E-MTAB-9392
Ontology highlight
ABSTRACT:
PROVIDER: E-MTAB-9392 | ExpressionAtlas | 2023-06-16
REPOSITORIES: ExpressionAtlas
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| E-MTAB-9392-analysis-methods.tsv | Tabular | |||
| E-MTAB-9392-analytics.tsv | Tabular | |||
| E-MTAB-9392-apply_fixes_zooma_mappings.done | Other | |||
| E-MTAB-9392-atlasExperimentSummary.Rdata | Rdata | |||
| E-MTAB-9392-configuration.xml | Xml |
Items per page: 5 1 - 5 of 24 |
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Project description:Role of Macrophage migration inhibitory factor (MIF) in pancreatic stellate cells (PSCs)
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Project description:The presence of activated pancreatic stellate cells (PSCs) in the pancreatic ductal adenocarcinoma (PDAC) microenvironment plays a significant role in cancer progression. Macrophage migration inhibitory factor (MIF) is overexpressed in PDAC tissues and expressed by both cancer and stromal cells. The expression status of MIF and its receptors in PDAC- associated fibroblasts or PSCs and its pathophysiological roles are yet to be elucidated. The next-generation sequencing technique was adapted to check the effect of MIF absence on the expression of other genes in mice (mPSCs).
2022-09-28 | E-MTAB-9392 | biostudies-arrayexpress
Project description:Cancer-associated fibroblasts (CAFs), although considered as the most abundant pancreatic ductal adenocarcinoma (PDAC) stromal cells playing a critical role in tumor progression and chemoresistance, are not yet directly druggable. Here we report that focal adhesion kinase (FAK) activity (evaluated based on 397 tyrosine phosphorylation level) in CAFs is highly increased compared to its activity in fibroblasts from healthy pancreas. Fibroblastic FAK activity is an independent prognostic marker for disease free and overall survival of PDAC patients (cohort of 120 PDAC samples). Genetic inactivation of FAK within fibroblasts (FAK-kinase-dead, KD) reduces fibrosis and immunosuppressive cell number within primary tumor and dramatically decreases tumor spread. Mechanistically, pharmacologic and genetic fibroblastic FAK inactivation reduces fibroblast migration/invasion, decreases extracellular matrix (ECM) expression and deposition by CAFs, and negatively impacts M2 macrophage polarization and migration. Thus, FAK activity within CAFs appears as an independent PDAC prognostic marker and a druggable driver of tumor cell invasion.
2020-08-19 | PXD018899 | Pride
Project description:Pancreatic cancers (PCs) are highly metastatic with poor prognosis, mainly due to delayed detection. We hypothesized that intercellular communication is critical for metastatic progression. Here, we show that PC-derived exosomes induce liver pre-metastatic niche formation in naïve mice and consequently increase liver metastatic burden. Uptake of PC-derived exosomes by Kupffer cells caused transforming growth factor β secretion and upregulation of fibronectin production by hepatic stellate cells. This fibrotic microenvironment enhanced recruitment of bone marrow-derived macrophages. We found that macrophage migration inhibitory factor (MIF) was highly expressed in PC-derived exosomes, and its blockade prevented liver pre-metastatic niche formation and metastasis. Compared to patients whose pancreatic tumors did not progress, MIF was markedly higher in exosomes from stage I PC patients who later developed liver metastasis. These findings suggest that exosomal MIF primes the liver for metastasis and may be a prognostic marker for the development of PC liver metastasis.
2015-03-16 | GSE66876 | GEO
Project description:Glutaminyl cyclase (QC) activity in macrophage cells is correlated with the gene expression of MCP-2 and QC-catalyzed N-terminal pGlu formation of MCPs is required for macrophage migration and provide new insights into the role of QC in the inflammation process.
2021-10-22 | GSE21082 | GEO
Project description:MicroRNAs (miRNAs) are short single-stranded RNA molecules that have a critical role in the regulation of gene expression. Alterations in miRNA expression levels have been observed in multiple tumor types and there is clear evidence on their active involvement in cancer development. Here, a comprehensive miRNA expression profiling in 16 pancreatic cancer cell lines and four normal pancreatic samples provided a specific molecular signature for pancreatic cancer and enabled us to identify 72 differentially expressed miRNAs with approximately half of them being up- and half downregulated in cancer cells as compared to normal samples. Of these, miR-31 was selected for further functional analyses based on its interesting M-bM-^@M-^\on-offM-bM-^@M-^] type expression profile, i.e. very low or even absent expression in normal pancreas and in six of the pancreatic cancer samples but extremely high expression in the remaining ten cell lines. Quite unexpectedly, both the inhibition of miR-31 in AsPC-1 and HPAF-II pancreatic cancer cells with high endogenous expression and forced expression of miR-31 in MIA PaCa-2 with low endogenous levels led to reduced cell proliferation, migration and invasion. More importantly, in AsPC-1 cells further enhancement of miR-31 also resulted in reduced cell migration and invasion, implicating that the level of miR-31 is critical for these phenotypes. We also identified novel miR-31 target genes, APBB2 and RSBN1, that might contribute to cancer pathogenesis. This study highlights a specific miRNA expression pattern in pancreatic cancer and reveals that manipulation of miR-31 expression leads to reduced cell migration and invasion in pancreatic cancer. 16 pancreatic cancer cell lines and 4 normal pancreatic RNA samples were hybridized on Agilent vs1 miRNA microarrays. Pool of four normal samples was hybridized on each slide to allow normalization between slides.
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Project description:Macrophage migration inhibitory factor is overproduced through EGR1 in TET2low resting monocytes
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Project description:The aim of this experiment was to investigate the role of MIF during wound healing using BALB/C MIF null mice and in the context of reduced estrogen-associated impaired healing using ovariectomized mice (a mouse model of age-associated delayed healing). Ageing is associated with delayed cutaneous wound healing resulting from reduced estrogen levels. Macrophage migration inhibitory factor (MIF - NCBI RefSeq: NM_010798) is thought to mediate the effects of estrogen on wound healing. Gene expression was compared between wounds from ovariectomized MIF null mice and controls.
2005-11-05 | E-MEXP-209 | biostudies-arrayexpress
Project description:Previously we have described the role of liver stellate cell exosomes in triggering macrophage migration and immune activation, we wanted to study what cargo in this exosomes were responsible for such activation. We found a few interesting mRNAs and siRNAs involved in the immune response pathway and cytokine production. We have found that Ectodysplasin A, a hepatokine, has an important role in stimulating the macrophage response and to be highly expressed in liver cirrhosis.
2022-01-31 | E-MTAB-11373 | biostudies-arrayexpress
Project description:Pancreatic cancer is an aggressive disease with a poor prognosis for which current standard chemotherapeutic treatment options offer little survival benefit. In recent years, receptor tyrosine kinases (RTK)s have garnered interest as therapeutic targets to augment or replace standard chemotherapeutic therapies because of their high expression levels in various cancers and their ability to promote cell growth, migration, and survival. Met and Ron, which are homologous RTKs activated by the ligands hepatocyte growth factor (HGF) and macrophage stimulating protein (MSP), respectively, are over-activated in many of the least treatable cancers. In pancreatic adenocarcinoma, Met expression is linked to poor patient survival and Ron expression is generally higher in tumor samples relative to normal tissue, although its prognostic significance in pancreatic cancer remains unclear. Despite the structural homology between Met and Ron, studies that have directly compared the functional outcomes of these systems in any context are limited. To address this, we sought to determine if the HGF/Met and MSP/Ron systems produce overlapping or divergent contributions towards a malignant phenotype by performing a characterization of MSP and HGF driven signaling, behavioral, and transcriptomic responses in pancreatic cancer cells in vitro. We found HGF and MSP both encouraged cell migration and activated the MAPK/Erk pathway both at the transcript and protein level. HGF uniquely increased proliferation in addition to regulating a wider variety of transcripts compared to MSP. Although HGF and MSP produced a differing breadth of responses, overlapping pro-cancer signaling, behavioral, and transcriptional effects suggest dual inhibition of the MSP/Ron and HGF/Met systems in pancreatic cancer may provide a more complete anti-cancer effect compared to individually targeting either system.
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