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

ABSTRACT: 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.

ORGANISM(S): Mus musculus

PROVIDER: GSE339002 | 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 [Hepatocyte_MYCN_ChIPseq]

Project description: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.

2026-08-24 | GSE339003 | GEO

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

Project description:MYCN reprograms postnatal cells toward embryonic-like transcriptional states and drives tumorigenesis

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

Project description:This SuperSeries is composed of the SubSeries listed below.

2026-08-24 | GSE339004 | GEO

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

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

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

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

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

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

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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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SOX2+ sustentacular cells are stem cells in the postnatal adrenal medulla

Project description:Renewal of the catecholamine-secreting chromaffin cell population of the adrenal medulla is necessary for physiological homeostasis throughout life. Definitive evidence for the presence or absence of an adrenomedullary stem cell has been enigmatic. In this work, we show that a subpopulation of uncommitted sustentacular cells, previously thought to be support cells, are in fact adrenomedullary stem cells. These postnatal cells express the transcription factor SOX2, and give rise to chromaffin cells of both the adrenaline and noradrenaline lineages in vivo and in vitro. We present comprehensive transcriptomic data of the mouse adrenal medulla as well as of purified SOX2+ adrenomedullary stem cell populations. Through genetic tracing, we show that postnatal stem cells specialise from embryonic Schwann Cell Precursors and identify this population in the normal adult human adrenal medulla.

2024-07-13 | GSE237125 | GEO

An ALYREF-MYCN coactivator complex drives neuroblastoma tumorigenesis through effects on USP3 and MYCN stability

Project description:To achieve the very high oncoprotein levels required to drive the malignant state, cancer cells utilise the ubiquitin proteasome system to regulate proteins involved in growth signalling pathways. Here we identify a transcriptional coactivator, ALYREF, expressed from the most common genetic copy number variation in childhood neuroblastoma, chromosome 17q21-ter gain. We show strong co-operativity between ALYREF and MYCN from transgenic models of neuroblastoma in vitro and in vivo. MYCN induced ALYREF transcription, and the two proteins formed a nuclear coactivator complex which stimulated transcription of the ubiquitin specific peptidase 3, USP3. We found that increased USP3 levels markedly reduced K-48- and K-63-linked ubiquitination of MYCN, thus driving up MYCN protein stability. In the MYCN-ALYREF-USP3 signal, ALYREF was required for MYCN effects on the malignant phenotype in vitro and that of USP3 on MYCN stability. Our data define a novel MYCN oncoprotein dependency state which provides rationale for future pharmacological studies.

2020-05-12 | GSE150303 | GEO

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