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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

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.

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

Project description:ATRX is one of the most frequently altered genes in solid tumors, and mutation is especially frequent in soft tissue sarcomas. However, the role of ATRX in tumor development and response to cancer therapies remains poorly understood. Here, we developed a primary mouse model of soft tissue sarcoma and showed that Atrx-deleted tumors were more sensitive to radiation therapy and to oncolytic herpesvirus. In the absence of Atrx, irradiated sarcomas had increased persistent DNA damage, telomere dysfunction, and mitotic catastrophe. Our work also showed that Atrx deletion resulted in downregulation of the CGAS/STING signaling pathway at multiple points in the pathway and was not driven by mutations or transcriptional downregulation of the CGAS/STING pathway components. We found that both human and mouse models of Atrx-deleted sarcoma had a reduced adaptive immune response, markedly impaired CGAS/STING signaling, and increased sensitivity to TVEC, an oncolytic herpesvirus that is currently FDA approved for the treatment of aggressive melanomas. Translation of these results to patients with ATRX-mutant cancers could enable genomically guided cancer therapy approaches to improve patient outcomes.

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

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Characterization of open chromatin regions and ATRX, DAXX, H3.3 and cGAS binding sites in BJ-hTERT cells mutant for ATRX, on cGAS WT or null background

Project description:Characterization of open chromatin regions and ATRX, DAXX, H3.3 and cGAS binding sites in BJ-hTERT cells mutant for ATRX, on cGAS WT or null background

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Epigenomic analysis of Atrx deficiency in murine glioma cells of orgin [Atrx ChIP]

Project description:The chromatin regulator ATRX is inactivated in large subsets of adult and pediatric glioma. Whether and how ATRX deficiency promotes oncogenesis by epigenomic dysregulation remains unclear. We found that Atrx loss, especially when coupled with Tp53 inactivation, promoted cell motility and modulated differentiation state in primary murine neuroepithelial progenitors, recapitulating characteristic disease phenotypes and molecular features. Moreover, Atrx deficiency induced widespread shifts in chromatin accessibility, histone composition, and gene transcription at vacant Atrx binding sites distributed across the genome. Finally, target genes mediating Atrx-deficient phenotypes in vitro exhibited similarly selective misexpression in ATRX-mutant human glioma tissues and cell lines. These findings demonstrate that, in appropriate physiological contexts, ATRX deficiency and its epigenomic sequelae are sufficient to induce disease-defining oncogenic phenotypes.

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Project description:Heterochromatin in the eukaryotic genome is rigorously controlled by the concerted action of protein factors and RNAs. Here, we investigate the RNA binding function of ATRX, a chromatin remodeler with roles in silencing of repetitive regions of the genome and in recruitment of the polycomb repressive complex 2 (PRC2). We identify ATRX RNA binding regions (RBRs) and discover that the major ATRX RBR lies within the N-terminal region of the protein, distinct from its PHD and helicase domains. Deletion of this ATRX RBR (ATRXRBR) compromises ATRX interactions with RNAs in vitro and in vivo and alters its chromatin binding properties. Genome-wide studies reveal that loss of RNA interactions results in a redistribution of ATRX on chromatin. Finally, our studies identify a role for ATRX-RNA interactions in regulating PRC2 localization to a subset of polycomb target genes.

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Examining the role of ATRX-RNA interactions in ATRX and PRC2 localization and gene expression.

Project description:We disrupted the RNA binding region in endogenous ATRX and tested localization of ATRX, EZH2 and H3K27me3 by CUT&RUN. We show that ATRX-RNA binding is important to regulate ATRX and PRC2 localization to specific genes.

2020-02-24 | GSE130452 | GEO

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