Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR23782100.fastq.gz | Fastqsanger.gz | |||
| SRR23782101.fastq.gz | Fastqsanger.gz | |||
| SRR23782102.fastq.gz | Fastqsanger.gz | |||
| SRR23782103.fastq.gz | Fastqsanger.gz | |||
| SRR23782104.fastq.gz | Fastqsanger.gz |
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Similar Datasets
Project description:Immunogenic cell death (ICD) inducers are valuable chemotherapeutic agents that elicit protective immune responses against tumors. However, the specific molecular targets directly associated with ICD remain less explored. Here, a Type II ICD inducer, Pt-ER, was validated as a bona fide ICD inducer with the ability to establish protection against colorectal cancer. Based on Pt-ER, several ICD-inducing photoactivable probes were designed to capture their potential targets. By integrating quantitative proteomics analysis, genetic method and biochemical assays, we identified that PTP1B is a direct target of Pt-ER and engages in ICD.
2026-02-02 | PXD065824 | Pride
Project description:Immunogenic cell death (ICD) in cancer represents a functionally unique therapeutic response that can induce tumor-targeting immune responses. ICD is characterized by the exposure and release of numerous damage-associated molecular patterns (DAMPs), which confer adjuvanticity to dying cancer cells. The spatiotemporally defined emission of DAMPs during ICD has been well described; whereas the epigenetic mechanisms that regulate ICD hallmarks have not yet been deeply elucidated. Here, we aimed to examine the involvement of miRNAs and their putative targets taking advantage from well-established in vitro models of ICD. To this end, B cell lymphoma (Mino) and breast cancer (MDA-MB-231) cell lines were exposed to two different ICD inducers: the combination of retinoic acid (RA) and interferon-alpha (IFN-a) and doxorubicin, and to non ICD inducers like gamma irradiation. Then, miRNA and mRNA profiles were studied by next generation sequencing. Co-expression analysis identified 16 miRNAs differentially modulated in cells subjected to ICD. Integrated miRNA-mRNA functional analysis revealed candidate miRNAs, mRNAs, and modulated pathways associated with Immune System Process (GO Term). In this sense, ICD induced a distinctive transcriptional signature hallmarked by regulation of antigen presentation, a crucial step for a proper immune system antitumor response activation. Interestingly, the major histocompatibility complex class I (MHC-I) pathway was upregulated whereas class II (MHC-II) was downregulated. Analysis of MHC-II associated transcripts and HLA-DR surface expression validated the inhibition of this pathway by ICD on lymphoma cells. miR-4284 and miR-212-3p were the strongest miRNAs upregulated by ICD associated with this event. It is well known that MHC-II expression on tumor cells facilitates the recruitment of CD4+ T cells. However, the interaction between tumor MHC-II and the inhibitory co-receptor LAG-3 on tumor-associated lymphocytes could provide an immunosuppressive signal that directly represses effector cytotoxic activity. In this context, MHC-II downregulation by ICD could enhance antitumor immunity. Overall, we found that the miRNA profile was significantly altered during ICD. Several miRNAs are predicted to be involved in the regulation of Class I and II MHC pathway, whose implication in ICD was demonstrated herein for the first time, which could eventually modulate tumor recognition and attack by the immune system.
2022-08-08 | E-MTAB-11799 | biostudies-arrayexpress
Project description:CD74 (invariant chain), expressed on B cells, is directly involved in shaping the B cell repertoire by regulating their survival in health and disease. Binding of its ligand, macrophage migration inhibitory factor (MIF), induces a cascade that results in CD74 intramembrane proteolysis, and the release of the CD74 intracellular domain (CD74-ICD). CD74-ICD translocates to the nucleus where it induces activation of transcription. In the current study, we characterized the transcription factor activity of CD74-ICD. Following histone modifications we are able to characterize CD74's binding sites as regulatory areas.
2022-11-03 | GSE181676 | GEO
Project description:In DRG neurons NRG1 type III intacellular domain (ICD) moves to the nucleus upon contact with Schwann cells. We aimed to investigate genes up/down regulated by ICD. We analyzed total RNA from DRG neurons over-expressing ICD comparing it to RNA from wild-type DRG neurons and RNA from DRG neurons over-expressing EGFP. We used 4 biological replicates and two technical replicates for each condition.
2014-09-26 | E-GEOD-61784 | biostudies-arrayexpress
Project description:The induction of immunogenic cell death (ICD) impedes tumor progression via both tumor cell-intrinsic and -extrinsic mechanisms, representing a robust therapeutic strategy. However, there remains a dearth of ICD-inducing targets. Employing kinome-wide CRISPR-Cas9 screening, we have identified NUAK1 as a potential target. The ICD-provoking effect of NUAK1 inhibition depends on the production of reactive oxygen species (ROS), consequent to the downregulation of NRF2-mediated antioxidant gene expression. Moreover, the mevalonate pathway/cholesterol biosynthesis, activated by XBP1s downstream of NUAK1 inhibition-induced endoplasmic reticulum stress, functions as negative feedback on ICD. Targeting the mevalonate pathway using HMGCR inhibitor statins amplifies NUAK1 inhibition-mediated ICD and antitumor activity, while cholesterol mitigates ICD by diminishing ROS. The combination of NUAK1 inhibitors and statins enhances the efficacy of anti-PD-1 therapy. Collectively, our study unveils the promise of blocking the mevalonate pathway in conjunction with ICD-targeted immunotherapies such as NUAK1 inhibition.
2024-12-10 | GSE264513 | GEO
Project description:The induction of immunogenic cell death (ICD) impedes tumor progression via both tumor cell-intrinsic and -extrinsic mechanisms, representing a robust therapeutic strategy. However, ICD-targeted therapy remains to be explored and optimized. Through kinome-wide CRISPR-Cas9 screen, NUAK1 is identified as a potential target. The ICD-provoking effect of NUAK1 inhibition depends on the production of reactive oxygen species (ROS), consequent to the downregulation of NRF2-mediated antioxidant gene expression. Moreover, the mevalonate pathway/cholesterol biosynthesis, activated by XBP1s downstream of ICD-induced endoplasmic reticulum stress, functions as a negative feedback mechanism. Targeting the mevalonate pathway with CRISPR knockout or HMGCR inhibitor simvastatin amplifies NUAK1 inhibition-mediated ICD and antitumor activity, while cholesterol dampers ROS, ICD and therefore tumor suppression. The combination of NUAK1 inhibitor and statin enhances the efficacy of anti-PD-1 therapy. Collectively, our study unveils the promise of blocking the mevalonate-cholesterol pathway in conjunction with ICD-targeted immunotherapy.
2024-12-11 | GSE283933 | GEO
Project description:Transient transfection of activated Notch1 (Notch1-ICD) decreases cellular proliferation and reduces the expression of a subset of neuroendocrine genes. We used microarrays to identify the gene expression changes 48 hours after overexpression of Notch1-ICD. mSCLC cells transfected with Notch1-ICD-ires-GFP were FACS sorted for GFP+ cells 48 hours after transfection. RNA was then extracted and hybridized to Affymetrix GeneChip® Mouse Gene 2.0 ST array.
2015-05-21 | E-GEOD-69091 | biostudies-arrayexpress
Project description:The goal of this study is to compare the different biological functions between nuclear (ICD)-TYRO3- and kinase dead (KD)-TYRO3-overexpressed cells by BRD3 occupancy profiling. We revel that ICD-TYRO3-overexpressed cell were particularly enriched in negatively regulate cell death, regulation of cell cycle, regulation of vascular permeability, positively regulation of EMT, cell-cell adhesion, and regulation of phosphorylation.
2024-11-08 | GSE188378 | GEO
Project description:The anti-tumor function of engineered T cells expressing chimeric antigen receptors (CARs) is dependent on signals transduced through intracellular signaling domains (ICDs). Different ICDs are known to drive distinct phenotypes, but systematic investigations into how ICD architectures direct T cell function—particularly at the molecular level—are lacking. Here, we use single-cell sequencing to map diverse signaling inputs to transcriptional outputs, focusing on a defined library of clinically relevant ICD architectures. Informed by these observations, we functionally characterize transcriptionally distinct ICD variants across various contexts to build comprehensive maps from ICD composition to phenotypic output. We identify a unique tonic signaling signature associated with a subset of ICD architectures that drives durable in vivo persistence and efficacy in liquid, but not solid, tumors. Our findings work toward decoding CAR signaling design principles, with implications for the rational design of next-generation ICD architectures optimized for in vivo function.
2024-07-13 | GSE264681 | GEO