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Epithelial XBP1 coordinates TP53-driven DNA damage responses and suppression of intestinal carcinogenesis

ABSTRACT: Epithelial XBP1 coordinates TP53-driven DNA damage responses and suppression of intestinal carcinogenesis

PROVIDER: PRJNA755990 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR15510523.fastq.gz	Fastqsanger.gz
	SRR15510524.fastq.gz	Fastqsanger.gz
	SRR15510525.fastq.gz	Fastqsanger.gz
	SRR15510526.fastq.gz	Fastqsanger.gz
	SRR15510527.fastq.gz	Fastqsanger.gz

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Epithelial XBP1 coordinates TP53-driven DNA damage responses and suppression of intestinal carcinogenesis

Project description:We assessed the impact of intestinal epithelial XBP1 in coordinating epithelial DNA damage responses. As our data revealed that low XBP1 activity in the context of chronic DNA damage is associated with both reduced p53 pathway activity and formation of tumors with metastaic potential in-vivo, we performed RNA sequencing of intestinal organoids (H2b/Xbp1fl/fl, H2bΔIEC, H2b/Xbp1ΔIEC, H2b/p53∆IEC) to identify a transcriptional program downstream of p53 that drives the tumorigenic in-vivo phenotype.

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Tp53 suppression promotes cardiomyocyte proliferation during zebrafish heart regeneration

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Expression data from IRE1a or XBP1 deficient mouse liver

Project description:IRE1a and XBP1 are key regulators of the unfolded protein response (UPR). XBP1 ablation causes profound hypolipidemia in mice, and triggers feedback activation of its upstream enzyme IRE1a, instigating regulated IRE1-dependent decay (RIDD), an mRNA degradation mechanism dependent on IRE1a's endoribonuclease activity. Comprehensive microarray analysis of XBP1 and/or IRE1a deficient liver identified genes involved in lipogenesis and lipoprotein metabolism as RIDD substrates, which might contribute to the suppression of plasma lipid levels by activated IRE1a. To identify RIDD substrate mRNAs and direct XBP1 targets in the liver, we performed a comprehensive comparative microarray analysis of three groups of RNA samples: WT and XBP1 deficient mice, WT and IRE1a deficient mice untreated or injected with tunicamycin, and XBP1 deficient mice injected with luciferase or IRE1a siRNA.

2012-10-17 | E-GEOD-40515 | biostudies-arrayexpress

Chromosome 9p21.3 Coordinates Cell Intrinsic and Extrinsic Tumor Suppression

Project description:Chromosome 9p21.3 Coordinates Cell Intrinsic and Extrinsic Tumor Suppression

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Expression data from IRE1a or XBP1 deficient mouse liver

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Chromosome 9p21.3 Coordinates Cell Intrinsic and Extrinsic Tumor Suppression [scRNA-seq]

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Project description:Regulatory T cell depletion causes compensatory immune suppression and accelerated pancreatic carcinogenesis.

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IRE1α-XBP1 controls T cell function in ovarian cancer by regulating mitochondrial activity

Project description:Tumors evade immune control by creating hostile microenvironments that perturb T cell metabolism and effector function. However, it remains unclear how intratumoral T cells integrate and interpret metabolic stress signals. Here we report that ovarian cancer (OvCa), an aggressive malignancy refractory to standard treatments and current immunotherapies, induces Endoplasmic Reticulum (ER) stress and activation of the IRE1α-XBP1 arm of the Unfolded Protein Response (UPR)10,11 in T cells to control their mitochondrial respiration and anti-tumor function. XBP1 upregulation in T cells isolated from human OvCa specimens was associated with decreased intratumoral T cell infiltration and reduced IFNG mRNA expression. Malignant ascites fluid obtained from OvCa patients inhibited glucose uptake and caused N-linked protein glycosylation defects in T cells, leading to IRE1α/XBP1-driven suppression of mitochondrial activity and IFN- production. Mechanistically, XBP1 induction limited the influx of glutamine necessary to sustain T cell mitochondrial respiration under glucose-deprived conditions by regulating the abundance of glutamine carriers. Restoring N-linked protein glycosylation, abrogating IRE1α-XBP1 activation or enforcing expression of glutamine transporters enhanced mitochondrial respiration in human T cells exposed to OvCa ascites. XBP1-deficient T cells in the metastatic OvCa milieu exhibited global transcriptional reprogramming and improved effector capacity. Accordingly, OvCa-bearing mice lacking XBP1 selectively in T cells demonstrated superior anti-tumor immunity, delayed malignant progression and increased overall survival. Therefore, controlling ER stress or targeting IRE1α-XBP1 signaling may help restore T cell metabolic fitness and anti-tumor capacity in cancer hosts.

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