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

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

PROVIDER: PRJNA1125401 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR29462191_1.fastq.gz	Fastqsanger.gz
	SRR29462191_2.fastq.gz	Fastqsanger.gz
	SRR29462192_1.fastq.gz	Fastqsanger.gz
	SRR29462192_2.fastq.gz	Fastqsanger.gz
	SRR29462193_1.fastq.gz	Fastqsanger.gz

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

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.

2024-06-25 | GSE270196 | GEO

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

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

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

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

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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

Identification of CTCF binding sites through CUT&RUN sequencing in the neuroblastoma cell line CLB-GA.

Project description:CUT&RUN sequencing to define binding sites for CTCF and IgG in the neuroblastoma cell line CLB-GA.

2023-02-23 | E-MTAB-12586 | biostudies-arrayexpress

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 treatments. Immune checkpoint blockade therapy against the PD-1/L1 axis shows limited efficacy in patients with neuroblastoma, and the cancer intrinsic immune regulatory network is poorly understood. Here, we leverage genome-wide CRISPR/Cas9 screens and identify H2AFY as a resistance gene to the clinically approved PD-1 blocking antibody nivolumab. Analysis of single-cell RNA-Seq datasets reveals that H2AFY mRNA is enriched in adrenergic cancer cells and is associated with worse patient survival. Genetic deletion of H2afy in MYCN-driven neuroblastoma cells reverts in vivo resistance to PD-1 blockade by eliciting activation of the adaptive and innate immunity. Mapping of the epigenetic and translational landscape demonstrates that H2afy deletion promotes cell transition to a mesenchymal-like state. With a multiomics approach, we uncovered H2AFY-associated genes that are functionally relevant and prognostic in patients. Altogether, our study elucidates the role of H2AFY as an epigenetic gatekeeper for cell states and immunogenicity in high-risk neuroblastoma.

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Identification of SOX11 binding sites through CUT&RUN sequencing in the neuroblastoma cell lines IMR-32, CLB-GA, NGP and SH-EP

Project description:CUT&RUN sequencing to define binding sites for SOX11 and IgG in the neuroblastoma cell lines IMR-32, CLB-GA and NGP as well as neuroblastoma cell line SH-EP after SOX11 overexpression for 48h. A SOX11 inducible overexpression system was generated using a Tet-on system.

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Transcriptonal and epigenetic profiling of neuroblastoma cells based on CD49b expression

Project description:This study was undertaken to assess heterogeneity within neuroblastoma cell populations, and to assess whether the integrin CD49b can distinguish different neuroblastoma phenotypes. Methods: We performed bulk RNA sequencing on Neuro-2a and SH-SY5Y neuroblastoma cells sorted based on CD49b expression, and CUT&RUN for H3K4me1 and H3K27ac on Neuro-2a cells sorted based on CD49b expression. Results: We find that CD49b expression identifies transcriptionally distinct neuroblastoma cell populations. High CD49b expression marks cells expressing mesenchymal genes, while lack of CD49 denotes cells expression neuronal genes. CUT&RUN analysis shows that CD49b distinguishes cells with distinct enhancer and super enhancer profiles. Conclusion: RNA sequencing and CUT&RUN demonstrate that neuroblastoma cell lines include heterogeneous populations.

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