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ARID1A suppresses R-loop mediated STING-Type I Interferon pathway activation of anti-tumor immunity

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Mus musculus

PROVIDER: GSE217807 | GEO | 2024/04/06

REPOSITORIES: GEO

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ARID1A suppresses R-loop mediated STING-Type I Interferon pathway activation of anti-tumor immunity (RNA-Seq)

Project description:Clinical trials have identified ARID1A mutations as enriched among patients who respond favorably to Immune Checkpoint Blockade (ICB) in several solid tumor types independent of microsatellite instability. We show that ARID1A loss in murine models is sufficient to induce anti-tumor immune phenotypes observed in ARID1A mutant human cancers, including increased CD8+ T cell infiltration and cytolytic activity. ARID1A deficient cancers upregulated an interferon (IFN) gene expression signature, the ARID1A-IFN signature, associated with increased R-loops and cytosolic single stranded DNA (ssDNA). Overexpression of the R-loop resolving enzyme, RNASEH2B, or cytosolic DNase, TREX1, in ARID1A deficient cells prevented cytosolic ssDNA accumulation and ARID1A-IFN gene upregulation. Further, the ARID1A-IFN signature and anti-tumor immunity were driven by STING dependent Type I IFN signaling, which was required for improved responsiveness of ARID1A mutant tumors to ICB treatment. These findings define a molecular mechanism underlying anti-tumor immunity in ARID1A mutant cancers.

2024-04-06 | GSE217803 | GEO

ARID1A suppresses R-loop mediated STING-Type I Interferon pathway activation of anti-tumor immunity (ChIP-Seq)

2024-04-06 | GSE217805 | GEO

ARID1A suppresses R-loop mediated STING-Type I Interferon pathway activation of anti-tumor immunity (ATAC-Seq)

2024-04-06 | GSE217804 | GEO

ARID1A suppresses R-loop mediated STING-Type I Interferon pathway activation of anti-tumor immunity (scRNA/TCR-seq)

2024-04-06 | GSE217806 | GEO

ARID1A suppresses R-loop mediated STING-Type I Interferon pathway activation of anti-tumor immunity

Project description:ARID1A suppresses R-loop mediated STING-Type I Interferon pathway activation of anti-tumor immunity

| PRJNA900585 | ENA

ARID1A suppresses R-loop mediated STING-Type I Interferon pathway activation of anti-tumor immunity (ChIP-Seq)

Project description:ARID1A suppresses R-loop mediated STING-Type I Interferon pathway activation of anti-tumor immunity (ChIP-Seq)

| PRJNA900583 | ENA

ARID1A suppresses R-loop mediated STING-Type I Interferon pathway activation of anti-tumor immunity (RNA-Seq)

Project description:ARID1A suppresses R-loop mediated STING-Type I Interferon pathway activation of anti-tumor immunity (RNA-Seq)

| PRJNA900581 | ENA

ARID1A suppresses R-loop mediated STING-Type I Interferon pathway activation of anti-tumor immunity (ATAC-Seq)

Project description:ARID1A suppresses R-loop mediated STING-Type I Interferon pathway activation of anti-tumor immunity (ATAC-Seq)

| PRJNA900584 | ENA

ARID1A suppresses R-loop mediated STING-Type I Interferon pathway activation of anti-tumor immunity (scRNA/TCR-seq)

Project description:ARID1A suppresses R-loop mediated STING-Type I Interferon pathway activation of anti-tumor immunity (scRNA/TCR-seq)

| PRJNA900586 | ENA

STING strengthens host anti-hantaviral immunity through an interferon-independent pathway.

Project description:Hantaan virus (HTNV), the prototype virus of hantavirus, could escape innate immunity by restraining type I interferon (IFN) responses. It is largely unknown whether there existed other efficient anti-hantaviral tactics in host cells. Here, we demonstrate that the stimulator of interferon genes (STING) strengthens the host IFN-independent anti-hantaviral immunity. HTNV infection activates RIG-I through IRE1-XBP 1-mediated ER stress, which further facilitates the subcellular translocation and activation of STING. During this process, STING triggers cellular autophagy by interacting with Rab7A, thus restricting viral replication. To note, the anti-hantaviral effects of STING are independent of canonical IFN signaling. Additionally, neither application of the pharmacological antagonist nor the agonist targeting STING could improve the outcomes of nude mice post HTNV challenge in vivo. However, the administration of plasmids exogenously expressing the mutant C-terminal tail (ΔCTT) STING, which would not trigger the type I IFN responses, protected the nude mice from lethal HTNV infection. In summary, our research revealed a novel antiviral pathway through the RIG-I-STING-autophagy pathway, which offered novel therapeutic strategies against hantavirus infection.

| S-EPMC10436061 | biostudies-literature

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