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

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

PROVIDER: PRJNA491481 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR7865944.fastq.gz	Fastqsanger.gz
	SRR7865945.fastq.gz	Fastqsanger.gz
	SRR7865946.fastq.gz	Fastqsanger.gz
	SRR7865947.fastq.gz	Fastqsanger.gz
	SRR8169718.fastq.gz	Fastqsanger.gz

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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

LMO1 Synergizes with MYCN to Promotes Neuroblastoma Initiation and Metastasis

Project description:High levels of LMO1 expression synergizes with MYCN to accelerate neuroblastomagenesis, enhance disease penetrance and promote widespread metastasis in zebrafish. Transcriptomic analysis of human neuroblasotma cells with programed expression of LMO1 vs vector control or neuroblastoma cells with differential endogenous LMO1 expression revealed that gene signitures affecting tumor cell-extracellular matrix interaction are significantly associated with high levels of LMO1 expression. Our findings provide compelling evidence for a major pathogenic role of LMO1 in MYCN-driven neuroblastoma.

2017-07-31 | GSE90087 | GEO

RNA-seq analysis after LMO1 or MYCN knockdown in Kelly cells

Project description:RNA-seq analysis was performed in Kelly neuroblastoma cell line to analyze gene expression changes after LMO1 or MYCN knockdown.

2019-11-10 | GSE118823 | GEO

ASCL1 is a MYCN- and LMO1-dependent member of the adrenergic neuroblastoma core regulatory circuitry

Project description:ASCL1 is a MYCN- and LMO1-dependent member of the adrenergic neuroblastoma core regulatory circuitry

| PRJNA548931 | ENA

RNA-seq analysis after LMO1 or MYCN knockdown in Kelly cells

Project description:RNA-seq analysis after LMO1 or MYCN knockdown in Kelly cells

| PRJNA486907 | ENA

ASCL1 is a MYCN- and LMO1-dependent member of the adrenergic neuroblastoma core regulatory circuitry.

Project description:A heritable polymorphism within regulatory sequences of the LMO1 gene is associated with its elevated expression and increased susceptibility to develop neuroblastoma, but the oncogenic pathways downstream of the LMO1 transcriptional co-regulatory protein are unknown. Our ChIP-seq and RNA-seq analyses reveal that a key gene directly regulated by LMO1 and MYCN is ASCL1, which encodes a basic helix-loop-helix transcription factor. Regulatory elements controlling ASCL1 expression are bound by LMO1, MYCN and the transcription factors GATA3, HAND2, PHOX2B, TBX2 and ISL1-all members of the adrenergic (ADRN) neuroblastoma core regulatory circuitry (CRC). ASCL1 is required for neuroblastoma cell growth and arrest of differentiation. ASCL1 and LMO1 directly regulate the expression of CRC genes, indicating that ASCL1 is a member and LMO1 is a coregulator of the ADRN neuroblastoma CRC.

| S-EPMC6901540 | biostudies-literature

SCL and LMO1 reprogram thymocytes into self-renewing cells.

Project description:The SCL and LMO1 oncogenic transcription factors reprogram thymocytes into self-renewing pre-leukemic stem cells (pre-LSCs). Here we report that SCL directly interacts with LMO1 to activate the transcription of a self-renewal program coordinated by LYL1. Gene expression profiles of thymocytes from SCL-LMO1 transgenic and age-matched non transgenic Cd3Îµ-/- mice were compared to identify candidate genes that confer self-renewal capability to pre-leukemic thymocytes.

2015-11-05 | E-GEOD-74659 | biostudies-arrayexpress

Gene expression profiling of MYCN-driven neuroblastoma tumor development in the TH-MYCN mouse model.

Project description:Neuroblastoma is an embryonic tumor arising from immature sympathetic nervous system progenitor cells. MYCN and ALK are driver oncogenes both of which are specifically expressed during early neurogenesis. This is in line with the assumption that neuroblastoma arises through disruption of normal developmental processes. MYCN has a broad impact on the tumor phenotype; however, the details of the MYCN driven oncogenic program are far from clear. In order to gain further insight into the role of gene expression during neuroblastoma initiation and progression, we evaluated gene expression profiles of hyperplastic ganglia and tumors isolated from MYCN transgenic mice.

2016-02-28 | E-MTAB-3247 | 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

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