{"doi":"10.1101/2024.02.11.579816","title":"BPTF cooperates with MYCN and MYC to link neuroblastoma cell cycle control to epigenetic cellular states","abstract":"<jats:title>Abstract</jats:title>\n                <jats:p>\n                  The nucleosome remodeling factor BPTF is required for the deployment of the MYC-driven transcriptional program. Deletion of one\n                  <jats:italic>Bptf</jats:italic>\n                  allele delays tumor progression in mouse models of pancreatic cancer and lymphoma. In neuroblastoma, MYCN cooperates with the transcriptional core regulatory circuitry (CRC). High\n                  <jats:italic>BPTF</jats:italic>\n                  levels are associated with high-risk features and decreased survival. BPTF depletion results in a dramatic decrease of cell proliferation. Bulk RNA-seq, single-cell sequencing, and tissue microarrays reveal a positive correlation of\n                  <jats:italic>BPTF</jats:italic>\n                  and CRC transcription factor expression. Immunoprecipitation/mass spectrometry shows that BPTF interacts with MYCN and the CRC proteins. Genome-wide distribution analysis of BPTF and CRC in neuroblastoma reveals a dual role for BPTF: 1) it co-localizes with MYCN/MYC at the promoter of genes involved in cell cycle and 2) it co-localizes with the CRC at super-enhancers to regulate cell identity. The critical role of BPTF across neuroblastoma subtypes supports its relevance as a therapeutic target.\n                </jats:p>","journal":null,"year":null,"id":621355,"datarank":0.20794415416798362,"base_score":1.3862943611198906,"endowment":1.3862943611198906,"self_citation_contribution":0.20794415416798362,"citation_network_contribution":0.0,"self_endowment_contribution":0.20794415416798362,"citer_contribution":0.0,"corpus_percentile":null,"corpus_rank":null,"citation_count":3,"citer_count":0,"citers_with_citation_signal":0,"citers_with_endowment":0,"datacite_reuse_total":0,"is_dataset":false,"is_dataset_confidence":null,"is_data_producer":false,"deposit_databanks":null,"is_oa":false,"file_count":0,"downloads":0,"has_version_chain":false,"published_date":null,"fair_score":null,"fair_percentile":null,"algorithm_id":"datarank_citation_only_1hop_v6","ranking_scope":"data_only","authors":[{"id":1604384,"name":"Jaime Martínez-de-Villarreal","orcid":null,"position":1,"is_corresponding":false},{"id":550692,"name":"Khushbu Patel","orcid":"0000-0002-3269-7442","position":2,"is_corresponding":false},{"id":1604385,"name":"Jorge Martínez-Torrecuadrada","orcid":null,"position":3,"is_corresponding":false},{"id":810051,"name":"Liron D. Grossmann","orcid":"0000-0002-0692-8921","position":4,"is_corresponding":false},{"id":1604386,"name":"Giovanna Roncador","orcid":null,"position":5,"is_corresponding":false},{"id":1604387,"name":"Mariona Cubells","orcid":null,"position":6,"is_corresponding":false},{"id":1604388,"name":"Alvin Farrell","orcid":null,"position":7,"is_corresponding":false},{"id":1604389,"name":"Nathan Kendsersky","orcid":null,"position":8,"is_corresponding":false},{"id":1419702,"name":"Sergio Sabroso-Lasa","orcid":null,"position":9,"is_corresponding":false},{"id":1604390,"name":"Lucía Sancho-Temiño","orcid":null,"position":10,"is_corresponding":false},{"id":1604391,"name":"Kyabeth Torres","orcid":null,"position":11,"is_corresponding":false},{"id":29526,"name":"Daniel Martinez","orcid":null,"position":12,"is_corresponding":false},{"id":1604392,"name":"Javier Muñoz Perez","orcid":null,"position":13,"is_corresponding":false},{"id":1131850,"name":"Fernando García","orcid":"0000-0002-1384-3862","position":14,"is_corresponding":false},{"id":1604393,"name":"Jenny Pogoriler","orcid":null,"position":15,"is_corresponding":false},{"id":305846,"name":"Lucas Moreno","orcid":"0000-0002-0708-1670","position":16,"is_corresponding":false},{"id":240511,"name":"John M. Maris","orcid":"0000-0002-8088-7929","position":17,"is_corresponding":false},{"id":451234,"name":"Francisco X. Real","orcid":"0000-0001-9501-498X","position":18,"is_corresponding":false},{"id":1604383,"name":"Irene Felipe","orcid":null,"position":0,"is_corresponding":false}],"reference_count":0,"raw_metadata":{"has_enrichment":true,"resolved":true,"title":"BPTF cooperates with MYCN and MYC to link neuroblastoma cell cycle control to epigenetic cellular states","abstract":"<jats:title>Abstract</jats:title>\n                <jats:p>\n                  The nucleosome remodeling factor BPTF is required for the deployment of the MYC-driven transcriptional program. Deletion of one\n                  <jats:italic>Bptf</jats:italic>\n                  allele delays tumor progression in mouse models of pancreatic cancer and lymphoma. In neuroblastoma, MYCN cooperates with the transcriptional core regulatory circuitry (CRC). High\n                  <jats:italic>BPTF</jats:italic>\n                  levels are associated with high-risk features and decreased survival. BPTF depletion results in a dramatic decrease of cell proliferation. Bulk RNA-seq, single-cell sequencing, and tissue microarrays reveal a positive correlation of\n                  <jats:italic>BPTF</jats:italic>\n                  and CRC transcription factor expression. Immunoprecipitation/mass spectrometry shows that BPTF interacts with MYCN and the CRC proteins. Genome-wide distribution analysis of BPTF and CRC in neuroblastoma reveals a dual role for BPTF: 1) it co-localizes with MYCN/MYC at the promoter of genes involved in cell cycle and 2) it co-localizes with the CRC at super-enhancers to regulate cell identity. The critical role of BPTF across neuroblastoma subtypes supports its relevance as a therapeutic target.\n                </jats:p>","is_dataset_classified":null,"base_score":1.3862943611198906,"endowment":1.3862943611198906,"datacite_reuse_total":0,"file_count":0,"downloads":0,"views":0,"has_version_chain":false,"is_dataset":false,"is_oa":false,"pmid":"38405949","pmcid":null,"openalex_id":"https://openalex.org/W4391743446","authors":[],"funders":[],"total_grants":0,"fwci":null,"citation_percentile":null,"influential_citations":0,"citation_trend":[{"year":2025,"count":3}],"oa_status":"green","license":null,"oa_locations":[{"url":"https://www.biorxiv.org/content/biorxiv/early/2024/02/12/2024.02.11.579816.full.pdf","host_type":"repository"},{"url":"https://www.biorxiv.org/content/biorxiv/early/2024/02/12/2024.02.11.579816.full.pdf","host_type":"repository"},{"url":"https://syndication.highwire.org/content/doi/10.1101/2024.02.11.579816","host_type":"publisher"},{"url":"https://doi.org/10.1101/2024.02.11.579816","host_type":"repository"},{"url":"https://pubmed.ncbi.nlm.nih.gov/38405949","host_type":"repository"},{"url":"https://www.ncbi.nlm.nih.gov/pmc/articles/10888818","host_type":"repository"}],"fields_of_study":["Neuroblastoma Research and Treatments","Protein Degradation and Inhibitors","Cancer, Hypoxia, and Metabolism"],"mesh_terms":[],"keywords":["Epigenetics","Neuroblastoma","Suppressor","Biology","Link (geometry)","Cell cycle","Control (management)","Histone","Cell","Cell biology","Genetics","Gene","Computer science"],"sdg_mappings":[{"sdg_number":0,"sdg_label":"Good health and well-being"}],"linked_datasets":[],"clinical_trials":[],"software_tools":[],"database_accessions":[],"source":"live","citation_network_status":"fetched"},"created_at":"2026-08-03T14:12:38.045587Z","pmid":null,"pmcid":null,"fwci":null,"citation_percentile":null,"influential_citations":0,"oa_status":null,"license":null,"views":0,"total_file_size_bytes":0,"version_count":0,"fair_f":null,"fair_a":null,"fair_i":null,"fair_r":null,"fair_zscore":null,"fair_rationale":null,"fair_model":null,"fair_agent_version":null,"fair_fulltext_source":null,"fair_has_llm":null,"fair_computed_at":null,"clinical_trials":[],"software_tools":[],"db_accessions":[],"linked_datasets":[],"topics":[]}