AHNAK, regulated by the OSM/OSMR signaling, enhances keratinocyte proliferation and differentiation in PLCA patients
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE214120 | GEO | 2022/09/27
REPOSITORIES: GEO
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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: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.
2011-09-29 | E-GEOD-27480 | biostudies-arrayexpress
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.
2021-08-30 | GSE161359 | GEO
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.
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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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Project description:Oncostatin M (OSM) is a member of the interleukin-6 (IL-6) family of cytokines. OSM has been found to have distinct anti-inflammatory and pro-inflammatory properties in various cellular and disease contexts. OSM signals through a receptor complex that includes OSMRbeta and activates downstream signaling through the JAK/STAT, MAPK/ERK and PI3K/AKT pathways. To investigate the anti- and/or pro-inflammatory roles of OSM signaling in the context of adult hematopoiesis, we utilized the readily available Cre-driven conditional knockout Osmrfl/fl mouse model B6;129-Osmrtm1.1Nat/J. This model contains loxP sites flanking exon 2, which is the first coding exon of the Osmr gene. We crossed Osmrfl/fl mice to an interferon-inducible Mx1-Cre allele that is classically utilized to study adult hematopoiesis given its high efficiency of expression and recombination in adult hematopoietic cells. We developed a PCR assay to evaluate recombination of the Osmrfl allele. In Osmrfl/fl Mx1-Cre mice, we observed complete recombination of the Osmrfl allele and loss of exon 2 in hematopoietic (bone marrow) as well as non-hematopoietic (liver, lung, kidney) tissues. To evaluate Osmr mRNA expression downstream of exon 2, real-time PCR was utilized with TaqMan probes that anneal to an amplicon spanning Osmr exons 17 and 18. Using this assay, reduced Osmr transcript was observed in kidney samples from Osmrfl/fl Mx1-Cre mice compared to Mx1-Cre controls. However, Osmr transcript levels were similar in bone marrow, lung, and liver samples from Osmrfl/fl Mx1-Cre compared to Mx1-Cre control mice, suggesting that transcript is being produced despite loss of exon 2. Western blots revealed that liver cells from Osmrfl/fl Mx1-Cre mice had complete loss of OSMR protein. In contrast, bone marrow, kidney, and lung cells from Osmrfl/fl Mx1-Cre mice had reduced levels of OSMR protein. Together, our data suggest that the B6;129-Osmrtm1.1Nat/J model should be utilized with caution as loss of exon 2 of Osmr variably impacts mRNA and protein expression in a tissue-dependent context.
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Project description:The cytokine Oncostatin M (OSM) promotes cancer progression by acting as central node for multicellular interactions between cancer cells and surrounding stromal cells. OSM is mainly secreted by myeloid cells and the oncostatin M receptor (OSMR) is expressed by cancer cells and cancer associated fibroblasts (CAFs), among others. To understand the effect of OSM in triple negative breast cancer cells, a small and well-annotated Clariom S gene microarray was performed in OSM-overexpressing (MDA-MB-231-hOSM) and control (MDA-MB-231-hC) MDA-MB-231 cells.
2022-02-02 | GSE195774 | GEO
Project description:Heterocellular OSM-OSMR signalling drives pancreatic cancer growth and metastasis through functional fibroblast reprogramming
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Project description:To identify molecular mechanism underlying the protection from diet-induced hepatic steatosis in AHNAK deficiency mice, we examined microarray analysis with liver sample from HFD-fed AHNAK KO and WT mice. Two-condition experiment, regular chow (CD) -fed WT vs. CD-fed AHNAK KO and High fat diet(HFD)-fed WT vs. HFD-fed AHNAK KO mice. Biological replicates: 3 control, One replicate per array.
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