BPTF is required for c-MYC transcriptional activity and in vivo tumorigenesis View Full Text


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Article Info

DATE

2016-01-05

AUTHORS

Laia Richart, Enrique Carrillo-de Santa Pau, Ana Río-Machín, Mónica P. de Andrés, Juan C. Cigudosa, Víctor J. Sánchez-Arévalo Lobo, Francisco X. Real

ABSTRACT

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. More... »

PAGES

10153

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    http://scigraph.springernature.com/pub.10.1038/ncomms10153

    DOI

    http://dx.doi.org/10.1038/ncomms10153

    DIMENSIONS

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