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

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

PROVIDER: PRJNA799749 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR17712049_1.fastq.gz	Fastqsanger.gz
	SRR17712049_2.fastq.gz	Fastqsanger.gz
	SRR17712050_1.fastq.gz	Fastqsanger.gz
	SRR17712050_2.fastq.gz	Fastqsanger.gz
	SRR17712051_1.fastq.gz	Fastqsanger.gz

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Hijacking a neurodevelopmental epigenomic program in metastatic dissemination of medulloblastoma

Project description:Hijacking a neurodevelopmental epigenomic program in metastatic dissemination of medulloblastoma

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

Project description: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 [ATAC-Seq]

Project description: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 [Cut & Run]

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 | GSE194216 | GEO

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

2023-02-28 | GSE194215 | GEO

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

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.

2024-05-06 | GSE266048 | GEO

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

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miRNA expression profiles of pediatric medulloblastoma

Project description:The main cause of death in medulloblastoma is recurrence associated with leptomeningeal dissemination. Although the molecular basis of medulloblastoma has received considerable attention over the past decade, the role of microRNAs (miRNAs) in the acquisition of metastatic phenotype remains poorly understood. This study aimed to identify miRNA involved in leptomeningeal dissemination and to elucidate its target mechanisms. We analyzed miRNA expression profiles of 29 medulloblastomas according to the presence of cerebrospinal fluid (CSF) seeding. The differential expressed miRNAs (DEmiRNAs) were validated on 29 medulloblastoma tissues and three medulloblastoma cells. The biological function of the selected miRNA was evaluated using in vitro studies. A total of 12 DEmiRNAs were identified including miRNA-192 in medulloblastoma with seeding. The reduced expression of miRNA-192 was confirmed in tumor seeding group and the medulloblastoma cells. Overexpression of miRNA-192 inhibited cellular proliferation targeting dihydrofolate reductase (DHFR). MiRNA-192 decreased cellular anchoring via repression of integrin subunits (Î±V, Î²1, and Î²3) and CD47. Medulloblastoma with seeding showed specific DEmiRNAs compared with those without seeding. MicroRNA-192 suppresses leptomeningeal dissemination of medulloblastoma through modulating cell proliferation and anchoring ability. leptomeningeal dissemination in 29 pediatric medulloblastoma patients

2015-12-31 | E-GEOD-66968 | biostudies-arrayexpress

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