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Oncogenic KRAS-dependent stromal interleukin-33 directs the pancreatic microenvironment to promote tumor growth [bulk RNA-seq]

ABSTRACT: This experiment was designed to investigate the intrinsic effect of interleukin-33 (IL-33) on pancreatic cancer associated fibroblasts. IL-33 wildtype (WT) or IL-33 knockout (KO) fibroblasts were grown with or without tumor conditioned media to stimulate cancer-associated fibroblast (CAF) polarization and harvested for bulk RNA sequencing.

ORGANISM(S): Mus musculus

PROVIDER: GSE269889 | GEO | 2024/06/26

REPOSITORIES: GEO

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Oncogenic KRAS-dependent stromal interleukin-33 directs the pancreatic microenvironment to promote tumor growth [scRNA-seq]

Project description:Here, we sought to understand the function of stromal interleukin-33 (IL-33) in PanIN and PDA. We collected pancreatic tissues from various mouse models of PanIN and PDA for single cell RNA sequencing to assess IL-33 expression across the microenviornment. We also implanted syngeneic orthotopic pancreatic tumors into mice harboring a conditional stromal IL-33 knockout and sequenced the resulting tumors.

2024-06-26 | GSE269888 | GEO

Knockdown of interleukin-33 in human fibroblasts

Project description:Interleukin (IL)-33 is a cytokine that appears to mediate fibrosis by signaling via its receptor ST2 (IL-33R/IL1RL1). It is also, however, a protein that after synthesis is sorted to the cell nucleus, where it appears to affect chromatin folding. Here we describe a novel role for nuclear IL-33 in regulating the fibroblast phenotype in murine kidney fibrosis driven by unilateral ureteral obstruction. Transcriptional profiling of IL-33-deficient kidneys 24h after ligation revealed enhanced expression of fibrogenic genes and enrichment of gene sets involved in extracellular matrix formation and remodeling. These changes relied on intracellular effects of IL-33, because they were not reproduced by treatment with a neutralizing antibody to IL-33 that prevents IL-33R/ST2L receptor signaling nor were they observed in IL33R/ST2-deficient kidneys. To further explore the intracellular function of IL-33, we established transcription profiles of human fibroblasts, observing that knockdown of IL-33 skewed the transcription profile from an inflammatory towards a myofibroblast phenotype, reflected in higher levels of COL3A1, COL5A1 and transgelin protein, as well as lower expression levels of IL6, CXCL8, CLL7 and CCL8. In conclusion, our findings suggest that nuclear IL-33 in fibroblasts dampens the initial profibrotic response until persistent stimuli, as enforced by UUO, can override this protective mechanism.

2020-05-06 | GSE149917 | GEO

Glioma cells response Interleukin-33 (IL-33) [microarray]

Project description:Determination of the molecular mechanism of IL33 on glioma cells Since IL-33 is known to associate with chromatin and regulate transcriptional activity and that nuclear expression of IL-33 increases glioma progression, we determined Nuclear IL-33 regulates the expression and secretion of inflammatory cytokines in glioma cells. Using these parameters 340 genes were induced by the ectopic expression of IL-33 and an additional 377 genes were downregulated. Gene ontology terms over-represented in the genes induced by IL-33 include three major clusters that associate with cytokine activity and inflammation

2020-08-21 | GSE153486 | GEO

Gene expression profile of RAW264.7 monocytes treated with or without IL-33

Project description:Molecular mechanisms underlying the cancer stroma in metastasis is largely unknown. Here we show that cancer-associated fibroblasts (CAFs) produce high levels of IL-33 that acted on tumor-associated macrophages (TAMs) to induce the M1 to M2 transition. Genome profiling of metastasis-related genes in the IL-33-stimulated TAMs showed a > 200-fold increase of metalloproteinase 9 (MMP9). Signaling analysis demonstrated the IL-33-ST2-NFkB-MMP9-laminin pathway that mediates cancer metastasis. In mouse and human fibroblast-rich pancreatic cancers, genetic deletion of IL-33, ST2 and MMP9 markedly blocked metastasis. Pharmacological inhibition of NFkB and MMP9 also blocked cancer metastasis. Deletion of IL-33, ST2 and MMP9 restored laminin, a key basement membrane component associated to tumor microvessels. Together, our data provide novel mechanistic insights on the IL-33-NFkB-MMP9-laminin axis that mediates the CAF-TAM-committed cancer metastasis. Thus, targeting the CAF-TAM-vessel interaction provides an outstanding therapeutic opportunity for cancer treatment.

2018-11-30 | GSE97657 | GEO

A proteomic landscape of the spatiotemporal influence of Interleukin-33 (IL-33) in monocytes

Project description:Interleukin-33 (IL-33), a member of the IL-1 superfamily cytokines, is an endogenous danger signal and a nuclear-associated cytokine. It is one of the essential mediators of both innate and adaptive immune responses. Aberrant IL-33 signaling has been demonstrated to play a defensive role against various infectious and inflammatory diseases. Although the signaling responses mediated by IL-33 have been previously reported, the temporal signalingdynamicsare yet to be explored. Towards this end,we applied quantitative temporal phosphoproteomics analysis to elucidate pathways and proteins induced by IL-33 in THP1 monocytes. Employing TMT labeling-based quantitation and titanium dioxide (TiO2)-based phosphopeptide enrichment strategy followed by mass spectrometry analysis, we identified 14,515 phosphorylation sites mapping to 4,174 proteins across (0 min to 240 mins)time points.

2022-02-16 | PXD028673 | Pride

Mouse immune cells response Interleukin-33 (IL-33) [nanostring]

Project description:To validate the modulation of inflammatory genes by ectopic IL-33, we performed Gene expression analysis using the nCounter Mouse v2 Inflammation Panel. This result validated a significant increase in a number of anti-inflammatory cytokines in the IL-33+ xenografts that were absent in the DNLS xenografts

2020-08-21 | GSE153488 | GEO

Dataset of spatiotemporal influences of interleukin IL-1 family cytokine: Interleukin-33 on cellular signal transduction pathways

Project description:Interleukin-33 (IL-33) is a member of the IL-1 family of cytokines that play a central role in the regulation of immune responses. IL-33 signaling, from the early signaling events triggered by the ligand-activated receptor to result in activation of early and late signaling events, such as proteome changes. In this study, THP1 (monocyte) cell line model was stimulated with IL-33 (50 ng/ml) for varying duration (5, 10, 15, 30, 40, 60, 120 and 240 mins). We carried out in-depth proteomic analysis using high-resolution LC-MS/MS. Our analysis resulted in the identification of 64,030 peptides corresponding to 7947 protein groups. Differentially regulated proteins identified in this study could be targeted for developing an inflammatory immune response.

2022-02-17 | PXD024385 | Pride

Glioma cells response Interleukin-33 (IL-33) [microarray]

Project description:Glioma cells response Interleukin-33 (IL-33) [microarray]

| PRJNA642838 | ENA

Mouse immune cells response Interleukin-33 (IL-33) [nanostring]

Project description:Mouse immune cells response Interleukin-33 (IL-33) [nanostring]

| PRJNA642836 | ENA

The alarmin interleukin-33 drives protective antiviral CD8+ T cell responses

Project description:Pathogen-associated molecular patterns decisively influence antiviral immune responses, whereas the contribution of endogenous signals of tissue damage, also known as “damage-associated molecular patterns” or “alarmins”, remains ill-defined. We show that interleukin-33 (IL-33), an alarmin released from necrotic cells, is necessary for potent CD8+ T cell (CTL) responses to replicating, prototypic RNA and DNA viruses in mice. IL-33 signaled through its receptor on activated CTLs, enhanced clonal expansion in a MyD88-dependent, CTL-intrinsic fashion, determined polyfunctional effector cell differentiation and was necessary for virus control. Moreover, recombinant IL-33 augmented vaccine-induced CTL responses. Radio-resistant cells of the splenic T cell zone produced IL-33, and efficient CTL responses required IL-33 from radio-resistant cells but not from hematopoietic cells. Thus, alarmin release by radio-resistant cells orchestrates protective antiviral CTL responses. 2 groups (wt vs. ST-/- P14 cells), 3 replicates per group.

2012-02-27 | E-GEOD-34392 | biostudies-arrayexpress

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