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Next Generation Sequencing Facilitates Quantitative Analysis of SETD6 Knock-out and stable expression of TWIST1 in Glioblastoma cells

ABSTRACT: Next Generation Sequencing Facilitates Quantitative Analysis of SETD6 Knock-out and stable expression of TWIST1 in Glioblastoma cells

PROVIDER: PRJNA772191 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR16465587.fastq.gz	Fastqsanger.gz
	SRR16465588.fastq.gz	Fastqsanger.gz
	SRR16465589.fastq.gz	Fastqsanger.gz
	SRR16465590.fastq.gz	Fastqsanger.gz
	SRR16465591.fastq.gz	Fastqsanger.gz

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Next Generation Sequencing Facilitates Quantitative Analysis of SETD6 Knock-out and stable expression of TWIST1 in Glioblastoma cells

Project description:The goal of this study was to identifiy shared target genes for SETD6 and TWIST1 in Glioblastoma.

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Next Generation Sequencing Facilitates Quantitative Analysis of Wild Type and TWIST1 knock out U87 xenograft mice transcriptomes

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TWIST1 methylation by SETD6 selectively antagonizes LINC-PINT expression in Glioblastoma multiforme

Project description:Glioblastoma multiforme (GBM) is the most common and aggressive malignant brain tumor among adults, which is characterized by high invasion, migration and proliferation abilities. One important process that contributes to the invasiveness of GBM is the epithelial to mesenchymal transition (EMT). EMT is regulated by a set of defined transcription factors which tightly regulate this process, among them is the basic helix-loop-helix family member, TWIST1. Here we show that TWIST1 is methylated on lysine-33 at chromatin by SETD6, a methyltransferase with expression levels correlating with poor survival in GBM patients. RNA-seq analysis in U251 GBM cells suggested that both SETD6 and TWIST1 regulate cell adhesion and migration processes. We further show that TWIST1 methylation attenuates the expression of the long-non-coding RNA, LINC-PINT, thereby suppressing EMT in GBM. Mechanistically, TWIST1 methylation represses the transcription of LINC-PINT by increasing the occupancy of EZH2 and the catalysis of the repressive H3K27me3 mark at the LINC-PINT locus. Under un-methylated conditions, TWIST1 dissociates from the LINC-PINT locus, allowing the expression of LINC-PINT which leads to increased cell adhesion and decreased cell migration. Together, our findings unravel a new mechanistic dimension for selective expression of LINC-PINT mediated by TWIST1 methylation.

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TWIST1 expression is associated with high-risk neuroblastoma and promotes primary and metastatic tumor growth

Project description:Our aim was to investigate the contribution of TWIST1 on Neuroblastoma (NB) tumor formation and dissemination using TWIST1 knock-out (KO) in the SK-N-Be2C cell line.

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