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Dynamic Chromatin Alteration Induces Oncogenic Hijacking by Nuclear Factor I Family Proteins for Medulloblastoma Progression

ABSTRACT: Dynamic Chromatin Alteration Induces Oncogenic Hijacking by Nuclear Factor I Family Proteins for Medulloblastoma Progression

PROVIDER: PRJNA1008757 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR25750700_1.fastq.gz	Fastqsanger.gz
	SRR25750700_2.fastq.gz	Fastqsanger.gz
	SRR25750701_1.fastq.gz	Fastqsanger.gz
	SRR25750701_2.fastq.gz	Fastqsanger.gz
	SRR25750702_1.fastq.gz	Fastqsanger.gz

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Dynamic Chromatin Alteration Induces Oncogenic Hijacking by Nuclear Factor I Family Proteins for Medulloblastoma Progression

Project description:The cancer-specific epigenome is the critical scaffold on which genetic programs work to positively promote cancer growth and progression. Understanding and appropriately disrupting this epigenome will lead to the discovery of new, more extensive and effective therapies in addition to conventional personalized medicine that relies on genomic mutations. However, the epigenomic changes during the process from normal cells to cancer formation as well as the molecules involved in the maintenance of the aberrant epigenome are still poorly characterized, and the development of epigenome-based therapeutics is therefore undeniably stagnant. To address this issue, we here focus on SHH-subgroup medulloblastoma, a representative pediatric brain tumor for which we developed a reliable mouse model to capture the epigenomic changes that cerebellar granule cells, the cells of origin, undergo during tumorigenesis. By comparing the epigenomes of the different stages of transforming cells, we identified NFI family of developmental factors as oncogenic regulators in the epigenome of pre-cancerous and cancerous cells, which they also contribute to maintain. Furthermore, we report pharmacological experiments demonstrating that inhibition of NFIB methylation blocks tumor growth and increases sensitivity to molecularly targeted drugs by disrupting the cancer epigenome. Thus, this study is a unique example of how epigenomic studies of cancer have led directly to therapeutic insights, and similar approaches in various cancers would accelerate the establishment of novel therapies.

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Project description:Using ATAC-seq analysis from GNPs to MBSHH we discovered a massive modification in chromatin accessibility during MBSHH formation. Next, using integrative bioinformatics, we identified genes of the nuclear factor I (NFI) family that function as oncogenes on the MBSHH epigenome. We demonstrate not only that these genes are essential in the early stages of murine MBSHHs tumorigenesis, but also that their genetic silencing inhibits tumor growth in murine and human MBSHHs in vitro and in vivo. Finally, we discovered that NFIA/B are post-translationally modified by an activating methylation in MBSHH, making it possibility to target this pathway. Further studies revealed that pharmacological inhibition of this methylated NFIA/B hindered tumor proliferation, demonstrating the requirement of NFIA/B for tumor progression. Collectively our data shed light on the mechanism underlying the epigenome during the formation of the most malignant pediatric brain tumor and emphasizes the importance of deciphering cancer-specific epigenome for identification of new therapeutic avenues.

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