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CT26 sorted in vivo tumor cells with Trex1 KO

ABSTRACT: CT26 sorted in vivo tumor cells with Trex1 KO

PROVIDER: PRJEB72746 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	ERR12664744.fastq.gz	Fastqsanger.gz
	ERR12664745.fastq.gz	Fastqsanger.gz
	ERR12664746.fastq.gz	Fastqsanger.gz
	ERR12664747.fastq.gz	Fastqsanger.gz
	ERR12664748.fastq.gz	Fastqsanger.gz

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CT26 sorted in vivo tumor cells with Trex1 KO

Project description:The DNA exonuclease TREX1 degrades endogenous cytosolic DNA. Cytosolic DNA triggers the cGAS/STING pathway which increases type I interferon. To investigate the physiological significance of TREX1 loss on in vivo tumor growth, we implanted control and TREX1-deficient CT26 tumor cells into immunocompetent BALB/c hosts.Tumor cells were collected 7 days after tumors reached around 200mm3.

2024-03-12 | E-MTAB-13816 | biostudies-arrayexpress

The exonuclease TREX1 constitutes an innate immune checkpoint limiting cGAS/STING-mediated anti- tumor immunity

Project description:Given that TREX1-deficient tumor cells showed a growth delay in immunocompetent but not immunodeficient hosts, we characterize the consequences of CT26 tumor-intrinsic TREX1 loss on the host immune system by performing single-cell RNA sequencing on intra-tumoral immune cells sorted from control and TREX1 KO CT26 tumors.

2024-03-12 | E-MTAB-13823 | biostudies-arrayexpress

Single-cell sequencing of CD45-positive and CD45 negative cells from the lungs of WT, Trex1 KO, Trex1;Ifngr1 DKO, and cGas-KI/+;Vav-icre mice

Project description:Trex1 KO is one of the animal models with activated cGAS. Here, we will compare the lung tissue of mice with hematopoietic overexpression of cGAS to see if it exhibits a phenotype similar to that of Trex1 KO.

2024-07-09 | GSE271340 | GEO

Microarray of Trex1 WT and Trex1 KO hearts on RAG2KO background

Project description:Heart ventricle tissue was harvested from Trex1/RAG2 DKO mice and from Trex1WT/RAG2KO littermate controls. RNA was extracted, and an Affymetrix Mouse 430 2.0 gene chip analysis was performed.

2008-08-22 | GSE11698 | GEO

Transcription profiling of mouse Trex1 WT and Trex1 KO hearts on RAG2KO background

Project description:Heart ventricle tissue was harvested from Trex1/RAG2 DKO mice and from Trex1WT/RAG2KO littermate controls. RNA was extracted, and an affymetrix Mouse 430 2.0 gene chip analysis was performed. Experiment Overall Design: Three pairs of littermates are included: 779/780, 4184/4185, and 4192/4193.

2008-10-25 | E-GEOD-11698 | biostudies-arrayexpress

TCR variable regions transcripts of CT26-shppp2r1a and CT26-scr samples

Project description:TCR variable regions transcripts of three CT26-shppp2r1a samples and three CT26-scr samples

2021-11-20 | GSE189092 | GEO

Inherited C-terminal TREX1 variants disrupt homology-directed repair to cause senescence and DNA damage phenotypes in Drosophila, mice, and humans

Project description:Age-related microangiopathy, also known as small vessel disease (SVD), causes damage to the liver, brain, kidney and retina. Based on the DNA damage theory of aging, we reasoned that genomic instability may underlie an SVD caused by dominant C-terminal variants in TREX1, the most abundant 3’-5’ DNA exonuclease in mammals. C-terminal TREX1 variants cause an adult-onset SVD known as retinal vasculopathy with cerebral leukoencephalopathy (RVCL or RVCL-S). In RVCL, an aberrant, C-terminally truncated TREX1 mislocalizes to the nucleus due to deletion of its ER-anchoring domain. Since RVCL pathology mimics that of the radiation injury, we reasoned that nuclear TREX1 promotes DNA damage. Here, we show that RVCL-associated TREX1 variants cause DNA damage in humans, mice, and Drosophila, and that cells expressing RVCL mutant TREX1 are more vulnerable to DNA damage induced by chemotherapy and cytokines that up-regulate TREX1, leading to depletion of TREX1-high cells in RVCL mice. RVCL-associated TREX1 mutants inhibit homology-directed repair (HDR), causing DNA deletions and vulnerablility to PARP inhibitors. In women with RVCL, we observe early-onset breast cancer, similar to patients with BRCA1/2 variants. Our results provide a new mechanistic basis linking aberrant TREX1 activity to the DNA damage theory of aging, premature senescence, and microvascular disease.

2024-05-30 | PXD051905 | Pride

Transcriptome profiling of wild-type (WT) and USP8 knockout (KO) CT26 cell lines

Project description:USP8 is one of DUBs and is frequently overexpressed or gain-of-function mutated in multiple types of human cancer. Importantly, USP8 has been identified as an immunomodulatory DUB as T cell-specific Usp8 deficiency disrupts regulatory T cell functions, leading to recruiting abundant CD8+ T cells in colons and resulting in the inflammatory bowel disease in mice. However, whether targeting USP8 can enhance anti-tumor immunity has not been reported. To further explore the physiological function of USP8, we performed the transcriptomic analysis to comprehensively understand which signaling pathways are mainly regulated by USP8 in cancer cells. Usp8 WT and KO CT26 cells were harvested for RNA-sequencing (RNA-seq).

2022-02-14 | GSE164558 | GEO

Loss of Trex1 in dendritic cells is sufficient to trigger systemic autoimmunity

Project description:Biallelic defects of the gene encoding for the intracellular enzyme 3â repair exonuclease (Trex)1 cause Aicardi-GoutiÃ¨res syndrome (AGS), a rare monogenic, lupus-like autoimmune disease, while heterozygous Trex1 loss of function alleles are associated with systemic lupus erythematosus (SLE). Trex1-/- mice develop lethal autoimmune multi-organ inflammation, which results from a chronic type I IFN response triggered by intracellular accumulation of a putative nucleic acid substrate of Trex1. This pathogenic nucleic acid is detected by the broadly, but not ubiquitously, expressed cytosolic DNA sensor cGAS, raising the question whether there are specific cell types that respond to Trex1 deficiency by production of IFN and induce autoimmunity. We generated mice with conditional knock out of the Trex1 gene and demonstrated that loss of Trex1 throughout the hematopoietic system and even selective loss in dendritic cells is sufficient to cause IFN release and autoimmunity. B cells showed no transcriptional response to Trex1 deficiency. Trex1-/- keratinocytes produced IFN but did not induce skin inflammation, whereas loss of Trex1 in cardiomyocytes triggered neither IFN response nor pathology. Trex1-deficient neurons and astrocytes did not release IFN in the CNS. In contrast, mice with selective inactivation of Trex1 in long-living CNS macrophages such as microglia locally produced IFN but did not reproduce the mild encephalitis seen in Trex1-/- mice. Collectively, individual cell types differentially respond to the loss of Trex1 and dendritic cells seem promising candidates for experiments addressing the molecular pathomechanism in Trex1 deficiency. We sorted CD19-positive B cells from spleens of Trex1fl/fl CD19-Cre+ and Trex1fl/fl CD19-Cre- mice and isolated total RNA for library construction to perform mRNA deep sequencing.

2016-08-01 | E-GEOD-77693 | biostudies-arrayexpress

Induced loss of TREX1 in host cells inflames the tumor micromilieu and invigorates CTL-mediated cancer control

Project description:Activation of local innate immunity in tumor tissue, aiming at induction of adaptive responses, is a major concept in cancer immunotherapy. The cGAS/STING pathway triggers type I IFN and pro-inflammatory cytokine responses upon detection of cytosolic DNA and can robustly enhance anti-tumor immunity. The DNase 3’ repair exonuclease 1 (TREX1) is a central component of cellular DNA disposal preventing accumulation of endogenous DNA in the cytosol, activation of cGAS and cell-intrinsic innate immune responses. While constitutive TREX1-deficiency causes severe mendelian autoimmunity, temporary pharmacological inhibition of the enzyme may represent an efficient means to activate anti-tumor immunity. Induced inactivation of the Trex1 gene in mice (TREX1 iKO) resulted in improved immune control of established syngeneic tumors that was type I IFN- and CD8+ T cell-dependent. This was associated with a dramatic increase of immune cell infiltration of tumor tissue while other (non-tumor) tissues were not or marginally affected. TREX1 iKO triggered an inflammatory switch of intra-tumoral monocyte, macrophage and dendritic cell populations, associated with enhanced antigen presentation capacity. Invigoration of CD8 T cell responses was reflected in robust increase in cells differentiating along the exhaustion trajectory but expressing significant signatures of effector function. Combination of TREX1 iKO with immune checkpoint inhibition synergistically promoted tumor control. In addition to improved anti-tumor immunity upon loss of TREX1 in host cells, we also show that cancer cell-specific TREX1 deficiency synergizes with irradiation and checkpoint inhibition to enable tumor rejection and formation of long-term memory. We conclude that pharmacological TREX1 inhibition is a promising therapeutic approach to boost anti-tumor immunity.

2025-05-04 | GSE290383 | GEO

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