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CDK5RAP3 is activated by master TFs and regulates ER-Phagy in neuroblastoma

ABSTRACT: CDK5RAP3 is activated by master TFs and regulates ER-Phagy in neuroblastoma

PROVIDER: PRJNA1083459 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR28213092_1.fastq.gz	Fastqsanger.gz
	SRR28213092_2.fastq.gz	Fastqsanger.gz
	SRR28213093_1.fastq.gz	Fastqsanger.gz
	SRR28213093_2.fastq.gz	Fastqsanger.gz
	SRR28213094_1.fastq.gz	Fastqsanger.gz

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CDK5RAP3 is activated by master TFs and regulates ER-Phagy in neuroblastoma

Project description:Cyclin-dependent kinase 5 regulatory subunit associated protein 3(CDK5RAP3) is regulated by master TFs in neuroblastoma, and its functions in neuroblastoma are yet unclear. Herein, we observed a significantly elevated CDK5RAP3 expression level in neuroblastoma, which was associated with a poor prognosis in patients. CDK5RAP3 promotes the growth of neuroblastoma cells both in vitro and in vivo. Mechanistically, defective CDK5RAP3 interferes with UFMylation system, thereby triggering endoplasmic reticulum(ER)-Phagy. Additionally, we provide evidence that CDK5RAP3 maintains stability of MEIS2, a master TF in neuroblastoma, and in turn contributes high expression of CDK5RAP3. Overall, our findings shed light on the molecular mechanisms through which CDK5RAP3 promotes tumor progression and suggest that its inhibition may represent a novel therapeutic strategy in neuroblastoma.

2024-04-27 | GSE260772 | GEO

ER stress impairs the insulin signaling pathway through mitochondrial damage in SH-SY5Y human neuroblastoma cells

Project description:This SuperSeries is composed of the following subset Series: GSE24497: ER stress impairs the insulin signaling pathway through mitochondrial damage in SH-SY5Y human neuroblastoma cells (part 1) GSE24499: ER stress impairs the insulin signaling pathway through mitochondrial damage in SH-SY5Y human neuroblastoma cells (part 2) Refer to individual Series

2010-10-07 | E-GEOD-24500 | biostudies-arrayexpress

Transcription Factor Activating Protein 4 is synthetically lethal and a master regulator of MYCN-amplified neuroblastoma

Project description:Despite the identification of MYCN amplification as an adverse prognostic marker in neuroblastoma, MYCN inhibitors have yet to be developed. Here, by integrating evidence from a whole genome shRNA library screen and the computational inference of master regulator proteins, we identify Transcription Factor Activating Protein 4 (TFAP4) as a critical effector of MYCN amplification in neuroblastoma, providing a novel synthetic lethal target. We demonstrate that TFAP4 is a direct target of MYCN in neuroblastoma cells, and that its expression and activity strongly negatively correlate with neuroblastoma patient survival. Silencing TFAP4 selectively inhibits MYCN-amplified neuroblastoma cell growth both in vitro and in vivo, in xenograft mouse models. Mechanistically, silencing TFAP4 induces neuroblastoma differentiation, as evidenced by increased neurite outgrowth and up-regulation of neuronal markers. Taken together, our results demonstrate that TFAP4 is a master regulator of MYCN-amplified neuroblastoma and may represent a valuable novel therapeutic target.

2017-11-15 | GSE102652 | GEO

Occupancy profiling of IRF2BP2, MYCN, AP-1 and SOX11 by CUT&Tag from Neuroblastoma cells

Project description:MYCN and SOX11 are master transcription factors (TFs) in neuroblastoma by directly occupying each other's and their own super-enhancers (SEs). Additionally, Master TFs cooperatively co-occupy the same SE components, which promotes the expression of IRF2BP2 involved in cell survival. We also observed the significant enrichment of the AP-1 family at the binding sites of IRF2BP2. In the present study, CUT&Tag (Cleavage Under Targets and Tagmentation) analysis was performed to explore the target of IRF2BP2, MYCN, AP-1 and SOX11 in NB cells.

2024-06-24 | GSE246065 | GEO

Occupancy profiling of HAND2, MEIS2 and TCF4 by CUT&Tag from Neuroblastoma cells

Project description:HAND2, MEIS2 and TCF4 are master transcription factors (TFs) in neuroblastoma and create an interconnected core regulatory circuitry (CRC) by directly occupying each other's and their own super-enhancers (SEs), which leads to high levels of each TF expression inside the CRC. Additionally, CRC TFs cooperatively co-occupy the same SE components, which promotes the expression of genes involved in cell identity and cell-type-specific activities. Super-enhancer-mediated CRC enriched at key oncogenes in neuroblastoma. In the present study, CUT&Tag (Cleavage Under Targets and Tagmentation) analysis was performed to explore the target of HAND2, MEIS2 and TCF4 in NB cells.

2024-05-06 | GSE234337 | GEO

Reduced ER-mitochondria connectivity promotes neuroblastoma multidrug resistance

Project description:Most cancer deaths result from progression of therapy resistant disease, yet our understanding of this phenotype is limited. Cancer therapies generate stress signals that act upon mitochondria to initiate apoptosis. Mitochondria isolated from neuroblastoma cells were exposed to tBid or Bim, death effectors activated by therapeutic stress. Multidrug resistant tumor cells obtained from children at relapse had markedly attenuated Bak and Bax oligomerization and cytochrome c release (surrogates for apoptotic commitment) in comparison with patient-matched tumor cells obtained at diagnosis. Electron microscopy identified reduced endoplasmic reticulum-mitochondria contacts (ERMCs) in therapy resistant cells, and genetically or biochemically reducing ERMCs in therapy sensitive tumors phenocopied resistance. ERMCs serve as platforms to transfer Ca2+ and bioactive lipids to mitochondria. Reduced Ca2+ transfer was found in some but not all resistant cells, and inhibiting transfer did not attenuate apoptotic signaling. In contrast, reduced ceramide synthesis and transfer was common to resistant cells and its inhibition induced stress resistance. We identify ERMCs as physiologic regulators of apoptosis via ceramide transfer and uncover a previously unrecognized mechanism for cancer multidrug resistance.

2021-11-18 | ST002054 | MetabolomicsWorkbench

Transient ER binding and p300 redistribution support a physiological squelching model for immediate ER-repressed genes

Project description:Selective transcriptional activation and repression of genes throughout signaling cascades and development are poorly understood. Transcription factors (TF) orchestrate patterns and magnitude of transcriptional response, but TF action, or inaction, is highly dependent upon TF kinetics, distance from genes, chromatin architecture, and the local occupancy of other TFs. We integrated genomic transcription, chromosome looping, TF binding, and chromatin structure data to analyze the molecular cascade that results from estradiol-induced (E2) signaling in human MCF-7 breast cancer cells and addressed the context-specific nature of gene regulation. We analyzed kinetic ChIP-seq that profiled the master regulator of the E2-mediated response, estrogen receptor (ER), and found that transient ER binding sites are specifically associated with enhancers of repressed genes. We performed replicate ChIP-seq experiments prior to estrogen treatment and 2min, 5min, 10min, 40min, and 160min after E2 treatment.

2014-08-04 | E-GEOD-54855 | biostudies-arrayexpress

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

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

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

| PRJNA491481 | ENA

Transcription profiling by array of mouse promyelocyte granulocytes with activated MYC-ER protein

Project description:The mouse promyelocyte (MPRO) granulocyte cell model expressing the MYC-ER fusion protein encoding transgene was used as a system to perform gene expression profiling in a granulocytic cell setting of low endogenous MYC expression (differentiated MYC-ER MPROs, D4) where we then activated the MYC-ER protein for 24 h with 4-OHT (D5T) as compared to a EtOH vehicle treated control (D5E).

2011-06-01 | E-MEXP-2794 | biostudies-arrayexpress

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