2026-05-22T00:57:54Zhttps://repisalud.isciii.es/rest/oai/request

oai:repisalud.isciii.es:20.500.12105/78562025-05-30T08:51:32Zcom_20.500.12105_2173com_20.500.12105_2051col_20.500.12105_19597

00925njm 22002777a 4500 dc Richart, Laia author Carrillo-de-Santa-Pau, Enrique author Río-Machín, Ana author de Andrés, Mónica P author Cigudosa, Juan C author Lobo, Víctor J Sánchez-Arévalo author Real Arribas, Francisco author 2016-01-05 c-MYC oncogene is deregulated in most human tumours. Histone marks associated with transcriptionally active genes define high-affinity c-MYC targets. The mechanisms involved in their recognition by c-MYC are unknown. Here we report that c-MYC interacts with BPTF, a core subunit of the NURF chromatin-remodelling complex. BPTF is required for the activation of the full c-MYC transcriptional programme in fibroblasts. BPTF knockdown leads to decreased c-MYC recruitment to DNA and changes in chromatin accessibility. In Bptf-null MEFs, BPTF is necessary for c-MYC-driven proliferation, G1-S progression and replication stress, but not for c-MYC-driven apoptosis. Bioinformatics analyses unveil that BPTF levels correlate positively with c-MYC-driven transcriptional signatures. In vivo, Bptf inactivation in pre-neoplastic pancreatic acinar cells significantly delays tumour development and extends survival. Our findings uncover BPTF as a crucial c-MYC co-factor required for its biological activity and suggest that the BPTF-c-MYC axis is a potential therapeutic target in cancer. Nat Commun. 2016 ;7:10153. 10.1038/ncomms10153 2041-1723 2041-1723 Nature communications 26729287 http://hdl.handle.net/20.500.12105/7856 BPTF is required for c-MYC transcriptional activity and in vivo tumorigenesis