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Inflammatory cytokines induce novel cancer dependencies

ABSTRACT: Inflammatory cytokines induce novel cancer dependencies

PROVIDER: PRJNA1120334 | ENA |

REPOSITORIES: ENA

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Inflammatory cytokines induce novel cancer dependencies

Project description:Tumor cells respond and adapt to environmental stresses, including cytokine-mediated inflammation, to facilitate growth in hostile environments. However, cytokine responses also induce transcriptional and cell state changes that may predispose tumor cells to new vulnerabilities, which remain largely unexplored. Here, we performed in vitro genome-scale CRISPR loss-of-function screens in eight cancer models exposed to IFNγ, IFNβ, or TNFα to map context-specific genetic vulnerabilities. We identified members of the GPI transamidase complex and the lipid phosphatase FITM2 as interferon-specific cancer dependencies. Tumor-specific deletion of GPI transamidase subunits or FITM2 dramatically enhanced response to immune checkpoint blockade in vivo. By integrating functional genomics, metabolomics and pharmacological blockade, we determined that loss of FITM2 predisposed cancer cells to IFNγ-driven endoplasmic reticulum and oxidative stress, culminating in a paraptosis-like cell death. Our study provides a comprehensive profiling of tumor-intrinsic dependencies governing responses to inflammatory cytokines, thereby presenting promising avenues for therapeutic intervention.

2025-09-04 | GSE269110 | GEO

Inflammatory Cytokines Induce Sustained CTLA-4 Cell Surface Expression on Human MAIT Cells

Project description:Inflammatory Cytokines Induce Sustained CTLA-4 Cell Surface Expression on Human MAIT Cells

| PRJNA986479 | ENA

Inflammatory Cytokines Induce Sustained CTLA-4 Cell Surface Expression on Human MAIT Cells

Project description:Mucosal-associated invariant T (MAIT) cells acquire effector function in response to proinflammatory signals, which synergize with TCR-mediated signals. We asked if cell-intrinsic regulatory mechanisms exist to curtail MAIT cell effector function akin to the activation-induced expression of inhibitory receptors by conventional T cells. We examined human MAIT cells from blood and oral mucosal tissues by RNA sequencing and found differential expression of immunoregulatory genes, including CTLA-4, by MAIT cells isolated from tissue. Using an ex vivo experimental setup, we demonstrate that inflammatory cytokines were sufficient to induce CTLA-4 expression on the MAIT cell surface in the absence of TCR signals. Even brief exposure to the cytokines IL-12, IL-15, and IL-18 was sufficient for sustained CTLA-4 expression by MAIT cells. These data suggest that control of CTLA-4 expression is fundamentally different between MAIT cells and conventional T cells. We propose that this mechanism serves to limit MAIT cell-mediated tissue damage.

2023-06-23 | GSE235566 | GEO

Human FcγRIIa mediates osteoclastogenesis through a novel noncanonical pathway independent of RANKL and inflammatory cytokines

Project description:Human FcγRIIa mediates osteoclastogenesis through a novel noncanonical pathway independent of RANKL and inflammatory cytokines

| PRJNA560202 | ENA

Shear Stresses Associated with Cardiopulmonary Bypass Activate Expression Inflammatory Cytokines and Induce Necroptosis in Monocytes Via Calcium Dependent Signaling

Project description:Shear Stresses Associated with Cardiopulmonary Bypass Activate Expression Inflammatory Cytokines and Induce Necroptosis in Monocytes Via Calcium Dependent Signaling

| PRJNA601661 | ENA

The human pancreatic islet transcriptome: impact of pro-inflammatory cytokines

Project description:We have used RNA-seq to identify transcripts, including splice variants, expressed in human islets of Langerhans under control condition or following exposure to the pro-inflammatory cytokines interleukin-1β (IL-1β) and interferon-γ (IFN-γ). A total of 29,776 transcripts were identified as expressed in human islets. Expression of around 20% of these transcripts was modified by pro-inflammatory cytokines, including apoptosis- and inflammation-related genes. Chemokines were among the transcripts most modified by cytokines. Interestingly, 35% of the genes expressed in human islets undergo alternative splicing as annotated in RefSeq, and cytokines caused substantial changes in spliced transcripts. Nova1, previously considered a brain-specific regulator of mRNA splicing, is expressed in islets. 25/41 of the candidate genes for type 1 diabetes are expressed in islets, and cytokines modified expression of several of these transcripts. 5 human islet of Langerhans preparations examined under 2 conditions (control and cytokine treatment)

2012-03-09 | E-GEOD-35296 | biostudies-arrayexpress

Polarizing Cytokines and Staphylococcus aureus Cooperatively Induce Atopic Dermatitis-Like Transcriptomes

Project description:Polarizing Cytokines and Staphylococcus aureus Cooperatively Induce Atopic Dermatitis-Like Transcriptomes

| PRJNA727535 | ENA

PBECs stimulated with pro-inflammatory cytokines and P. aeruginosa

Project description:Comparison of libraries derived from primary human bronchial epithelial cells which are [i] unstimulated, [ii] stimulated with the pro-inflammatory cytokines IL1beta and TNFalpha and [iii] stimulated with heat-inactivated Pseudomonas aeruginosa (strain PAO1). Keywords: other

2005-02-02 | E-GEOD-2056 | biostudies-arrayexpress

Transcription profiling of human melanoma cell lines treated or not with inflammatory cytokines

Project description:Melanomas are often infiltrated by activated inflammatory cells. Thus, melanoma cells are very likely stimulated by inflammatory cytokines. In order to assess the impact of common inflammatory cytokines, we investigated the gene expression profile of melanoma cell lines before and after cytokine treatment in vitro. Experiment Overall Design: 5 human melanoma cell lines were treated with either IFN-Î± 1,000 U/ml, IFN-Î³ 100 U/ml or TNF-Î± 10 ng/ml for 72 hours, or were left untreated. We analyzed their expression profile with Affymetrix expression arrays.

2009-12-19 | E-GEOD-19428 | biostudies-arrayexpress

Polarizing Cytokines and Staphylococcus aureus Cooperatively Induce Atopic Dermatitis-Like Transcriptomes

Project description:Background: Atopic dermatitis (AD) is a common inflammatory skin disease with a TH2 immune polarity and is often colonized with Staphylococcus aureus. Despite recent advances in understanding Staphylococcus species infection and the impact of polar TH cytokines on the skin, the interactions between these factors in AD pathology are poorly understood. Methods: AD-related key immune biomarkers were measured by quantitative real-time PCR in human keratinocytes exposed heat-killed S. epidermidis or S. aureus with/without polar T-cell derived cytokines such as IFN-γ (TH1), IL-4/IL-13 (TH2), and IL-22 (TH22). Further analysis was performed by RNA-sequencing to define broader responses in both Staphylococcus species and polar cytokines. The similarity of gene expression patterns in AD skin lesions and stimulated keratinocytes was evaluated by gene-set variation analysis (GSVA). Results: Gene expression analysis exhibited distinct immune responses in keratinocytes depending on individual bacterial or polar cytokine exposure. Besides, numerous genes were synergistically upregulated by the combination exposure of bacteria and polar TH cytokines. Moreover, GSVA revealed that combined exposure of S. aureus and IL-4 + IL-13 exhibited significantly higher correlations with a genomic signature of AD skin lesions than their single exposure or combinations of other polar TH cytokines. Conclusions: Our findings provide novel insights into AD-related transcriptional activation and illustrate a potentially novel pathogenic function of S. aureus and IL-4/IL-13 interactions in AD.

2021-12-31 | GSE173902 | GEO

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