MYC regulates ribosome biogenesis and mitochondrial gene expression programs through its interaction with host cell factor–1
ribosome biogenesis
Proto-Oncogene Proteins c-myc
DOI:
10.7554/elife.60191
Publication Date:
2021-01-08T14:03:08Z
AUTHORS (14)
ABSTRACT
The oncoprotein transcription factor MYC is a major driver of malignancy and highly validated but challenging target for the development anticancer therapies. Novel strategies to inhibit may come from understanding co-factors it uses drive pro-tumorigenic gene expression programs, providing their role in activity understood. Here we interrogate how one co-factor, host cell (HCF)–1, contributes human Burkitt lymphoma setting. We identify genes connected mitochondrial function ribosome biogenesis as direct MYC/HCF-1 targets demonstrate modulation MYC–HCF-1 interaction influences growth, metabolite profiles, global patterns, tumor growth vivo. This work defines HCF-1 critical places biological context, highlights focal point novel anti-MYC
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