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Gene expression of HCT116 cells after stimulation with oncostatin M (OSM)

ABSTRACT: To evaluate gene expression profiles in intestinal epithelial cells (IEC) after OSM stimulation, we have employed whole genome microarray expression profiling as a discovery platform to identify relevant genes which are potentially of interest to reveal the role of OSM in intestinal inflammation. The most strongly up-regulated genes were SERPINS, which belong to the family of serin peptidase inhibitors with antiprotease activities, most of them serine and cysteine proteases. SERPINB4, SERPINB3 and SERPINA3 were the genes with the strongest up-regulation, also verified in qPCR. OSM-induced SERPIN up-regulation may contribute to anti-apoptotic and proliferative effects of OSM in IEC.

ORGANISM(S): Homo sapiens

PROVIDER: GSE53295 | GEO | 2014/12/13

SECONDARY ACCESSION(S): PRJNA231619

REPOSITORIES: GEO

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Gene expression of HCT116 cells after stimulation with oncostatin M (OSM)

Project description:To evaluate gene expression profiles in intestinal epithelial cells (IEC) after OSM stimulation, we have employed whole genome microarray expression profiling as a discovery platform to identify relevant genes which are potentially of interest to reveal the role of OSM in intestinal inflammation. The most strongly up-regulated genes were SERPINS, which belong to the family of serin peptidase inhibitors with antiprotease activities, most of them serine and cysteine proteases. SERPINB4, SERPINB3 and SERPINA3 were the genes with the strongest up-regulation, also verified in qPCR. OSM-induced SERPIN up-regulation may contribute to anti-apoptotic and proliferative effects of OSM in IEC. HCT116 cells were starved overnight with medium containing 1% FCS after reaching 70% confluency. On the next day, cells were stimulated in quadruplicates with 100 ng/mL OSM or left unstimulated. RNA was isolated 6 hours after stimulation and RNA concentration and purity was measured.

2014-12-13 | E-GEOD-53295 | biostudies-arrayexpress

Oncostatin M (OSM) and Leukemia Inhibitory factor (LIF) treatment of osteoblasts via LIF and OSM receptors

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.

2016-08-17 | GSE83418 | GEO

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.

2011-09-29 | E-GEOD-27480 | biostudies-arrayexpress

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

2011-09-30 | GSE27480 | GEO

Oncostatin M effects in IMR90 cells

Project description:The JAK2 mutation V617F is detectable in a majority of patients with Ph-negative myeloproliferative neoplasms (MPN). Enforced expression of JAK2 V617F in mice induces myeloproliferation and bone marrow (BM) fibrosis suggesting a causal role for the JAK2 mutant in the pathogenesis of MPN. However, little is known about mechanisms and effector molecules contributing to JAK2 V617F-induced myeloproliferation and fibrosis. Here we show that JAK2 V617F promotes expression of oncostatin M (OSM) in neoplastic myeloid cells. Correspondingly, OSM was found to be overexpressed in the BM and elevated in the serum of patients with JAK2 V617F+ MPN. In addition, OSM secreted by JAK2 V617F+ cells stimulated growth of fibroblasts and microvascular endothelial cells and induced the production of angiogenic and profibrogenic cytokines (HGF, VEGF, and SDF-1) in BM fibroblasts. All effects of MPN cell-derived OSM were blocked by a neutralizing anti-OSM antibody, whereas the production of OSM in MPN cells was effectively suppressed by a pharmacologic JAK2 inhibitor or RNAi-mediated knockdown of JAK2. In summary, JAK2 V617F-mediated upregulation of OSM may contribute to fibrosis, neoangiogenesis, and the cytokine storm observed in JAK2 V617F+ MPN, suggesting that OSM could serve as a novel therapeutic target molecule in these neoplasms. IMR90 cells were treated with a single dose of rh Oncostatin M (10ng/ml).

2013-01-29 | E-GEOD-29655 | biostudies-arrayexpress

Oncostatin M effects in IMR90 cells

2013-01-29 | GSE29655 | GEO

Oncostatin experiment

Project description:Cultured epidermal keratinocytes treated with OsM 1, 4, 24 & 48hrs, and Skinethic epidermal substitutes treated 1, 4, 24, 48h & 7days, each with untreated control Keywords: Time course

2005-06-18 | GSE2822 | GEO

Oncostatin M signaling drives cancer-associated skeletal muscle wasting

Project description:Investigating muscle wasting in a murine model of cancer cachexia, we identified Oncostatin M (OSM) as a potential mediator of inflammatory responses in skeletal muscle. OSM is a member of the IL-6 family of cytokines and has crucial functions in cell growth, differentiation, and inflammation. Our results demonstrate that OSM induces muscle atrophy. To understand if its effect is specific or it is a general effect of IL6 family cytokines, primary myotubes were treated with OSM, IL6 and LIF for 48hrs. Our findings showed that OSM potently induces muscle wasting in differentiated myotubes.

2024-03-21 | GSE222208 | GEO

The genes regulated by JAK2 and Lnc-BM in breast cancer brain metastasis cells (231-BM, derived from MDA-MB-231 cells) treated with Oncostatin M (OSM)

Project description:A long noncoding RNA (Lnc-BM) mediates JAK2 activity in 231-BM cells treated with OSM. Emerging evidence has shown that the effect of JAK2 is mainly mediated by three downstream signaling pathways including the AKT, MAPK, and STAT1/3/5 pathways. To determine the signaling pathways that are regulated by Lnc-BM, we performed gene expression microarray analysis on cells with Lnc-BM depletion or JAK2 KO and compared them to their corresponding controls following OSM stimulation.

2017-03-01 | GSE79534 | GEO

Oncostatin M neutralization in E. coli pneumonia

Project description:Oncostatin M (OSM) is an IL-6 family cytokine that is necessary for neutrophil recruitment in pneumonia by inducing STAT3-dependent production of CXCL5. We used microarrays to identify additional pathways affected by OSM neutralization in the lungs during pneumonia.

2021-03-08 | GSE155283 | GEO

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