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IRF3 prevents colorectal tumorigenesis via inhibiting the nuclear translocation of β-catenin

ABSTRACT: IRF3 prevents colorectal tumorigenesis via inhibiting the nuclear translocation of β-catenin

PROVIDER: PRJNA655560 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR12397900_1.fastq.gz	Fastqsanger.gz
	SRR12397900_2.fastq.gz	Fastqsanger.gz
	SRR12397901_1.fastq.gz	Fastqsanger.gz
	SRR12397901_2.fastq.gz	Fastqsanger.gz
	SRR12397902_1.fastq.gz	Fastqsanger.gz

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IRF3 prevents colorectal tumorigenesis via inhibiting the nuclear translocation of β-catenin

Project description:Occurrence of Colorectal cancer（CRC）is relevant with gut microbiota. However, role of IRF3, a key signaling mediator in innate immune sensing, has been barely investigated in CRC. Here, we unexpectedly found that the IRF3 deficient mice are hyper-susceptible to the development of intestinal tumor in AOM/DSS and Apcmin/+ models. Genetic ablation of IRF3 profoundly promotes the proliferation of intestinal epithelial cells via aberrantly activating Wnt signaling. Mechanically, IRF3 in resting state robustly associates with the active β-catenin in the cytoplasm, thus preventing its nuclear translocation and cell proliferation, which can be relieved upon microbe-induced activation of IRF3. In accordance, the survival of CRC is clinically correlated with the expression level of IRF3. Therefore, our study identifies IRF3 as a negative regulator of the Wnt/β-catenin pathway and a potential prognosis marker for Wnt-related tumorigenesis, and describes an intriguing link between gut microbiota and CRC via the IRF3-β-catenin axis.

2020-09-16 | GSE155777 | GEO

IRF3 prevents colorectal tumorigenesis via inhibiting the nuclear translocation of β-catenin.

Project description:Occurrence of Colorectal cancer (CRC) is relevant with gut microbiota. However, role of IRF3, a key signaling mediator in innate immune sensing, has been barely investigated in CRC. Here, we unexpectedly found that the IRF3 deficient mice are hyper-susceptible to the development of intestinal tumor in AOM/DSS and Apcmin/+ models. Genetic ablation of IRF3 profoundly promotes the proliferation of intestinal epithelial cells via aberrantly activating Wnt signaling. Mechanically, IRF3 in resting state robustly associates with the active β-catenin in the cytoplasm, thus preventing its nuclear translocation and cell proliferation, which can be relieved upon microbe-induced activation of IRF3. In accordance, the survival of CRC is clinically correlated with the expression level of IRF3. Therefore, our study identifies IRF3 as a negative regulator of the Wnt/β-catenin pathway and a potential prognosis marker for Wnt-related tumorigenesis, and describes an intriguing link between gut microbiota and CRC via the IRF3-β-catenin axis.

| S-EPMC7666182 | biostudies-literature

Macropahge-specific Irf3 prevents viral inflammation

Project description:Macropahge-specific Irf3 prevents viral inflammation

| PRJNA1112164 | ENA

Macropahge-specific Irf3 prevents viral inflammation

Project description:Viral inflammation contributes to pathogenesis and mortality during respiratory virus infections. We recently uncovered Irf3, a critical component of innate antiviral immune responses, interacts with pro-inflammatory transcription factor NF-kB, and inhibits its activity. Irf3, using this mechanism, suppresses inflammatory gene expression in virus-infected cells and mice. In this study, we evaluated the cells responsible for Irf3-mediated suppression of viral inflammation using newly engineered conditional Irf3Δ/Δ mice. Irf3Δ/Δ mice, upon respiratory virus infection, showed increased susceptibility and mortality. Irf3 deficiency caused enhanced inflammatory gene expression, lung inflammation, immunopathology, and damage, which were accompanied by increased infiltration of pro-inflammatory macrophages. Deletion of Irf3 in macrophages (Irf3-MKO) displayed, similar to Irf3Δ/Δ mice, increased inflammatory responses, macrophage infiltration, lung damage, and lethality, indicating Irf3 in these cells suppressed lung inflammation. RNA-seq analyses revealed enhanced NF-kB-dependent gene expression along with activation of inflammatory signaling pathways in infected Irf3MKO lungs. Targeted analyses revealed activated MAPK signaling in Irf3MKO lungs. Therefore, Irf3 inhibited inflammatory signaling pathways in myeloid cellsmacrophages to prevent viral inflammation and pathogenesis.

2024-08-16 | GSE267631 | GEO

Inhibiting or depleting AHCY prevents senescence induction

Project description:Inhibiting or depleting AHCY prevents senescence induction

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Irf3 phenotyping

Project description:The interferon regulatory factors IRF3 and IRF7 are key players in the regulation of type I and III IFN genes. In this study, we analyzed the role of IRF3 and IRF7 for the host response to influenza A virus infections in Irf3-/-, Irf7-/- and Irf3-/-Irf7-/- knock-out mice.

2016-11-02 | GSE77600 | GEO

IRF3 and ZBP1

Project description:IRF3 and ZBP1

| PRJNA686391 | ENA

Gene expression in IRF3-/- peritoneal macrophage infected with VSV

Project description:IRF3 is one of the most critical transcription factor in down stream of pattern recognition receptors (such as toll-like receptor and RIG-I-like receptor) signalling pathway. IRF3 is known to induce the expression of type I IFN gene upon virus infection. To furter examine the role of IRF3 in virus-induced gene expression, we preformed microarray analysis in IRF3-/- peritoneal macrophages infected with VSV, and found that IRF3 suppresses the expression of Il12b gene. Peritoneal macrophages from WT of IRF3-/- B6 mice were infected with VSV(1 M.O.I. ) for 6 hous, and then subjected to microarray analysis.

2012-05-19 | E-GEOD-37855 | biostudies-arrayexpress

RACK1 prevents premature differentiation of epidermal progenitors by inhibiting IRF6 expression

Project description:RACK1 prevents premature differentiation of epidermal progenitors by inhibiting IRF6 expression

| PRJNA751366 | ENA

Oxygen enhances antiviral innate immunity through maintenance of EGLN1-catalysed proline hydroxylation of IRF3

Project description:Oxygen is essential for aerobic organisms, but little is known about its role in antiviral immunity. Here, we report that during responses to viral infection, the hypoxic conditions repress antiviral-responsive genes independently of HIF signalling. EGLN1 was identified as a key mediator of the enhancement exerted by the oxygen on antiviral innate immune responses. Under sufficient oxygen conditions, EGLN1 maintains its prolyl hydroxylase activity to catalyse hydroxylation of IRF3 at proline 10. This modification enhances IRF3 phosphorylation, dimerisation, and nuclear translocation, leading to subsequent IRF3 activation. Furthermore, mice and zebrafish with Egln1 deletion, treatment with the EGLN inhibitor, FG4592, or mice carrying an Irf3 P10A mutation are more susceptible to viral infections. These findings not only reveal a direct link between oxygen and antiviral responses, but also provide insights into the mechanisms by which oxygen regulates innate immunity

2024-01-18 | GSE253181 | GEO

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