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AVEN is an indirectly druggable mediator of neuroblastoma cell tumorigenicity and chemotherapy resistance [RNA-seq]

ABSTRACT: AVEN is an indirectly druggable mediator of neuroblastoma cell tumorigenicity and chemotherapy resistance [RNA-seq]

PROVIDER: PRJNA540519 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR8992770.fastq.gz	Fastqsanger.gz
	SRR8992771.fastq.gz	Fastqsanger.gz
	SRR8992772.fastq.gz	Fastqsanger.gz
	SRR8992765.fastq.gz	Fastqsanger.gz
	SRR8992766.fastq.gz	Fastqsanger.gz

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AVEN is an indirectly druggable mediator of neuroblastoma cell tumorigenicity and chemotherapy resistance

Project description:AVEN is an indirectly druggable mediator of neuroblastoma cell tumorigenicity and chemotherapy resistance

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AVEN is an indirectly druggable mediator of neuroblastoma cell tumorigenicity and chemotherapy resistance [microarray]

Project description:AVEN is an indirectly druggable mediator of neuroblastoma cell tumorigenicity and chemotherapy resistance [microarray]

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AVEN is an indirectly druggable mediator of neuroblastoma cell tumorigenicity and chemotherapy resistance [microarray]

Project description:Approximately half of children diagnosed with neuroblastoma have aggressive high-risk disease, against which current multimodal therapy has little success. New targets for therapeutic intervention are urgently needed. In a systems approach, we combined time-resolved mRNA-Seq with miRNA profiling in a model of neuroblastoma differentiation treated with or without the clinically approved histone deacetylase inhibitor, panobinostat. Treatment most strongly regulated miR-630, which strongly downregulated AVEN, an inhibitor of apoptosis. Here we characterized AVEN for the first time in neuroblastoma pathogenesis, disclosed its epigenetic regulation and discovered correlations between AVEN expression and resistance to chemotherapy. High-level AVEN expression in 649 primary neuroblastomas negatively correlated with patient survival. Stably enforcing AVEN expression in BE(2)-C cells markedly promoted growth as subcutaneous xenografts in mice, while CRISP/Cas9-mediated AVEN knockout in BE(2)-C cells substantially reduced xenograft growth and enhances the efficacy of systemic doxorubicin treatment. Cell-based assays, flow cytometric cell cycle analyses and SILAC experiments demonstrate that AVEN is required for neuroblastoma proliferation.

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AVEN is an indirectly druggable mediator of neuroblastoma cell tumorigenicity and chemotherapy resistance [RNA-seq]

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AVEN is an indirectly druggable mediator of neuroblastoma cell tumorigenicity and chemotherapy resistance

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

2023-07-30 | GSE130524 | GEO

System-Wide Analysis Reveals a Complex Network of Tumor-Fibroblast Interactions Involved in Tumorigenicity

Project description:Weâve undertaken a genome-wide approach to identify and test genes in fibroblasts that are both induced upon interaction with basal breast cancer cells in culture and upregulated in stromal cells from primary human breast cancers. Several of the upregulated genes encode secreted growth factors or cytokines. Using RNAi and a co-injection tumorigenicity assay, we determined that the majority of secreted factors selected for functional validation played significant, yet functionally diverse, roles in promoting tumorigenicity. Rather than a single major mediator, these results indicate multiple points of intervention to prevent fibroblasts from supporting basal breast cancer. Additionally, we show that breast cancer subtypes differ markedly in the expression of these and other stromally secreted proteins using data from microdissected stromal samples. Induction of genes in four different fibroblast strains (HFFF2, HFF1, CCD1112Sk and Wi38) upon coculture with Cal51 and MDAMB231 human basal breast cancer cell lines. Monocultures of each group are used as the experimental control with each group having 3-4 independent biological replicates.

2013-11-21 | E-GEOD-41678 | biostudies-arrayexpress

System-Wide Analysis Reveals a Complex Network of Tumor-Fibroblast Interactions Involved in Tumorigenicity

Project description:We’ve undertaken a genome-wide approach to identify and test genes in fibroblasts that are both induced upon interaction with basal breast cancer cells in culture and upregulated in stromal cells from primary human breast cancers. Several of the upregulated genes encode secreted growth factors or cytokines. Using RNAi and a co-injection tumorigenicity assay, we determined that the majority of secreted factors selected for functional validation played significant, yet functionally diverse, roles in promoting tumorigenicity. Rather than a single major mediator, these results indicate multiple points of intervention to prevent fibroblasts from supporting basal breast cancer. Additionally, we show that breast cancer subtypes differ markedly in the expression of these and other stromally secreted proteins using data from microdissected stromal samples.

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Microplitis mediator

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Epigenetic regulation of MYC modulates glioblastoma tumorigenicity

Project description:One aspect of intra-tumoral heterogeneity in glioblastoma involves subpopulations of cells capable of self-renewal and indefinite propagation. Conceptually, this capacity is frequently treated as a static property. Here we provide data suggesting that tumorigenicity in glioblastomais a dynamic property that can be acquired or lost. Integrated expression analyses suggest that tumorigenicity is determined by the level of MYC expression relative to a threshold. Transitions between tumorigenic and non-tumorigenic cell states are associated with changes in histone modifications at the MYC locus, suggesting tumorigenicity is epigenetically regulated.

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Epigenetic regulation of MYC modulates glioblastoma tumorigenicity

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