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Hijacking a neurodevelopmental epigenomic program in metastatic dissemination of medulloblastoma

ABSTRACT: Hijacking a neurodevelopmental epigenomic program in metastatic dissemination of medulloblastoma

PROVIDER: PRJNA799747 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR17712108_1.fastq.gz	Fastqsanger.gz
	SRR17712108_2.fastq.gz	Fastqsanger.gz
	SRR17712109_1.fastq.gz	Fastqsanger.gz
	SRR17712109_2.fastq.gz	Fastqsanger.gz
	SRR17712110_1.fastq.gz	Fastqsanger.gz

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Hijacking a neurodevelopmental epigenomic program in metastatic dissemination of medulloblastoma [Cut & Run]

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Hijacking a neurodevelopmental epigenomic program in metastatic dissemination of medulloblastoma [RNA-Seq]

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Hijacking a neurodevelopmental epigenomic program in metastatic dissemination of medulloblastoma [RNA-Seq]

Project description:How dysregulation of neurodevelopment relates to medulloblastoma (MB), the most common pediatric brain tumor, remains elusive. Here, we uncovered a neurodevelopmental epigenomic program being hijacked to induce MB metastatic dissemination. Unsupervised analyses by integrating publicly available datasets with our newly generated data revealed that SMARCD3/BAF60C regulates DAB1-mediated Reelin signaling in Purkinje cell migration and MB metastasis by orchestrating cis-regulatory elements (CREs) at the DAB1 locus. We further identified that a core set of transcription factors, enhancer of zeste homolog 2 (EZH2) and nuclear factor I X (NFIX), coordinates with the CREs at the SMARCD3 locus to form a chromatin hub for controlling SMARCD3 expression in the developing cerebellum and metastatic MB. Elevated SMARCD3 activates Reelin/DAB1-mediated Src kinase signaling, resulting in MB response to Src inhibition. These data deepen our understanding of how neurodevelopmental programming influences disease progression and provide a potential therapeutic option for MB patients.

2023-02-28 | GSE194213 | GEO

Hijacking a neurodevelopmental epigenomic program in metastatic dissemination of medulloblastoma [Cut & Run]

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Hijacking a neurodevelopmental epigenomic program in metastatic dissemination of medulloblastoma [ATAC-Seq]

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Hijacking a neurodevelopmental epigenomic program in metastatic dissemination of medulloblastoma

Project description:This SuperSeries is composed of the SubSeries listed below.

2023-02-28 | GSE194217 | GEO

Therapeutic radiation drives leptomeningeal dissemination of medulloblastoma [scRNA-seq]

Project description:In this study, we examine the effect of radiation on the transcriptional profile of medulloblastoma tumor cells and its microenvironment that could potentially be leading to metastatic dissemination.

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Therapeutic radiation drives leptomeningeal dissemination of medulloblastoma [bulkRNA-seq]

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HDAC and NFκB antagonists synergistically inhibit growth and metastatic dissemination of MYC-driven medulloblastoma

Project description:Aberrant oncogenic activation of MYC drives tumorigenesis in the most aggressive subset of medulloblastoma, the most common malignant brain tumor in childhood. Metastatic dissemination at diagnosis and at recurrence is commonly observed in MYC-driven medulloblastomas. Since these tumors display remarkable resistance to standard multimodal therapeutic approaches, epigenetic modulators commonly altered in these tumors are highly promising targets for novel therapeutic approaches. Here, we report on a cross-entity, high-throughput epigenetic drug screen to evaluate therapeutic vulnerabilities in the most common malignant primary brain tumors. Specifically, we performed a primary screen including 78 epigenetic inhibitors and a secondary screen including 20 histone deacetylase inhibitors (HDACi) to compare response profiles in atypical teratoid/rhabdoid tumor (AT/RT, n=11), medulloblastoma (n=14), and glioblastoma (n=14). This unbiased approach revealed preferential activity of HDACi in MYC-driven medulloblastoma. Importantly, the class I selective HDACi CI-994 showed significant cell viability reduction mediated by induction of apoptosis in MYC-driven medulloblastoma, with little to no activity in non-MYC-driven medulloblastoma, AT/RT, and glioblastoma in vitro. Notably, CI-994 displayed antitumoral effects at the primary site and the metastatic compartment in two orthotopic mouse models of MYC-driven medulloblastoma. Furthermore, synergistic drug screening and RNA sequencing revealed NFκB pathway induction as a mechanism of resistance to CI-994 treatment. Taken together, our findings identified MYC pathway activation as a predictive biomarker for epigenetic treatment intervention in high-risk medulloblastoma and provide a preclinical rationale for further exploration of CI-994 combined with NFκB pathway inhibitors in the treatment of MYC-driven medulloblastoma.

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