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.
Recommended CitationPopay, Tessa M.; Wang, Jing; Adams, Clare M.; Howard, Gregory Caleb; Codreanu, Simona G.; Sherrod, Stacy D.; McLean, John A.; Thomas, Lance R.; Lorey, Shelly L.; Machida, Yuichi J.; Weissmiller, April M.; Eischen, Christine M.; Liu, Qi; and Tansey, William P., "MYC regulates ribosome biogenesis and mitochondrial gene expression programs through its interaction with host cell factor-1." (2021). Department of Cancer Biology Faculty Papers. Paper 174.
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