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Response of several cell lines originated from liver, skin and colon to stimulation by IFNg, hyper-IL6, IL27 and OSM, investigated at microRNA level

ABSTRACT: In this study 6 cell lines originated from liver, skin and colon tumours as well as 3 non-tumour cell lines from the same organs were profiled with and without stimulation by 4 cytokines: IFNg, hyper-IL6, IL27 and OSM. The main objective was investigation of downstream effects of the stimulation if these cancer cell lines as well as in healthy tissues at microRNA level.

ORGANISM(S): Homo sapiens

SUBMITTER: Iris Behrmann

PROVIDER: E-MTAB-9118 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Response of several cell lines originated from liver, skin and colon to stimulation by IFNg, hyper-IL6, IL27 and OSM, investigated at mRNA level

Project description:In this study 6 cell lines originated from liver, skin and colon tumours as well as 3 non-tumour cell lines from the same organs were profiled with and without stimulation by 4 cytokines: IFNg, hyper-IL6, IL27 and OSM. The main objective was investigation of downstream effects of the stimulation if these cancer cell lines as well as in healthy tissues.

2018-10-01 | E-MTAB-6080 | biostudies-arrayexpress

Crosstalk between very different family members: How STAT3 activating IL6-type cytokines inhibit the IFNg-like responses of IL27 in hepatocellular carcinoma cells

Project description:Interleukin-27 (IL27) is a type-I-cytokine of the IL6/IL12 family predominantly secreted by activated macrophages and dendritic cells. Best understood are the effects of IL27 on immune cells where it has been described to have pro- or anti-inflammatory properties, either promoting TH1 responses or suppressing TH1 and TH2 responses. The action on other cell types is less well studied. In the liver, IL27 expression was observed to be upregulated in patients with hepatitis B, and sera of hepatocellular carcinoma (HCC) patients contain significantly elevated levels of IL27 compared to healthy controls or patients with hepatitis and/or liver cirrhosis. We previously reported interferon-gamma-like antiviral activity of IL27 in hepatic cells. Here we further studied the effects of IL27 on HCC cells in comparison to other cytokines. We were especially interested in the relevance of the IL27-induced STAT3 activation. Thus we compared its response with those induced by IFNg (STAT1-dominated response) or IL6-type cytokines (IL6, Hyper-IL6 or OSM) (STAT3-dominated response). We find that in hepatocytes, IL27 induces an IFNg-like, STAT1-dependent transcriptional response, but we do not find an effective STAT3-dependent response. The availability of STAT1 seems critical in the shaping of the IL27 response, as the siRNA knock-down of STAT1 revealed its ability to induce the acute-phase protein gamma-fibrinogen, a typical IL6 family characteristic. Moreover, we describe a crosstalk between the signaling of IL6-type cytokines and IL27: responses to the gp130-engaging cytokine IL27 (but not those to IFNs) can be inhibited by IL6-type cytokine pre-stimulation, likely by a SOCS3-mediated mechanism. This experiment represents microarray analysis of three hepatocellular carcinoma cell lines treated with IL-27, IFNg, hyper-IL6 or OSM in combination with shRNA knockdown of STAT3.

2017-07-05 | E-MTAB-4570 | biostudies-arrayexpress

Primary healthy liver cells under hyper-IL6 stimulation (miRNA)

Project description:In this study, primary health liver cells obtained from patients with colon cancer and liver metastasis were stimulated with hyper-IL-6 for 6, 24, 48 and 72 h or kept untreated. Both mRNA and miRNA levels were characterized (this is miRNA dataset).

2019-02-28 | E-MTAB-6572 | biostudies-arrayexpress

Intraperitoneal activation of myeloid cells clears ascites and reveals IL27-dependent regression of metastatic ovarian cancer.

Project description:Patients with metastatic ovarian cancer (OvCa) have a 5-year survival rate of less than 30% due to persisting dissemination of chemoresistant cells in the peritoneal fluid and the immunosuppressive microenvironment in the peritoneal cavity. Here, we report that intraperitoneal administration of β-glucan and IFNγ (BI) induced robust tumor regression in clinically relevant models of metastatic OvCa. BI induced tumor regression by controlling fluid tumor burden and activating localized antitumor immunity. β-glucan alone cleared ascites and eliminated fluid tumor cells by inducing intraperitoneal clotting in the fluid and Dectin-1-Syk-dependent NETosis in the omentum. In omentum tumors, BI expanded a novel subset of immunostimulatory IL27+ macrophages and neutralizing IL27 impaired BI efficacy in vivo. Moreover, BI directly induced IL27 secretion in macrophages where single agent treatment did not. Finally, BI extended mouse survival in a chemoresistant model and significantly improved chemotherapy response in a chemo-sensitive model. In summary, we propose a new therapeutic strategy for the treatment of metastatic OvCa.

2024-10-22 | GSE278380 | GEO

A miR-494 dependent feedback loop regulates ER stress (ANAN-376 Project)

Project description:Defects in stress responses are important contributors in many chronic conditions including cancer, cardiovascular disease, diabetes, and obesity-driven pathologies like non-alcoholic steatohepatitis (NASH). Specifically, endoplasmic reticulum (ER) stress is linked with these pathologies and control of ER stress can ameliorate tissue damage. MicroRNAs have a critical role in regulating diverse stress responses including ER stress. Here we show that miR-494-3p plays a functional role during ER stress. ER stress inducers (tunicamycin and thapsigargin) robustly increase the expression of miR-494 in vitro in an ATF6 dependent manner. Surprisingly, miR-494 pretreatment dampens the induction and magnitude of ER stress in response to tunicamycin in endothelial cells. Conversely, inhibition of miR-494 increases ER stress de novo and amplifies the effects of ER stress inducers. Using Mass Spectrometry (TMT-MS) we identified many proteins that are downregulated by both tunicamycin and miR-494 in cultured human umbilical vein endothelial cells (HUVECs). Among these, we found 6 transcripts which harbor a putative miR-494 binding site. Our data indicates that ER stress driven miR-494 may act in a feedback inhibitory loop to dampen downstream ER stress signaling. We propose that RNA-based approaches targeting miR-494 or its targets may be attractive candidates for inhibiting ER stress dependent pathologies in human disease.

2021-09-09 | PXD019992 | Pride

Bulk ATAC-seq of IL27 treated OT-1 cells

Project description:Bulk ATAC-seq of IL27 treated OT-1 cells

| PRJEB82071 | ENA

Cancer cell-endothelial intercellular transfer alters the endogenous miRNA profile and phenotype of recipient endothelial cells

Project description:Metastasis is a major cause of mortality, and remains a final frontier in the search for a cure for cancer. While there has been much research on the ‘seed’ (metastatic tumor cells) and the ‘soil’ (colonized host tissue), interactions between metastatic cancer cells and stromal endothelial cells, which occur at multiple stages during metastasis, are less well understood. Here we report a dynamic regulation of the endothelium by cancer cells through the formation of nanoscale intercellular membrane bridges, which act as physical conduits for intercellular communication in vitro and in vivo, including horizontal transfer of microRNAs (miRNA). The communication between the tumor cell and the endothelium upregulates markers associated with pathological endothelium, which is reversed by pharmacological inhibition of these nanoscale conduits. These results lead us to define the notion of “metastatic hijack”: cancer cell-induced transformation of healthy endothelium into pathological endothelium via horizontal communication through the nanoscale conduits. Pharmacological perturbation of these nanoscale membrane bridges decreases metastatic foci in syngeneic- and human xenograft-breast cancer models. Targeting the formation of these nanoscale membrane bridges may potentially emerge as a new therapeutic opportunity in the management of metastatic cancer. A miRNA microarray was used to evaluate the transport of endogenous microRNAs. The intercellular transfer-ve and intercellular transfer+ve samples were sorted from the same endothelial cell population with the only difference being the occurrence of intercellular transport. The heat map shows potential miRNA candidates for exogenous transfer on two independent biological replicates. These miRNA candidates were significantly up-regulated in the cells receiving transfer of intercellular contents. HUVECs that were not exposed to cancer cells were used as a baseline control.

2015-09-04 | E-GEOD-72679 | biostudies-arrayexpress

Liver cell lines under hyper-IL6 stimulation (mRNA)

Project description:In this study, two hepatic cell lines were stimulated with hyper-IL-6 for 6, 24, 48 and 72 h or kept untreated.

2022-06-30 | E-MTAB-10646 | biostudies-arrayexpress

cDC1 derived IL27 regulates the transcriptional profile of SI-LP Th subsets

Project description:cDC1 derived IL27 regulates the transcriptional profile of SI-LP Th subsets

| PRJNA903146 | ENA

Primary healthy liver cells under hyper-IL6 stimulation (mRNA)

Project description:In this study, primary healthy liver cells obtained from patients with colon cancer and liver metastasis were stimulated with hyper-IL-6 for 6, 24, 48 and 72 h or kept untreated. Both mRNA and miRNA levels were characterized (this is mRNA dataset).

2019-02-28 | E-MTAB-6571 | biostudies-arrayexpress

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