Richart, LaiaCarrillo-de-Santa-Pau, EnriqueRío-Machín, Anade Andrés, Mónica PCigudosa, Juan CLobo, Víctor J Sánchez-ArévaloReal Arribas, Francisco2019-07-042019-07-042016-01-05Nat Commun. 2016 ;7:10153.2041-1723http://hdl.handle.net/20.500.12105/7856c-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.engVoRhttp://creativecommons.org/licenses/by-nc-sa/4.0/AnimalsAntigens, NuclearCell LineCell ProliferationAtribución-NoComercial-CompartirIgual 4.0 Internacional26729287711015310.1038/ncomms101532041-1723Nature communicationsopen access