ArticleNature communications2019
A NOTCH feed-forward loop drives reprogramming from adrenergic to mesenchymal state in neuroblastoma.
Article in Nature communications, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 112 papers.
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Who cites it
112 citing papers in PubMed.
- Hypoxia during GPC2-CAR T-cell manufacturing compromises cell expansion and cytotoxic capacity.Cytotherapy · 2026Article
- Alternative Splicing of the NF-Y Subunit, NF-YA, in Neuroblastoma Phenotype Heterogeneity.Cancers · 2026Review
- Multi‑omics identification of MSI2 as a super-enhancer‑driven vulnerability in MYCN‑amplified neuroblastoma.Journal of translational medicine · 2026Article
- Review
- Repurposing statins and phenothiazines to treat chemoresistant neuroblastoma.EMBO molecular medicine · 2026Article
- YAP1 Enhances Mesenchymal-Type Gene Expression in Human Adrenergic-Type Neuroblastoma Cells.Cancers · 2026Article
- Rho GTPases signaling mediates aggressiveness and differentiation in neuroblastoma tumors.Cell communication and signaling : CCS · 2026Article
- Article
- Epigenetic crosstalk in neuroblastoma development and progression.Frontiers in cell and developmental biology · 2026Review
- Integrative precision oncology in neuroblastoma: multi-omics biomarkers, molecular targets, and immunotherapeutic strategies.Frontiers in oncology · 2026Review
- Review
- Emerging small molecule strategies target cancer stem cells through ferroptosis and metabostemness.Discover oncology · 2025Review
- Transcriptomic and epigenetic profiling of neuroblastoma states in response to RBM39 degrader.Scientific data · 2025Article
- Chromosomal instability degrades developmental phenotypes essential for anti-GD2 immunotherapy outcomes in high-risk neuroblastoma.Cell reports. Medicine · 2025Article
- RBM39 degrader invigorates innate immunity to eradicate neuroblastoma despite cancer cell plasticity.Nature communications · 2025Article
- Extracellular Matrix Topography Drives Adrenergic to Mesenchymal Transition in Neuroblastoma.Advanced materials (Deerfield Beach, Fla.) · 2025Article
- Sensitive detection of minimal residual disease and immunotherapy targets by multi-modal bone marrow analysis in high-risk neuroblastoma - a multi-center study.Journal of experimental & clinical cancer research : CR · 2025Article
- Lineage dependence of the neuroblastoma surfaceome defines tumor cell state-dependent and -independent immunotherapeutic targets.Neuro-oncology · 2025Article
- Emerging Trends in Neuroblastoma Diagnosis, Therapeutics, and Research.Molecular neurobiology · 2025Review
- Longitudinal single-cell multiomic atlas of high-risk neuroblastoma reveals chemotherapy-induced tumor microenvironment rewiring.Nature genetics · 2025Article
52 more citing papers are in PubMed but not listed here.
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18 authors.
Funding
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Abstract
Transition between differentiation states in development occurs swift but the mechanisms leading to epigenetic and transcriptional reprogramming are poorly understood. The pediatric cancer neuroblastoma includes adrenergic (ADRN) and mesenchymal (MES) tumor cell types, which differ in phenotype, super-enhancers (SEs) and core regulatory circuitries. These cell types can spontaneously interconvert, but the mechanism remains largely unknown. Here, we unravel how a NOTCH3 intracellular domain reprogrammed the ADRN transcriptional landscape towards a MES state. A transcriptional feed-forward circuitry of NOTCH-family transcription factors amplifies the NOTCH signaling levels, explaining the swift transition between two semi-stable cellular states. This transition induces genome-wide remodeling of the H3K27ac landscape and a switch from ADRN SEs to MES SEs. Once established, the NOTCH feed-forward loop maintains the induced MES state. In vivo reprogramming of ADRN cells shows that MES and ADRN cells are equally oncogenic. Our results elucidate a swift transdifferentiation between two semi-stable epigenetic cellular states.
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