Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Gene expression changes of tumor microenvironment (TME) after STING activation

ABSTRACT: Gene expression changes of tumor microenvironment (TME) after STING activation

PROVIDER: PRJNA554008 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Similar Datasets

Gene expression changes of tumor microenvironment (TME) after STING activation

Project description:The results revealed dramatic differences between the STING-activated and STING-deficient TMEs.

2019-07-12 | GSE134129 | GEO

Gene expression changes of intraperitoneal tumor microenvironment after STING activation

Project description:Gene expression changes of intraperitoneal tumor microenvironment after STING activation

| PRJNA670654 | ENA

Gene expression changes of intraperitoneal tumor microenvironment after STING activation

Project description:The results revealed dramatic differences between the STING-activated and Control tumors

2020-10-23 | GSE159825 | GEO

STING activation promotes robust immune response and NK cell- mediated tumor regression in glioblastoma models

Project description:Immunotherapy has had a tremendous impact on cancer treatment in the past decade, with hitherto unseen responses at advanced and metastatic stages of the disease. However, the aggressive brain tumor glioblastoma (GBM) is highly immunosuppressive and remains largely refractory to current immunotherapeutic approaches. The cGAS-STING cytoplasmic double stranded DNA (dsDNA) sensing pathway has emerged as a next-generation immunotherapy target with potent local immune stimulatory properties. Here, we investigated the status of the STING pathway in GBM and the modulation of the brain tumor microenvironment (TME) with the STING agonist ADU-S100. Our data reveal the presence of STING in human GBM specimens, where it stains strongly in the tumor vasculature. We show that human GBM explants can respond to STING agonist treatment by secretion of inflammatory cytokines. In murine GBM models, we show a profound shift in the tumor immune landscape after STING agonist treatment, with massive infiltration of the tumor-bearing hemisphere with innate immune cells including inflammatory macrophages, neutrophils and NK populations. Treatment of established murine intracranial GL261 and CT-2A tumors by biodegradable ADU-S100-loaded intracranial implants demonstrated a significant increase in survival in both models and long-term survival with immune memory in GL261. Responses to treatment were abolished by NK cell depletion. This study reveals therapeutic potential and deep remodeling of the TME by STING activation in GBM and warrants the further examination of STING agonists alone or in combination with other immunotherapies such as cancer vaccines, CAR T cells, NK therapies or immune checkpoint blockade.

2022-06-28 | GSE206604 | GEO

ExoSTING, an extracellular vesicle loaded with STING agonists, promotes tumor immune surveillance

Project description:Cyclic dinucleotide (CDN) agonists of the STimulator of InterferoN Genes (STING) pathway have shown immune activation and tumor clearance in pre-clinical models. However, CDNs administered intratumorally also promote STING activation leading to direct cytotoxicity of many cell types in the tumor microenvironment (TME), systemic inflammation due to rapid tumor extravasation of the CDN, and immune ablation in the TME. These result in a failure to establish immunological memory. ExoSTING, an engineered extracellular vesicle (EV) exogenously loaded with CDN, enhances the potency of CDN and preferentially activates antigen presenting cells in the TME. Following intratumoral injection, exoSTING was retained within the tumor, enhanced local Th1 responses and recruitment of CD8+ T cells, and generated systemic anti-tumor immunity to the tumor. ExoSTING at therapeutically active doses did not induce systemic inflammatory cytokines, resulting in an enhanced therapeutic window. ExoSTING is a novel, differentiated therapeutic candidate that leverages the natural biology of EVs to enhance the activity of CDNs.

2021-03-13 | GSE168784 | GEO

Targeting IRE1α reprograms the tumor microenvironment and enhances anti-tumor immunity in prostate cancer

Project description:Unfolded protein response (UPR) is a central stress response pathway in normal cells that is hijacked by tumor cells for their survival. However, how activation of UPR in cancer cells shapes the tumor microenvironment (TME) remain largely unexplored. Here, we investigated the role of IRE1Î±-XBP1s on modulation of TME dynamics in prostate cancer (PCa).

2024-08-28 | PXD044287 | Pride

NK cell proteome reponse to tumor microenvironment

Project description:To elucidate the mechanisms that regulate metabolic suppression versus sustained metabolic fitness in NK cells in the tumor microenvironment (TME), we assessed global differences in protein levels via proteomics in NK cells exposed to the TME or control media.

2021-04-12 | PXD016996 | Pride

Cancer cell non-autonomous tumor progression from chromosomal instability

Project description:Chromosomal instability (CIN) is a driver of cancer metastasis and immune evasion. Yet, the extent to which this effect depends on the immune system remains unknown. Here we show that CIN-induced chronic activation of the cGAS-STING pathway in cancer cells induces signal re-wiring downstream of STING, promoting a pro-metastatic tumor microenvironment (TME). Using ContactTracing, a newly developed, validated, and benchmarked tool to infer conditionally-dependent cell-cell interactions from single cell transcriptomic data, we identify a cancer cell-derived STING-dependent ER stress response that remodels a TME replete with immune suppressive myeloid cells and dysfunctional T cells. Simultaneously, CIN-induced chronic STING activation leads to interferon-specific tach-yphylaxis reinforcing immune suppression. Reversal of CIN, depletion of cancer cell STING, or inhibition of ER stress signaling upends CIN-dependent effects on the TME and suppresses metastasis in immune competent, but not severely immune compromised settings. Treatment with STING inhibitors reduces CIN-driven metastasis in melanoma, breast, and colorectal cancer. Finally, we show that CIN and pervasive cGAS activation in micronuclei are associated with ER stress signaling, immune suppression, and metastasis in human triple-negative breast cancer; highlighting a viable strategy to identify and therapeutically intervene in tumors spurred by CIN-induced inflammation.

2023-06-20 | GSE189856 | GEO

Novel prognostic implications of complement activation in the tumor microenvironment for de novo metastatic BRAF V600E mutant colorectal cancer

Project description:Prognosis of metastatic BRAF V600E mutant colorectal cancer (CRC) is poor, and the prognostic implications of immune contextures in the tumor microenvironment (TME) for CRC remain elusive. Complement activation in the TME was significantly associated with poor OS and was correlated with TAM M2 in patients with de novo metastatic BRAF V600E mutant CRC.

2022-11-08 | GSE211576 | GEO

BJ cyto-nuclear translocation upon STING activation

Project description:The goal of this project is to identify changes of cyto-nuclear import upon STING activation by cGAMP. BJ cells stably expressing TurboID-NES were treated with biotin to label cytoplasmic proteins, after which cells were further treated with or without cGAMP to activate STING signaling. Cells were then fractionated to collect the nuclei. The biotinylated proteins in the nuclear pellets were purified by streptavidin beads for mass spectrometry analysis.

2024-09-19 | PXD049018 | Pride

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data