defines cohorts of genes that are implicated for the phenotypes observed. Importantly, we have identified 15 OSM induced genes that are involved in at least one of these key functions and are up-regulated in both OSMR over-expressing cell-lines and tumours. These genes can serve as markers of OSM signalling in OSMR over-expressing SCCs and represent suitable targets for functional characterisation. Gene expression of 4 cervical SCC cell lines analysed (2 with and 2 without OSMR overexpression) at 6 different time-points, with 3 replicates at each time-point.

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Heterocellular OSM-OSMR signalling drives pancreatic cancer growth and metastasis through functional fibroblast reprogramming

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:Oncostatin M (OSM) and Leukemia Inhibitory Factor (LIF) signal within cells via the gp130 (Il6st) coreceptor bound either to the LIF receptor (LIFR) or the oncostatin M receptor (OSMR), but whether murine OSM can act through both receptors is controversial. Both LIF and OSM stimulate bone formation, inhibit adipocyte differentiation, and promote osteoclast differentiation, but our earlier work suggested this may depend on the receptor subtype used. This project aimed to identify those gene targets regulated by murine OSM via OSMR and LIFR by using wild type and OSMR null primary osteoblasts. Cells were differentiated to their most mature state (i.e. osteocytes) because the only prior target gene known to be regulated by murine OSM via the LIFR was an osteocyte-specific gene, sclerostin.

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2022-02-02 | GSE195775 | GEO

Characterization of an Osmr Conditional Knockout Mouse Model

Project description:Oncostatin M (OSM) is a member of the interleukin-6 (IL-6) family of cytokines and has been found to have anti-inflammatory and pro-inflammatory properties in various cellular and disease contexts. OSM signals through two receptor complexes, one of which includes OSMRb. Here, we investigated OSM-OSMRb signaling in adult mouse hematopoietic stem cells (HSCs) using the conditional Osmrfl/fl mouse model B6;129-Osmrtm1.1Nat/J. We crossed Osmrfl/fl mice to interferon-inducible Mx1-Cre, which is robustly induced in adult HSCs. From these mice, we isolated HSCs by flow cytometry, stimulated with or without recombinant OSM for 1 hour, and assessed gene expression changes in control versus Osmr knockout HSCs by RNA-seq. This data may be utilized to investigate OSMRb-dependent and -independent OSM signaling as well as the transcriptional effects of an IL-6 family cytokine on mouse HSCs to further define its anti-inflammatory versus pro-inflammatory properties.

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