Transcriptomic and epigenetic profiling of neuroblastoma states in response to RBM39 degrader
Year: 2025
Type: data-paper
Abstract: Neuroblastoma accounts for approximately 15% of all pediatric cancer-related deaths, largely due to disease relapse following intensive multimodal therapy. A critical barrier to cure neuroblastoma is the emergence of therapy-resistant tumor cells. Neuroblastoma comprises two major cell states, adrenergic (ADRN) and mesenchymal (MES), which are believed to interconvert and contribute to therapeutic resistance through lineage plasticity. To investigate the mechanisms underlying this plasticity, we subjected human and murine neuroblastoma models to repeated treatment with indisulam, a molecular glue compound that selectively degrades the splicing factor RBM39, until full drug resistance emerged. We then generated datasets from these models, including bulk transcriptomic data, ATAC-seq, and H3K27ac CUT&Tag. These data comprehensively characterize transcriptomic and epigenetic landscapes of resistant ADRN and MES neuroblastoma cell states. We present this resource to facilitate reuse by the scientific community. These datasets may support efforts to decipher lineage switching, identify regulators of therapy resistance, and discover potential therapeutic vulnerabilities in resistant neuroblastoma.
Source: Scientific Data
Authors: Hongjian Jin, Jie Fang, Jason Myers, Shivendra Singh, Jun Yang
Language: English
Subfield: Neurology
Field: Medicine
Domain: Health Sciences
Open Access status: gold
Estimated APC paid: $2,490
Awards: G2074029610, G2631233060, Development of small molecules to target KDM4B, G3280730974, G4170786942, G4766096375, G4869702982, G5685867167, G5775726095, G7283801956, G8629949615, G9000027531, EXPLORE AND TARGET THE EPIGENETIC VULNERABILITY OF PAX3-FOXO1-DRIVEN RHABDOMYOSARCOMA, Targetable epigenetic modifiers that promote neuroblastoma malignancy and plasticity, Targeting splicing vulnerability of neuroblastoma, Cancer Center Support Grant (CCSG)
OpenAlex ID: W4417149111
