ArticleNeuro-oncology2026
MBD3 deficiency decommissions the nucleosome remodeling and deacetylase complex and orchestrates the epigenetic regulation of gene expression to suppress neuroblastoma progression.
Article in Neuro-oncology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
backgroundNeuroblastoma is the most common extracranial solid tumor in children and accounts for 15% of childhood cancer deaths. The nucleosome remodeling and deacetylase (NuRD) complex is a major chromatin remodeling complex that regulates chromatin accessibility and gene transcription. However, its role in the pathogenesis of neuroblastoma remains poorly understood.
methodsThe genetic dependency and clinical significance of MBD3 in neuroblastoma were evaluated by analysis of public datasets. The function of MBD3 in neuroblastoma cell growth was evaluated by shRNA knockdown experiment. Cleavage under targets and tagmentation sequencing (CUT&Tag-seq), coupled with RNA-sequencing, was employed to explore the mechanisms involved in the epigenetic regulation executed by NuRD decommissioning following MBD3 deficiency.
resultsHere we find that MBD3 is the most lineage-selective dependency among the nonenzymatic subunits of the NuRD complex in neuroblastoma. Knockdown of MBD3 induces cell cycle arrest and apoptosis, and inhibits neuroblastoma growth in vivo. Mechanistically, MBD3 deficiency leads to decommissioning of the NuRD complex and dissociation of the EZH2-PRC2 complex from chromatin, thereby orchestrating the epigenetic regulation of gene expression by modulating the balance between histone acetylation and methylation. NuRD decommissioning upon MBD3 deficiency selectively downregulates the expression of core regulatory transcription factors and upregulates a tumor suppressor, SRCIN1, collectively suppressing neuroblastoma progression.
conclusionsOur data identify MBD3 and the NuRD complex as potential therapeutic targets in neuroblastoma, highlighting the critical role of epigenetic regulation in tumor maintenance. Targeting this pathway may offer a novel strategy to selectively impair neuroblastoma cell survival and improve outcomes.
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