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Epigenetic regulation of cell state by H2AFY governs immunogenicity in high-risk neuroblastoma

ABSTRACT: Epigenetic regulation of cell state by H2AFY governs immunogenicity in high-risk neuroblastoma

PROVIDER: PRJNA987526 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR25022266_1.fastq.gz	Fastqsanger.gz
	SRR25022266_2.fastq.gz	Fastqsanger.gz
	SRR25022267_1.fastq.gz	Fastqsanger.gz
	SRR25022267_2.fastq.gz	Fastqsanger.gz
	SRR25022268_1.fastq.gz	Fastqsanger.gz

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Epigenetic regulation of cell state by H2AFY governs immunogenicity in high-risk neuroblastoma

Project description:Childhood neuroblastoma with MYCN-amplification is classified as high-risk and often relapses after intensive treatment regimen. Immune checkpoint blockade therapy shows limited efficacy in neuroblastoma patients and the cancer intrinsic immune regulatory network is poorly understood. Here, we leveraged genome-wide CRISPR/Cas9 screens in a human co-culture system and identified H2AFY as a resistance gene to nivolumab. Genetic deletion of H2afy in MYCN-driven neuroblastoma cells reverted in vivo resistance to PD-1 blockade by eliciting concurrent activation of the adaptive and innate immunity. Analysis of single-cell RNA sequencing datasets revealed that H2AFY mRNA was enriched in adrenergic cancer cells and was associated with patient survival. Mapping of the epigenetic and translational landscape demonstrated that H2afy deletion promoted cell transition to a malignant mesenchymal-like state. With a multi-omics approach, we uncovered H2AFY-associated genes that were functionally relevant and prognostic in patients. Altogether, our study elucidates the role of H2AFY as an epigenetic gatekeeper for cell state and immunogenicity in high-risk human neuroblastoma.

2023-09-01 | GSE235736 | GEO

Epigenetic regulation of cell state by H2AFY governs immunogenicity in high-risk neuroblastoma [CUT&RUN]

2024-06-25 | GSE270196 | GEO

Epigenetic regulation of cell state by H2AFY governs immunogenicity in high-risk neuroblastoma [CRISPR/Cas9 screen]

2024-08-22 | GSE275390 | GEO

Epigenetic regulation of cell state by H2AFY governs immunogenicity in high-risk neuroblastoma [CUT&RUN]

Project description:Epigenetic regulation of cell state by H2AFY governs immunogenicity in high-risk neuroblastoma [CUT&RUN]

| PRJNA1125401 | ENA

Epigenetic regulation of cell state by H2AFY governs immunogenicity in high-risk neuroblastoma [CRISPR/Cas9 screen]

Project description:Epigenetic regulation of cell state by H2AFY governs immunogenicity in high-risk neuroblastoma [CRISPR/Cas9 screen]

| PRJNA1150587 | ENA

miRNA expression profiling in high-risk neuroblastoma

Project description:In the present study we evaluated the miRNA expression profile of 31 high risk, stage 4 neuroblastoma patients.

2009-06-27 | GSE16444 | GEO

Network-based, cross-cohort discovery of transcriptional mechanisms presiding over maintenance of high-risk neuroblastoma subtype state

Project description:Network-based analysis of neuroblastoma samples from two large cohorts identified master regulator proteins controlling the transcriptional state of three high-risk molecular subtypes. In particular, a TEAD4-MYCN positive feedback loop emerged as the core regulatory motif of a small protein module presiding over implementation and stability of the subtype associated with MYCN amplification. Specifically, MYCN transcriptionally activates TEAD4, which in turn activates MYCN both transcriptionally and post-translationally. The resulting MYCN-TEAD4 positive feedback loop plays a critical role in maintaining aberrant activity of a 10-protein regulatory module that causally regulates the transcriptional state of this subtype. Consistently, loss of TEAD4 activity induces core module activity collapse and abrogates neuroblastoma cell viability in vitro and in vivo, thus suggesting novel therapeutic strategies for this important childhood cancer. Study of the transcriptional control by TEAD4 and MYCN positive feedback loop using RNA-seq profiles of TEAD4 and MYCN shRNA knockdowns in neuroblastoma BE2 cells. ChIP-Seq analysis using TEAD4 antibody in BE2 cells.

2016-07-18 | E-GEOD-84389 | biostudies-arrayexpress

Oligonucleotide array CGH in high-risk neuroblastoma tumors

Project description:We performed array CGH in high-risk neuroblastoma tumors in order to compare genome aberrations with expression of small non-coding RNAs.

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miRNA expression profiling in high-risk neuroblastoma

Project description:In the present study we evaluated the miRNA expression profile of 31 high risk, stage 4 neuroblastoma patients. We compared miRNA expression profiles of 14 long-survivors (alive with an overall survival time > 36 months) and 17 short-survivors (dead of disease within 36 months from diagnosis. Deaths due to toxicity were censored).

2010-05-16 | E-GEOD-16444 | biostudies-arrayexpress

Nano-targeted double-edged induction of ferroptosis eradicates high-risk neuroblastoma

Project description:High-risk neuroblastoma is a devastating malignancy with few therapeutic options. We identify withaferin A (WA) as a natural ferroptosis inducing agent in neuroblastoma, which acts through a novel double-edged mechanism. WA targets and inactivates glutathione peroxidase 4, as well as increases intracellular labile Fe(II) upon excessive activation of heme oxygenase-1, which both independently result in ferroptosis. This double-edged mechanism results in a high efficacy of WA compared to etoposide in killing a heterogeneous panel of high-risk neuroblastoma cells, and in suppressing neuroblastoma xenografts growth and relapse rate. Nano-targeting of WA allows systemic application and suppressed tumor growth due to an enhanced targeting to the tumor site. Collectively, our data propose a novel therapeutic strategy to kill cancer cells by ferroptosis. High-risk neuroblastoma is a devastating malignancy with few therapeutic options. We identify withaferin A (WA) as a natural ferroptosis inducing agent in neuroblastoma, which acts through a novel double-edged mechanism. WA targets and inactivates glutathione peroxidase 4, as well as increases intracellular labile Fe(II) upon excessive activation of heme oxygenase-1, which both independently result in ferroptosis. This double-edged mechanism results in a high efficacy of WA compared to etoposide in killing a heterogeneous panel of high-risk neuroblastoma cells, and in suppressing neuroblastoma xenografts growth and relapse rate. Nano-targeting of WA allows systemic application and suppressed tumor growth due to an enhanced targeting to the tumor site. Collectively, our data propose a novel therapeutic strategy to kill cancer cells by ferroptosis.

2018-05-01 | GSE112384 | GEO

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