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

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

PROVIDER: PRJNA562258 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR10022447_1.fastq.gz	Fastqsanger.gz
	SRR10022447_2.fastq.gz	Fastqsanger.gz
	SRR10022448_1.fastq.gz	Fastqsanger.gz
	SRR10022448_2.fastq.gz	Fastqsanger.gz
	SRR10022449_1.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.

2020-08-15 | GSE136213 | GEO

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 [ChIP-seq]

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

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

Project description:Up-regulation of the neuropeptide NTS in a subgroup of lung cancers has been linked to poor prognosis. However, the regulatory pathway centered on NTS in lung cancer remains unclear. Here we identified the NTS specific enhancer in lung adenocarcinoma cells. The AF4/FMR2 (AFF) family protein AFF1 occupies the NTS enhancer and inhibits NTS transcription. Clustering analysis of lung adenocarcinoma gene expression data demonstrated that NTS is highly positively correlated with the expression of the oncogenic factor CPS1. Detailed analyses demonstrated that NTS antagonizes the IL6 pathway in regulating CPS1. Thus, our analyses revealed a novel NTS centered regulatory axis, consisting of AFF1 as a master transcription suppressor and IL6 as an antagonist in lung adenocarcinoma cells.

2021-03-23 | GSE164098 | GEO

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.

2020-10-28 | GSE147159 | GEO

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

Project description:Human Accelerated Regions (HARs) are conserved genomic loci that evolved at an accelerated rate in the human lineage and may underlie human-specific traits. We generated HARs and chimpanzee accelerated regions with an automated pipeline and an alignment of 251 mammalian genomes. Combining deep-learning with chromatin capture experiments in human and chimpanzee neural progenitor cells, we discovered a significant enrichment of HARs in topologically associating domains (TADs) containing human-specific genomic variants that change three-dimensional (3D) genome organization. Differential gene expression between humans and chimpanzees at these loci suggests rewiring of regulatory interactions between HARs and neurodevelopmental genes. Thus, comparative genomics together with models of 3D genome folding revealed enhancer hijacking as an explanation for the rapid evolution of HARs.

2022-12-21 | GSE183137 | GEO

An overlooked prebiotic: beneficial effect of dietary nucleotide supplementation on gut microbiota and metabolites in senescence-accelerated mouse prone-8 mice

Project description:Nucleotides (NTs) are regulatory factors in many biological processes and play important roles in the growth, development, and metabolism of living organisms. We used senescence-accelerated mouse prone-8 (SAMP8) to investigate the effects of NTs on the gut microbiota and metabolites. And the promoting effect of NTs on the growth of a probiotic (Lactobacillus casei) was explored through in vitro experiments. The results showed that the sequencing depth of 16S rDNA covered all microbial species in the feces of SAMP8. Supplementation with exogenous NTs to the diet enhanced the diversity of the gut microbiota, reduced the abundance of bacteria with negative effects on the body (such as Verrucomicrobia, Ruminococcaceae, Akkermansia and Helicobacter), and increased the abundance of the microbiota, which had beneficial effects on the mice (such as Lactobacillus, Candidatus saccharimonas and Lachnospiraceae_NK4A136_group). Metabonomic analysis showed that NT deficiency in the diet significantly affected metabolites in the mouse feces. The metabolites in mice supplemented with NTs tended to be normal (SAMR1). The differentially expressed metabolites caused by NT addition are involved in various pathways in the body, including linoleic acid metabolism, vitamin B6 metabolism, and histidine metabolism. Correlation analysis revealed a significant correlation between the gut microbiota and differentially expressed metabolites caused by the addition of NTs. In vitro experiments showed that NTs significantly promoted the growth, secretion of biofilm and extracellular polymeric substance of L. casei. NTs also promoted the ability of the crude extract of L. casei to resist the secretion of Shigella biofilm. Thus, NTs can regulate the abundance of the gut microbiota and alter the metabolic expression of the intestinal microbiome.

2022-03-21 | MTBLS4012 | MetaboLights

Effects of VNS on the NTS

Project description:Effects of VNS on the NTS

| PRJNA783894 | ENA