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CTCF orchestrated enhancer hijacking accelerated tumorigenesis through remodeling 3D chromosomal architecture in NTS locus [ChIP-seq]

ABSTRACT: CTCF orchestrated enhancer hijacking accelerated tumorigenesis through remodeling 3D chromosomal architecture in NTS locus [ChIP-seq]

PROVIDER: PRJNA562261 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR10022450_1.fastq.gz	Fastqsanger.gz
	SRR10022450_2.fastq.gz	Fastqsanger.gz
	SRR10022451_1.fastq.gz	Fastqsanger.gz
	SRR10022451_2.fastq.gz	Fastqsanger.gz

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CTCF orchestrated enhancer hijacking accelerated tumorigenesis through remodeling 3D chromosomal architecture in NTS locus

Project description:CTCF orchestrated enhancer hijacking accelerated tumorigenesis through remodeling 3D chromosomal architecture in NTS locus

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CTCF orchestrated enhancer hijacking accelerated tumorigenesis through remodeling 3D chromosomal architecture in NTS locus

Project description:We identified aberrant CTCF binding lead to a 3D chromosomal interactional driver in NTS locus that accelerates tumorigenesis of uveal melanoma. Both enhancer deletion and abolishing CTCF binding lead to the loss of chromosomal looping and triggered therapeutic efficacy in inhibiting tumorigenesis. Our study shed light on a functional chromosomal architecture induced enhancer hijacking, thereby provide novel concept of 3D-chromosomal conformation exploration.

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CTCF orchestrated enhancer hijacking accelerated tumorigenesis through remodeling 3D chromosomal architecture in NTS locus [RNA-seq]

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CTCF orchestrated enhancer hijacking accelerated tumorigenesis through remodeling 3D chromosomal architecture in NTS locus [ChIP-seq]

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CTCF orchestrated enhancer hijacking accelerated tumorigenesis through remodeling 3D chromosomal architecture in NTS locus [RNA-seq]

Project description:CTCF orchestrated enhancer hijacking accelerated tumorigenesis through remodeling 3D chromosomal architecture in NTS locus [RNA-seq]

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Suppression of the NTS-CPS1 regulatory axis by AFF1 in lung adenocarcinoma cells

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The role of NTS/NTSR1 signal in pancreatic cancer progression

Project description:Pancreatic cancer is one of the uncurable cancers and 5-year survival rate is still under 10 %. Therefore, it is urgent to identify a new molecular target for cure. In this study, the mouse serial transplantations by pancreatic orthotopic inoculation model were utilized for screening of new targets. The gene expression of highly malignant cancer cell lines, established in our previous study, showed increased expression of neurotensin receptor-1 (NTSR1). Re-analysis of clinical databases revealed that its expression was higher in pancreatic cancer dependent upon its stage. Overexpression of NTSR1 in SUIT-2 and Panc-1 cells accelerated tumorigenic and metastatic ability in vivo. RNA-sequence analysis revealed that MAPK and NF-kB signaling pathway were activated with neurotensin (NTS) stimulation in highly malignant cancer cell lines from Panc-1 cells. Moreover, NTS induced not only MMP-9, but also CTGF and other pro-inflammatory cytokines and chemokines. Administration of SR48692, a selective antagonist for NTSR1, suppressed tumorigenicity in vivo. These data suggested that NTSR1 can be a diagnostic marker and a new molecular target for pancreatic cancer treatment.

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Three-dimensional genome re-wiring in loci with Human Accelerated Regions

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Project description:Effects of VNS on the NTS

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