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Chromosome loop control of oncogenic MYC produces a common vulnerability in diverse cancers [HiChIP]

ABSTRACT: Chromosome loop control of oncogenic MYC produces a common vulnerability in diverse cancers [HiChIP]

PROVIDER: PRJNA438926 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR6855536_1.fastq.gz	Fastqsanger.gz
	SRR6855536_2.fastq.gz	Fastqsanger.gz

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Chromosome loop control of oncogenic MYC produces a common vulnerability in diverse cancers

Project description:Chromosome loop control of oncogenic MYC produces a common vulnerability in diverse cancers

| PRJNA358692 | ENA

Chromosome loop control of oncogenic MYC produces a common vulnerability in diverse cancers [HiChIP]

Project description:The majority of human cancers become highly dependent on a deregulated MYC oncogene, thus identifying a common mechanism underlying MYC regulation could provide valuable targets for therapy. We show here that diverse tumor-specific super-enhancers acquired throughout the 3Mb MYC insulated neighborhood functionally interact with a single conserved site occupied by CTCF protein in the MYC promoter. CRISPR-mediated deletion analysis shows that this common CTCF site is required for super-enhancer looping to the MYC promoter, high MYC expression and rapid cell proliferation in multiple cancers. Targeted methylation of the MYC enhancer anchor by a dCAS9-DNMT3A-3L fusion protein abrogates CTCF binding with consequent loss of MYC expression, suggesting a common vulnerability and a novel approach for therapeutic targeting of aggressive cancers.

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Chromosome loop control of oncogenic MYC produces a common vulnerability in diverse cancers [4C-seq]

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Chromosome loop control of oncogenic MYC produces a common vulnerability in diverse cancers [ChIP-seq]

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Chromosome loop control of oncogenic MYC produces a common vulnerability in diverse cancers

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

2016-12-24 | GSE92881 | GEO

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CTCF HiChIP data in A673 Ewing sarcoma cell lines (siCT & siSA2)

Project description:STAG2, a member of cohesin, is one of the most recurrently mutated genes in human cancer. Here, we investigated STAG2 function in the context of Ewing sarcoma, an aggressive bone tumor driven by EWS-FLI1 oncogene chimeric transcription factor. A673 Ewing sarcoma cell line was trasfected with siCT or 2 different siRNA targetting STAG2 during 72h and CTCF HiChIP experiments were preformed for each conditions. Analyses of HiChIP data show that STAG2 knowck-down alters CTCF-anchored loop extrusion.

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HiChIP data in A673 & TC71 Ewing cell lines (STAG1 and STAG2 knock-out)

Project description:STAG2, a member of cohesin, is one of the most recurrently mutated genes in human cancer. Here, we investigated STAG2 function in the context of Ewing sarcoma. Using a CRISPR/Cas9 approach, we generated two STAG2 knock-out isogenic clones (A673_SA2m#1 and TC71_SA2m#2) derived from A673 and TC71 STAG2 wild type (WT) Ewing sarcoma cell line. A STAG2 rescue model (A673_SA2r) was generated by correcting the CRISPR mutation in the A673_SA2m#1 model. These STAG1/2 proficient and deficient models were profiled by CTCF HiChIP experiments. STAG2 isogenic models were also profiled by H3K27ac HiChIP experiments. Analyses of HiChIP data allowed to show that STAG2 promotes CTCF-anchored loop extrusion and cis-promoter and -enhancer interactions.

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