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3D Chromatin Remodeling Potentiates Transcriptional Programs Driving Cell Invasion [Hi-C]

ABSTRACT: 3D Chromatin Remodeling Potentiates Transcriptional Programs Driving Cell Invasion [Hi-C]

PROVIDER: PRJNA760456 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR15712676_1.fastq.gz	Fastqsanger.gz
	SRR15712676_2.fastq.gz	Fastqsanger.gz
	SRR15712677_1.fastq.gz	Fastqsanger.gz
	SRR15712677_2.fastq.gz	Fastqsanger.gz
	SRR15712678_1.fastq.gz	Fastqsanger.gz

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3D Chromatin Remodeling Potentiates Transcriptional Programs Driving Cell Invasion

Project description:3D Chromatin Remodeling Potentiates Transcriptional Programs Driving Cell Invasion

| PRJNA760454 | ENA

3D Chromatin Remodeling Potentiates Transcriptional Programs Driving Cell Invasion [Hi-C]

Project description:Epigenetic mechanisms often play an important role in driving tumor progression towards metastasis. It is less clear that deregulation of chromatin architecture, including topologically associated domains (TADS), contributes to cancer progression. CTCF is a central regulator of three dimensional chromatin structure that undergoes copy number loss in over half of all breast cancers, but the impact of this defect on epigenetic programming and chromatin architecture remains obscure. We find that the reduced pools of CTCF in hemizygous models potentiates cell invasion. Underlying this phenotype is the activation of oncogenic networks including the PI3K signaling cascade, which presents therapeutic vulnerabilities, especially to mTOR inhibitors. Deregulation of these oncogenic pathways is largely due to the loss of CTCF insulation, allowing a reorganization of long-range chromatin contacts at the subTAD level that is associated with aberrant programming of H3K27 acetylation at enhancer/promoter regions. Thus, lowered CTCF levels lead to chromatin reorganization facilitating pro-invasive transcriptional programs.

2022-01-01 | GSE183378 | GEO

3D Chromatin Remodeling Potentiates Transcriptional Programs Driving Cell Invasion [RNA-Seq]

Project description:3D Chromatin Remodeling Potentiates Transcriptional Programs Driving Cell Invasion [RNA-Seq]

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3D Chromatin Remodeling Potentiates Transcriptional Programs Driving Cell Invasion [ChIP-Seq]

Project description:3D Chromatin Remodeling Potentiates Transcriptional Programs Driving Cell Invasion [ChIP-Seq]

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3D Chromatin Remodeling Potentiates Transcriptional Programs Driving Cell Invasion [RNA-Seq]

2022-01-01 | GSE183380 | GEO

3D Chromatin Remodeling Potentiates Transcriptional Programs Driving Cell Invasion [ChIP-Seq]

2022-01-01 | GSE183379 | GEO

3D Chromatin Remodeling Potentiates Transcriptional Programs Driving Cell Invasion

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

2022-01-01 | GSE183381 | GEO

Systematic identification of molecular pathways driving GBM invasion

Project description:Glioblastoma multiforme (GBM) is the most prevalent and deadliest adult brain tumor. To systematically characterize the pathways governing brain invasion, we developed a three-dimensional (3D) ex vivo organotypic invasion model with clinical relevance to GBM. We used this model to enrich for highly invasive GBM cell population. Using next-generation sequencing to transcriptomically profile highly invasive and poorly invasive GBM cell populations, we have identified a network of extracellular matrix (ECM) components, including multiple collagens and collagen-interacting proteins, which are upregulated by invading GBM cells and strongly correlate in expression with clinical glioma progression outcomes. We identify the interferon regulatory factor 3 (IRF3) as a direct transcriptional repressor of ECM factors in GBM and show that IRF3 acts as an endogenous suppressor of GBM invasion. Therapeutic activation of IRF3 by inhibiting casein kinase 2 (CK2) -- a negative regulator of IRF3 phosphorylation -- downregulated the expression of ECM factors and suppressed GBM invasion in ex vivo and in vivo models across a panel of patient-derived GBM cell lines representative of the main molecular GBM subtypes in the clinic. Our findings illustrate an integrated and systematic approach for the discovery of novel pathways regulating brain tumor invasion and provide a strong mechanistic insight into the notorious, yet poorly understood, invasion capacity of GBM tumors.

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Wnt-signaling potentiates nevogenesis.

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PHGDH heterogeneity potentiates cancer cell dissemination and metastasis

Project description:Cancer metastasis requires the transient activation of cellular programs enabling dissemination and seeding in distant organs. Genetic, transcriptional and translational heterogeneity contributes to this dynamic process. Metabolic heterogeneity has also been observed, yet its role for cancer progression is less explored. Here, we discover that loss of phosphoglycerate dehydrogenase (PHGDH) potentiates metastatic dissemination. Specifically, we find that heterogeneous or low PHGDH expression in primary tumors of breast cancer patients is associated with decreased metastasis free survival time. In mice, circulating tumor cells and early metastatic lesions are enriched with PHGDH low cancer cells and silencing PHGDH in primary tumors increases metastasis formation. Mechanistically, PHGDH protein interacts with the glycolytic enzyme phosphofructokinase (PFK) and the loss of this interaction activates the hexosamine – sialic acid pathway, which provides precursors for protein glycosylation. Consequently, aberrant protein glycosylation including increased sialylation of integrin αvβ3 occurs, which potentiates cell migration and invasion. Inhibition of sialic acid metabolism counteracts the metastatic capacity of PHGDH low cancer cells. In conclusion, while the catalytic activity of PHGDH supports cancer cell proliferation, low PHGDH protein expression non-catalytically potentiates cancer dissemination and metastasis formation. Thus, the presence of PHDGH heterogeneity in primary tumors may be considered a sign of tumor aggressiveness.

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