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Atrx deletion impairs cGAS-STING signaling and increases response to radiation and oncolytic herpesvirus in soft tissue sarcoma

ABSTRACT: Atrx deletion impairs cGAS-STING signaling and increases response to radiation and oncolytic herpesvirus in soft tissue sarcoma

PROVIDER: PRJNA698482 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR13594809_1.fastq.gz	Fastqsanger.gz
	SRR13594809_2.fastq.gz	Fastqsanger.gz
	SRR13594810_1.fastq.gz	Fastqsanger.gz
	SRR13594810_2.fastq.gz	Fastqsanger.gz
	SRR13594811_1.fastq.gz	Fastqsanger.gz

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Atrx deletion impairs cGAS-STING signaling and increases response to radiation and oncolytic herpesvirus in soft tissue sarcoma

Project description:RNA sequencing of isogenic ATRX wild-type (WT) and ATRX knockout (KO) paired isogenic cell lines treated with either 1.)interferon stimulatory DNA (ISD) and harvested 24 hours after treatment, 2)4 Gy ionizing radiation and harvested 36 hours after treatment, or 3) untreated control. These experiments help determine the differential impact of ATRX mutational status on cGAS-STING and type-I interferon signaling in soft tissue sarcoma.

2021-02-02 | GSE165878 | GEO

ATRX Deficiency Drives Aberrant Type I Interferon Signalling Through cGAS-Dependent Transcriptional Dysregulation [Cut&Tag: ATRX]

Project description:The X-linked α-thalassaemia intellectual disability syndrome (ATRX) protein is a chromatin remodeller involved in transcriptional regulation and genome stability. While the importance of ATRX in development and malignancy is well recognised, its role in innate immunity is less well defined. Here we describe three unrelated patients with ATR-X syndrome carrying missense mutations in the ATPase domain of ATRX, each manifesting features of severe inflammation accompanied by persistent upregulation of interferon-stimulated gene expression in whole blood. Studies in patient-derived cells, CRISPR-engineered fibroblasts and neuronal models demonstrate that ATRX loss-of-function mutations drive enhanced type I interferon signalling through a cGAS-dependent mechanism uncoupled from the DNA sensing activity of cGAS. Mechanistically, ATRX deficiency disrupts the chromatin distribution of DAXX and H3.3, with cGAS essential for the changes in nucleosome composition and gene expression mediated by loss of ATRX. Thus, our study highlights a previously unrecognized link between ATRX dysfunction and inflammation involving a non-canonical role of cGAS.

2026-08-24 | GSE329644 | GEO

RNA-sequencing of primary soft tissue sarcomas and cell lines with ATRX deletion

Project description:RNA sequencing of a primary tumors from a sarcoma genetically engineerted mouse model with activation of oncogenic Kras, deletion of p53 and deletion of Atrx, as compared to control sarcomas with identical genetic alterations but with wild-type Atrx. Tumors were either untreated or recieved 20 Gy of ionizing radiation and were harvested at 4 hrs, 3 day, or 6 day timepoints post treatment. For cell lines, isogenic ATRX wild-type (WT) and ATRX knockout (KO) paired isogenic cell lines treated with either 1.)interferon stimulatory DNA (ISD) and harvested 24 hours after treatment, 2)4 Gy ionizing radiation and harvested 36 hours after treatment, or 3) untreated control. These experiments help determine the differential impact of ATRX mutational status on cGAS-STING and type-I interferon signaling in soft tissue sarcoma.

2021-03-06 | GSE167537 | GEO

ATRX Deficiency Drives Aberrant Type I Interferon Signalling Through cGAS-Dependent Transcriptional Dysregulation [Quantseq_Anifrolumab]

2026-08-24 | GSE344583 | GEO

ATRX Deficiency Drives Aberrant Type I Interferon Signalling Through cGAS-Dependent Transcriptional Dysregulation [RNA-seq]

2026-08-24 | GSE344333 | GEO

ATRX Deficiency Drives Aberrant Type I Interferon Signalling Through cGAS-Dependent Transcriptional Dysregulation [CUT&Tag: H33]

2026-08-24 | GSE337574 | GEO

ATRX Deficiency Drives Aberrant Type I Interferon Signalling Through cGAS-Dependent Transcriptional Dysregulation [CUT&Tag: DAXX]

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Atrx deletion impairs CGAS/STING signaling and increases sarcoma response to radiation and oncolytic herpesvirus.

Project description: Not available

| S-EPMC10313374 | biostudies-literature

ATRX loss predicts poor outcomes and reveals a therapeutic vulnerability to TEAD inhibition in soft tissue sarcomas

Project description:ATRX is one of the most frequently altered genes in sarcoma and encodes an ATP-dependent chromatin remodeler implicated in maintaining heterochromatin. However, ATRX alterations have not been leveraged for sarcoma treatment. We observed loss of ATRX protein in 14% of soft tissue leiomyosarcoma (STLMS, n =127), 53% of uterine leiomyosarcoma (ULMS, n = 95), 37% of undifferentiated pleomorphic sarcoma (UPS, n = 82), and 8% of dedifferentiated liposarcoma (DDLPS, n = 84). ATRX loss was associated with significantly worse outcomes in ULMS, UPS, and DDLPS. ATRX knockout in sarcoma cells increased proliferation in cooperation with TP53 deletion. ATRX knockout led to chromatin de-repression and enrichment of PRDM4 and NFIX transcription factor (TF) motifs. PRDM4 and NFIX knockdown in ATRX-mutant sarcoma lines resulted in reduced proliferation and invasion suggesting epistatic relationship. Consistent with the known functional relationship between PRMD4 and YAP1, we observed that ATRX/TP53 KO cells were more sensitive to the TEAD inhibitor VT103 compared to TP53 KO and ATRX WT controls. Overall, our results identify ATRX loss as a prognostic factor of worse outcomes, implicate the ATRX-PRDM4-YAP1 axis as a novel underlying mechanism, and suggest use of TEAD inhibition as a potential therapeutic strategy for ATRX-deficient sarcomas.

2026-09-01 | GSE310906 | GEO

Mus musculus strain:129/SVJAe

Project description:Atrx deletion impairs cGAS-STING signaling and increases response to radiation and oncolytic herpesvirus in soft tissue sarcoma

| PRJNA694789 | ENA

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