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RNA-seq analysis after ASCL1 overexpression in GI-MEN cells [Part 1]

ABSTRACT: RNA-seq analysis was performed in a Neuroblastoma cell line (GI-MEN) to analyze gene expression changes after ASCL1 overexpression.

ORGANISM(S): Homo sapiens

PROVIDER: GSE214794 | GEO | 2023/11/21

REPOSITORIES: GEO

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ChIP-seq analysis for H3K27ac in GI-MEN DOX-ASCL1 cells and for ASCL1-HA in GI-MEN DOX-ASCL1-tag-HA cells.

Project description:ChIP-seq analysis was performed in an neuroblastoma cell line to analyze DNA bindings of H3K27ac in GI-MEN DOX-ASCL1 cells and ASCL1-HA in GI-MEN DOX-ASCL1-tag-HA cells.

2023-11-21 | GSE214791 | GEO

Cut & Run-seq analysis for transcription factors overexpression in GI-MEN cells

Project description:Cut & Run analysis was performed in an neuroblastoma cell line to analyze DNA bindings of ASCL1-tag-HA in GI-MEN ASCL1-tag-HA cells and GI-MEN ASCL1-tag-HA+4TFs cells; analyze DNA bindings of MYCN, PHOX2B and H3K27ac in, GI-MEN 4TFs cells, and GI-MEN ASCL1-tag-HA+4TFs cells.

2023-11-21 | GSE214793 | GEO

RNA-seq analysis after transcription factors overexpression in GI-MEN cells [Part 2]

Project description:RNA-seq analysis was performed in a Neuroblastoma cell line (GI-MEN) to analyze gene expression changes after ASCL1 ot other TFs overexpression.

2023-11-21 | GSE214795 | GEO

H3K27ac HiChIP analysis in GI-MEN DOX-ASCL1 cells

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ATAC-seq analysis for GI-MEN DOX-ASCL1 cells and GI-MEN DOX-ASCL1-4TFs cells.

Project description:ATAC-seq analysis was performed in an neuroblastoma cell line to analyze chromatin opening of Gi-MEN cells under four different conditions.

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ASCL1: a pioneer factor that induces subtype switching and characterizes adrenergic neuroblastoma

Project description:Neuroblastoma is an embryonic malignancy originating from early nerve cells. Neuroblastoma retains plasticity, interconverting between the mesenchymal (MES) and adrenergic (ADRN) states, which are controlled by different sets of transcription factors forming the core regulatory circuit (CRC). However, their functional roles and cooperative mechanisms in neuroblastoma pathogenesis are poorly understood. Here, we demonstrate that overexpression of ASCL1 in MES neuroblastoma cells opens closed chromatin at the promoters of key ADRN genes, accompanied by epigenetic activation and establishment of enhancer-promoter interactions, thereby initiating subtype switching. ASCL1 inhibits the TGFb-SMAD2/3 pathway but activates the BMP-SMAD1-ID3/4 pathway, serving as negative feedback to balance the function of ASCL1-TCF12 dimers. ASCL1 and other ADRN CRC members potentiate each other’s activity, increasing the expression of the original targets and inducing a new set of genes, thereby promoting conversion to ADRN neuroblastoma. Thus, via its pioneer factor function, ASCL1 serves as a master regulator that characterizes ADRN neuroblastoma.

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RNA-seq analysis after knockdown of ASCL1 gene in Kelly cells

Project description:RNA-seq analysis was performed in Kelly neuroblastoma cell line to analyze gene expression changes after ASCL1 knockdown.

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Project description:To compare the function of endogenous ASCL1 in different neuroblastoma cell contexts, we have used CRISPR-mediated deletion to compare the effects of ASCL1 deletion in a MYCN-amplified and an ALK-driven neuroblastoma line and assessed the impact of ASCL1 knockout on chromatin accessiblity genome-wide using ATAC-seq

2022-08-31 | GSE202629 | GEO

Expression data from P. aeruginosa colonizing the Murine GI Tract

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