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Stranded RNA-seq were performed on total RNA following ribosomal RNAs depletion (Ribo-zero removal kit, illumina) for glioblastoma stem cell

ABSTRACT: Stranded RNA-seq were performed on total RNA following ribosomal RNAs depletion (Ribo-zero removal kit, illumina) for glioblastoma stem cell

PROVIDER: PRJNA678319 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR13057287_1.fastq.gz	Fastqsanger.gz
	SRR13057287_2.fastq.gz	Fastqsanger.gz
	SRR13057288_1.fastq.gz	Fastqsanger.gz
	SRR13057288_2.fastq.gz	Fastqsanger.gz

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Stranded RNA-seq were performed on total RNA following ribosomal RNAs depletion (Ribo-zero removal kit, illumina) for 3 brain , 8 IDHwt and 5 IDHmut glioma samples.

Project description:Stranded RNA-seq were performed on total RNA following ribosomal RNAs depletion (Ribo-zero removal kit, illumina) for 3 brain , 8 IDHwt and 5 IDHmut glioma samples.

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Stranded RNA-seq were performed on total RNA following ribosomal RNAs depletion (Ribo-zero removal kit, illumina) for glioblastoma stem cell

Project description:In human, the 39 coding HOX genes and 18 referenced non-coding antisense transcripts are arranged in four genomic clusters named HOXA, B, C, and D. This highly conserved family belongs to the homeobox class of genes that encode transcription factors required for normal development. Therefore, HOX gene deregulation might contribute to the development of many cancer types. Here, we study HOX gene deregulation in adult glioma, a common type of primary brain tumor. We performed extensive molecular analysis of tumor samples, classified according to their isocitrate dehydrogenase (IDH1) gene mutation status, and of glioma stem cells. We found widespread expression of sense and antisense HOX transcripts only in aggressive (IDHwt) glioma samples, although the four HOX clusters displayed DNA hypermethylation. Integrative analysis of expression-, DNA methylation- and histone modification signatures along the clusters revealed that HOX gene upregulation relies on canonical and alternative bivalent CpG island promoters that escape hypermethylation. H3K27me3 loss at these promoters emerges as the main cause of widespread HOX gene upregulation in IDHwt glioma cell lines and tumors. Our study provides the first comprehensive description of the epigenetic changes at HOX clusters and their contribution to the transcriptional changes observed in adult glioma. It also identified putative "master" HOX proteins that might contribute to the tumorigenic potential of glioma stem cells.

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