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Integrated Enhancer Regulatory Network by Enhancer-Promoter Looping in Gastric Cancer (HiChIP)

ABSTRACT: Integrated Enhancer Regulatory Network by Enhancer-Promoter Looping in Gastric Cancer (HiChIP)

PROVIDER: PRJNA1039486 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR26798114_1.fastq.gz	Fastqsanger.gz
	SRR26798114_2.fastq.gz	Fastqsanger.gz
	SRR26798115_1.fastq.gz	Fastqsanger.gz
	SRR26798115_2.fastq.gz	Fastqsanger.gz
	SRR26798116_1.fastq.gz	Fastqsanger.gz

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ZNF143 deletion alters enhancer/promoter looping and CTCF/cohesin geometry [HiChIP]

Project description:ZNF143 deletion alters enhancer/promoter looping and CTCF/cohesin geometry [HiChIP]

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Integrated Enhancer Regulatory Network by Enhancer-Promoter Looping in Gastric Cancer

Project description:Integrated Enhancer Regulatory Network by Enhancer-Promoter Looping in Gastric Cancer

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Integrated Enhancer Regulatory Network by Enhancer-Promoter Looping in Gastric Cancer (4C)

Project description:Integrated Enhancer Regulatory Network by Enhancer-Promoter Looping in Gastric Cancer (4C)

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Integrated Enhancer Regulatory Network by Enhancer-Promoter Looping in Gastric Cancer (ChIP)

Project description:Integrated Enhancer Regulatory Network by Enhancer-Promoter Looping in Gastric Cancer (ChIP)

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Integrated Enhancer Regulatory Network by Enhancer-Promoter Looping in Gastric Cancer (HiChIP)

Project description:Enhancer as a cis-regulatory element (CRE), plays a critical role in gene regulation at many stages of cell growth. Meanwhile, enhancers in cancer cells also act as a regulator controlling oncogene transcription. In this study, we did a comprehensive analysis of long-range chromatin interactions, histone modifications, chromatin status, and expressions of two gastric cancer (GC) cell lines, compared with a human normal epithelial cell line. We found that GC-specific enhancers marked by histone modifications in gastric cancer can activate a population of genes including some oncogenes by enhancer-promoter (E-P) interactions. In addition, motif analysis of E-P interacted enhancers showed that three GC-specific TF sequences may regulate enhancer-interacting gene activation. We found MYB which is crucial for GC cellular growth and is activated by TCF7 regulated E-P loop. To validate this mechanism, we applied CRISPRi (dCas9-KRAB) induced transcriptional regulatory element inactivation in our target enhancer, the growth assay resulted in significant inhibition of cell growth in two GC cell lines. In conclusion, we found oncogene activation by aberrant loop formation that contributes to tumorigenesis in GC.

2024-04-22 | GSE247536 | GEO

Integrated Enhancer Regulatory Network by Enhancer-Promoter Looping in Gastric Cancer (RNA-seq)

Project description:Integrated Enhancer Regulatory Network by Enhancer-Promoter Looping in Gastric Cancer (RNA-seq)

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Integrated Enhancer Regulatory Network by Enhancer-Promoter Looping in Gastric Cancer (ChIP)

2024-04-22 | GSE247537 | GEO

Integrated Enhancer Regulatory Network by Enhancer-Promoter Looping in Gastric Cancer (4C)

2024-04-22 | GSE262406 | GEO

ZNF143 deletion alters enhancer/promoter looping and CTCF/cohesin geometry [HiChIP]

Project description:The transcription factor ZNF143 contains seven tandem zinc fingers and is involved in 3D genome construction; however, the mechanism by which ZNF143 functions in chromatin looping remains unclear. Here, we show that ZNF143 directionally recognizes diverse genomic sites and is required for chromatin looping between these sites. In addition, ZNF143 is located between CTCF and cohesin at numerous CTCF sites and ZNF143 removal narrows the space between CTCF and cohesin. Moreover, genetic deletion of ZNF143, in conjunction with acute CTCF depletion, revealed that ZNF143 and CTCF collaborate to regulate higher-order genome organization. Thus, ZNF143 is recruited by CTCF to the CTCF sites to regulate TAD formation and genome compartmentalization whereas directional recognition of DNA motifs directly by ZNF143 itself regulates promoter activity via chromatin looping.

2023-11-07 | GSE236635 | GEO

FOXF1 promoter-putative enhancer chromatin looping

Project description:To determine if there is a physical interaction between the FOXF1 promoter and putative enhancer sequences ~250kb upstream of the promoter chromosome conformation capture-on-chip (4C) analysis was performed. An unanticipated and tremendous amount of the non-coding sequences of the human genome are transcribed. Long non-coding RNAs (lncRNAs) are non-protein coding transcripts longer than 200 nucleotides and their functions remain enigmatic. We demonstrate that deletions of lncRNA genes cause a lethal lung developmental disorder, Alveolar Capillary Dysplasia with Misalignment of Pulmonary Veins (ACD/MPV), with parent of origin effects. We identify non-coding overlapping deletions 250 kb upstream to FOXF1 in nine patients with ACD/MPV that arose de novo specifically on the maternally inherited chromosome and delete a fetal lung-specific EST, part of an lncRNA. These deletions define distant cis-regulatory region that harbors a differentially methylated CpG island, binds GLI2 depending on the methylation status of this CpG island, and physically interacts with and up-regulates the FOXF1 promoter, consistent with the absence of the fetal lung-transcribed lncRNA perturbing FOXF1 regulation. LncRNA-mediated chromatin interactions may be responsible for position effect phenomenon and potentially cause many disorders of human development. 4C analysis using 16q24.1 specific 3x720K arrays demonstrated physical interaction between the FOXF1 promoter and distant putative regulatory sequences, about 250 kb upstream in human pulomonary microvascular endothelial cells; 2 biological replicates performed; this chromatin looping was not detected in lymphoblasts that do not express FOXF1 and hence serve as a negative control.

2012-07-10 | E-GEOD-39256 | biostudies-arrayexpress

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