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MYC regulates ribosome biogenesis and mitochondrial gene expression programs through its interaction with host cell factor-1


Popay TM , Wang J , Adams CM , Howard GC , Codreanu SG , Sherrod SD , McLean JA , Thomas LR , Lorey SL , Machida YJ , Weissmiller AM , Eischen CM , Liu Q , Tansey WP , . eLife. 2021 1 8; 10().


The oncoprotein transcription factor MYC is a major driver of malignancy and a highly validated but challenging target for the development of anticancer therapies. Novel strategies to inhibit MYC may come from understanding the co-factors it uses to drive pro-tumorigenic gene expression programs, providing their role in MYC activity is understood. Here we interrogate how one MYC co-factor, host cell factor (HCF)-1, contributes to MYC activity in a human Burkitt lymphoma setting. We identify genes connected to mitochondrial function and ribosome biogenesis as direct MYC/HCF-1 targets and demonstrate how modulation of the MYC-HCF-1 interaction influences cell growth, metabolite profiles, global gene expression patterns, and tumor growth in vivo. This work defines HCF-1 as a critical MYC co-factor, places the MYC-HCF-1 interaction in biological context, and highlights HCF-1 as a focal point for development of novel anti-MYC therapies.

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