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ASCL1 over-expression in neuroblastoma cell lines [RNA-seq]

ABSTRACT: To compare the function of overexpressed ASCL1 in two MYCN-amplified neuroblastoma cell contexts, we have used a doxycycline-inducible lentivirus system to induce ASCL1 overexpression in SK-N-BE(2)C and IMR-32 cell lines, and assessed the transcriptome wide impact of ASCL1 overexpression using RNA-seq.

ORGANISM(S): Homo sapiens

PROVIDER: GSE213430 | GEO | 2026/03/28

REPOSITORIES: GEO

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ASCL1 chromatin binding in neuroblastoma cell lines [ChIP-seq]

Project description:To compare the ASCL1 protein binding to chromatin in two MYCN-amplified neuroblastoma cell contexts, we have used a doxycycline-inducible lentivirus system to induce ASCL1 overexpression in SK-N-BE(2)C and IMR-32 cell lines, and assessed ASCL1 binding using ChIP-seq.

2026-03-28 | GSE213247 | GEO

Comparative ASCL1 interactome analysis reveals CDK2-Cyclin A2 as suppressors of differentiation in MYCN-amplified neuroblastoma

Project description:Neuroblastoma is a heterogeneous paediatric cancer arising from developmentally arrested neuronal precursors, where restoring differentiation offers therapeutic promise. ASCL1, a pro-neural transcription factor, is widely expressed in neuroblastoma and can drive either proliferation or differentiation depending on the cellular context. Here, we show that distinct MYCN-amplified neuroblastoma cell lines exhibit differing cell cycle and differentiation responses to ASCL1 overexpression. By comparing genome-wide ASCL1 chromatin binding, transcriptional changes, and protein-protein interactions, we found that ASCL1 binds more extensively to neuronal proteins in a cell line that is more susceptible to ASCL1-driven differentiation, but associates with cell cycle regulators in less responsive cells. We show that CDK2-Cyclin A2 bind ASCL1 in less responsive cells, with CDK-mediated phosphorylation of ASCL1 limiting the ability of ASCL1 to drive differentiation. Our study reveals that context-dependent interactions of ASCL1 with protein partners on the chromatin control its ability to re-engage a differentiation program in neuroblastoma.

2026-04-07 | PXD056448 | Pride

RNA-seq analysis of ASCL1-induced neuronal differentiation in WT and MED25 knockout Glioblastoma Stem Cells

Project description:Glioblastoma stem cells were infected with lentivirus expressing a control (gRNA-AAVS1) or MED25 targeting gRNA to assess the role of MED25 in the stem cell compartment of Glioblastoma stem cells. Cells were the subjected to doxycycline-induced ASCL1 overexpression (+DOX) to induced neuronal differentiation.

2023-06-01 | GSE166979 | GEO

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.

2023-12-08 | PXD037670 | Pride

RNA-seq of IMR-5/75 neuroblastoma cell line upon TBX2 and/or MYCN knockdown

Project description:RNA-seq upon TBX2, MYCN or combination of TBX2 and MYCN knockdown in the neuroblastoma cell line IMR-5/75. Cells were transduced with two different shRNAs (shTBX2_2 and shTBX2_4) targeting TBX2 and a non-targeting control (NTC), and selected with puromycin. Cells were treated with doxycycline for shMYCN induction (with DOX or not). Analysis was performed three days upon TBX2 knockdown and two days upon MYCN knockdown, including six biological replicates per condition.

2018-08-16 | E-MTAB-6568 | biostudies-arrayexpress

The proneural transcription factor ASCL1 regulates cell proliferation and primes for differentiation in neuroblastoma [RNA-Seq]

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 transcriptome wide impact of ASCL1 knockout using RNA-seq

2022-08-31 | GSE202634 | GEO

The proneural transcription factor ASCL1 regulates cell proliferation and primes for differentiation in neuroblastoma [ATAC-seq]

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

Role of ASCL1 in human neural development

Project description:As a proneural gene, ASCL1 was reported to be important to neurogenesis. To better illustrate the role of ASCL1 in human telencephalon development, we genetically engineered an ASCL1 knockout (KO) hESC line and ASCL1 rescue (RE) hESC line, and then preformed RNA sequencing when WT, KO and RE were differentiated into neural progenitors in vitro. Our results showed that ASCL1 KO hESCs could be regularly maintained in vitro, and could be efficiently specified into neuroectoderm cells and following telencephalic neural progenitors. Remarkably, dorsal progenitors-derived from ASCL1 KO hESCs failed to differentiate into DCX positive neuroblasts. In addition, dorsal and ventral progenitors retained higher expression of VZ/ESVZ genes but had much lower expression of LSVZ genes after KO of ASCL1. Re-introducing of ASCL1 in KO hESCs through a doxycycline (Dox) inducible overexpression system reversed the gene expression changes induced by cortical progenitors with ASCL1 KO. Taken all these together, our results revealed a pivotal role of ASCL1 in both dorsal and ventral telencephalic development by progressing the cycling progenitors within the ESVZ to post-mitotic early born neurons in the LSVZ in human telencephalon.

2022-12-21 | GSE149096 | GEO

ASCL1 is directly activated by the LMO1 and MYCN oncogenes and is a master regulator of the differentiation program in neuroblastoma

Project description:Neuroblastoma is an embryonal tumor of the peripheral sympathetic nervous system. Elevated expression of the transcription factor LMO1 and the polymorphisms within this gene are associated with the susceptibility to develop neuroblastoma. LMO1 has been implicated as an oncogene in T-cell acute lymphoblastic leukemia; however, the transcriptional targets regulated by this protein in neuroblastoma cells are unknown. Here, we identify the genes and molecular pathways controlled by LMO1 in neuroblastoma cells. ChIP-seq analysis revealed that LMO1-bound regions are frequently co-occupied by GATA3 and MYCN proteins and are associated with active histone marks in neuroblastoma cells. RNA-seq analysis demonstrated that LMO1 regulates gene expression in a tumor type-specific manner. One high-confidence target gene directly regulated by LMO1 and MYCN is ASCL1, which is more highly expressed in adrenergic subtype of neuroblastoma cells as compared to normal neuronal cells. High levels of ASCL1 expression are associated with inferior overall survival in primary human neuroblastoma cases. ChIP-seq analysis identified a regulatory element controlling ASCL1 expression that is bound by LMO1, MYCN and the members of the core regulatory circuitry in neuroblastoma cells. Furthermore, ASCL1 is required for neuroblastoma cell growth and regulates genes responsible for repression of neuronal cell differentiation. Taken together, our results implicate ASCL1 as a critical downstream target of LMO1 in the molecular pathogenesis of neuroblastoma.

2019-11-09 | GSE120074 | GEO

Effects of MYCN knockdwon on miRNA expression in neuroblastoma cells

Project description:Global miRNAs expression profilling of SK-N-BE(2)-C cells after dsRNA-mediated knockdown of MYCN To identify MYCN-associated miRNAs, we carried out a small RNA-seq on MYCN knockdown in SK-N-BE(2)-C cells to profile the miRNA expression.

2016-05-16 | E-GEOD-72721 | biostudies-arrayexpress

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