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MYCN reprograms postnatal cells toward embryonic-like transcriptional states and drives tumorigenesis [Hepatocyte_MYCN_ChIPseq]

ABSTRACT: This study investigated the genome-wide chromatin occupancy of MYCN in primary mouse hepatocytes following Mycn induction. Chromatin immunoprecipitation followed by sequencing of MYCN-HA was performed in primary hepatocytes at day 3 and day 6 after Mycn induction. Luciferase-expressing hepatocytes subjected to the same anti-HA chromatin immunoprecipitation procedure were included as negative controls.

ORGANISM(S): Mus musculus

PROVIDER: GSE339003 | GEO | 2026/08/24

REPOSITORIES: GEO

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MYCN reprograms postnatal cells toward embryonic-like transcriptional states and drives tumorigenesis [Hepatocyte_RNAseq]

Project description:This study investigated the transcriptional responses induced by c-Myc and Mycn in primary mouse hepatocytes. Primary hepatocytes expressing luciferase, Mycn, or c-Myc were collected at 12 h, day 3, day 6, and day 12 after transgene induction and analyzed by RNA sequencing. The dataset was generated to compare the temporal transcriptional programs induced by Mycn and c-Myc during hepatocyte transformation.

2026-08-24 | GSE339001 | GEO

MYCN reprograms postnatal cells toward embryonic-like transcriptional states and drives tumorigenesis [Neuroblastoma_RNAseq]

Project description:This study investigated the transcriptional changes associated with Mycn-induced adrenal tumor development in mice. RNA sequencing was performed using luciferase-expressing adrenal medulla samples and Mycn-induced adrenal tumors collected at different times after transgene induction. The dataset was generated to characterize early and advanced transcriptional states during Mycn-driven adrenal tumorigenesis.

2026-08-24 | GSE339002 | GEO

Genome-wide binding of MYCN protein in MYCN-amplified neuroblastoma cell lines

Project description:The MYCN locus is amplified in about half of high-risk neuroblastoma tumors. To identify genomic loci occupied by MYCN protein in the MYCN-amplified neuroblastoma cell lines NGP, Kelly and NB-1643, we performed chromatin immunoprecipitation coupled with Next-Generation Sequencing (ChIP-seq) using an anti-MYCN antibody.

2017-08-02 | GSE94782 | GEO

Genome-wide mapping of MYCN binding in neuroblastoma cells

Project description:To identify the MYCN transcription factor binding sites across the genome, we performed chromatin immunoprecipitation followed by sequencing (ChIP-seq) using anti-MYCN and anti-IgG antibodies on a MYCN-amplified NB cell line, SK-N-BE(2)-C. Identification of MYCN binding in neuroblastoma cells.

2016-05-16 | E-GEOD-72640 | biostudies-arrayexpress

Genome-wide mapping of MYCN binding in neuroblastoma cells

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MYCN directly regulates TET1 expression to control 5-hmC distribution and enhance neuroblastoma cell migration in hypoxia [RNA-Seq]

Project description:We performed RNA-sequencing on inducible MYCN cell line SHEPTET21n on Day 4 post MYCN induction

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MYCN-mediates ferroptosis escape in accelerates tumorigenesis via UBE2C

Project description:MYCN is a common oncogenic alteration in tumors, representing one of the high-risk molecular subtypes of tumors. However, the functional role of MYCN in tumorigenesis remains to be elucidated. Here, we report that MYCN binds to the UBE2C promoter and upregulates its transcription, accelerating the progression of neuroectodermal tumor. The proteomic analysis of UBE2C-interacting proteins revealed TFRC, a well-known tumor suppressor, is a novel ubiquitin target of UBE2C. Subsequently, immunoprecipitation assay demonstrates UBE2C downregulate TFRC expression via ubiquitinoylation in neuroectodermal tumor. Suppression of UBE2C in tumor cells induced ferroptosis and increased sensitivity to the ferroptosis inducer erastin. Taken together, our findings reveal a novel MYCN-UBE2C-TFRC-ferroptosis regulatory cascade in controlling MYCN activation cell proliferation and tumor growth, pinpointing an unprecedented mechanism of MYCN-mediated evasion of ferroptosis escape in tumor. This study provides useful insights into the theoretical underpinning for therapy of MYCN activation tumors.

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MYC deregulation sensitizes cancer cells to N-myristoyltransferase inhibition - Th-MycN tumour proteomics

Project description:Human N-myristoyltransferases (NMTs) catalyze N-terminal protein N-myristoylation and are promising targets in cancer, with an emerging mechanistic rationale for targeted therapy. Here, we screened 245 cancer cell lines against IMP-1320, a potent NMT inhibitor (NMTi), and conducted pathway-level analyses to identify that deregulated MYC increases cancer cell sensitivity to NMTi. Proteomics on detergent-enriched membrane fractions in MYC or MYCN-deregulated cancer cell models revealed that cell death is associated at least in part with loss of membrane association of mitochondrial respiratory complex I. This is concurrent with loss of myristoylation and degradation of the complex I assembly factor NDUFAF4, and induction of mitochondrial dysfunction, driven by MYC or MYCN-deregulation. NMTi eliminated or suppressed MYC and MYCN-driven tumors in vivo without overt toxicity, suggesting that this constitutive co-translational protein modification can be targeted in MYC-driven cancers. This dataset comprises the proteomic data obtained from Th-MycN tumours, excised from 129SvJ mice treated intraperitoneally with vehicle or IMP1320 (25 mg/kg/day), on a three days on/four days off dosing schedule.

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MYCN regulated miRNAs

Project description:miRNAs which are differentially expressed upon MYCN overexpression (1h, 4h and 24h after induction) in a neuroblastoma line were detected using deep sequencing.

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Global transcriptome analysis in the MYCN-amplified neuroblastoma cell line IMR5-75 upon inducible MYCN-knockdown

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2016-09-08 | E-GEOD-80397 | biostudies-arrayexpress

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