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Epigenetic state determines inflammatory sensing in neuroblastoma [ATAC-seq]

ABSTRACT: Epigenetic state determines inflammatory sensing in neuroblastoma [ATAC-seq]

PROVIDER: PRJNA754359 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR15441715_1.fastq.gz	Fastqsanger.gz
	SRR15441715_2.fastq.gz	Fastqsanger.gz
	SRR15441716_1.fastq.gz	Fastqsanger.gz
	SRR15441716_2.fastq.gz	Fastqsanger.gz
	SRR15441717_1.fastq.gz	Fastqsanger.gz

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Epigenetic state determines inflammatory sensing in neuroblastoma

Project description:Epigenetic state determines inflammatory sensing in neuroblastoma

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Epigenetic state determines inflammatory sensing in neuroblastoma [RNA-seq]

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Epigenetic state determines inflammatory sensing in neuroblastoma [RNA-seq]

Project description:Immunotherapy has revolutionized cancer treatment, but many cancers are not impacted by currently available immunotherapeutic strategies. Here, we investigated inflammatory signaling pathways in neuroblastoma, a classically “cold” pediatric cancer. By testing the functional response of a panel of 20 diverse neuroblastoma cell lines to three different inflammatory stimuli, we found that all cell lines have intact interferon signaling and all but one lack functional cytosolic DNA sensing via cGAS-STING. However, dsRNA sensing via TLR3 was heterogeneous, as was signaling through other dsRNA sensors and TLRs more broadly. Seven cell lines showed robust response to dsRNA, six of which are in the mesenchymal epigenetic state, while all unresponsive cell lines are in the adrenergic state. Genetically switching adrenergic cell lines towards the mesenchymal state fully restored responsiveness. In responsive cells, dsRNA sensing results in the secretion of pro-inflammatory cytokines, enrichment of inflammatory transcriptomic signatures, and increased tumor killing by T cells in vitro. Using single cell RNA sequencing data, we show that human neuroblastoma cells with stronger mesenchymal signatures have a higher basal inflammatory state, demonstrating intra tumoral heterogeneity in inflammatory signaling that has significant implications for immunotherapeutic strategies in this aggressive childhood cancer.

2022-01-22 | GSE182051 | GEO

Epigenetic state determines inflammatory sensing in neuroblastoma [ATAC-seq]

2022-01-22 | GSE182041 | GEO

Epigenetic state determines inflammatory sensing in neuroblastoma

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2022-01-21 | GSE182052 | GEO

Metabolic state determines drug response in liver cancer

Project description:Metabolic state determines drug response in liver cancer

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MPTAC determines APP fragmentation via sensing sulfur amino acid catabolism

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Distinct SOX signature determines neuroblastoma origin and predicts clinical outcome

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Endothelial Cell Cycle State Determines Propensity for Arterial-Venous Fate

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Interpreting an apoptotic corpse as anti-inflammatory involves a chloride sensing pathway

Project description:Phagocytes in different tissues recognize and remove apoptotic cells via the process of efferocytosis. Although it is well-established that efferocytosis elicits an anti-inflammatory response by phagocytes, the molecules and mechanisms that enforce this response in phagocytes are still being defined. In attempting to decipher gene programs induced after a phagocyte ingests a dying cell, we uncovered a chloride-sensing signaling pathway that controls both the ‘appetite’ of a phagocyte and how a phagocyte responds after corpse uptake. First, we noted that within phagocytes that have ingested a corpse, the solute carrier 12 (SLC12) family members SLC12A2 and SLC12A4 are actively modulated. Interfering with SLC12A2, either genetically or pharmacologically, led to significantly enhanced corpse uptake per phagocyte, while loss of SLC12A4 inhibited corpse uptake. Interestingly, when phagocytes with disrupted SLC12A2 engulfed apoptotic corpses, the typical homeostatic efferocytosis signature was perturbed, characterized by loss of the canonical anti-inflammatory program and replaced by pro-inflammatory and oxidative stress-associated gene programs. In further mechanistic studies, we observed efferocytosis was also regulated by the chloride-sensing pathway upstream of SLC12A2, including the kinases WNK1-OSR1-SPAK, and this involved chloride entry/exit across the plasma membrane of phagocytes during corpse engulfment. We also show that the ‘switch’ to pro-inflammatory sensing of apoptotic cells is specifically due to disruption of the chloride-sensing pathway and not due to corpse overload or poor degradation, and that the pro-inflammatory gene signature can be reversed using a chloride ionophore. Collectively, these data identify the WNK1-OSR1-SPAK-SLC12A2/SLC12A4 chloride-sensing pathway and chloride flux in phagocytes as key modifiers of how a phagocyte interprets an engulfed apoptotic corpse.

2020-03-24 | GSE131860 | GEO

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