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BPTF cooperates with MYCN/MYC to link neuroblastoma cell cycle control with epigenetic cell states

GSE256511 Homo sapiens Expression profiling by high throughput sequencing 4 samples Submitted 2025/02/23 Platform GPL21697
Summary
The nucleosome remodeling factor BPTF is required for the deployment of the MYC-driven transcriptional program. Deletion of oneBptfallele delays tumor progression in mouse models of pancreatic cancer and lymphoma. In neuroblastoma, MYCN cooperates with the transcriptional core regulatory circuitry (CRC). HighBPTFlevels are associated with high-risk features and decreased survival. BPTFdepletion results in a dramatic decrease of cell proliferation. Bulk RNA-seq, single-cell sequencing, and tissue microarrays reveal a positive correlation ofBPTFand CRCtranscription factor expression. Immunoprecipitation/mass spectrometry shows that BPTF interacts with MYCN and the CRC. Genome-wide distribution analysis of BPTF and CRC in neuroblastoma reveals a dual role forBPTF: 1) it co-localizes with MYCN/MYC at the promoter of genes involved in cell cycle and 2) it co-localizes withthe CRC at super-enhancers to regulate cell identity. The critical role of BPTF across neuroblastoma subtypes supports its relevance as a therapeutic target.
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Also filed as BioProject PRJNA1079811 and SRA study SRP491437. Searching any of these in the dataset finder brings you back here.

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