MassIVE MSV000086896

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GNPS Metabolomics Workbench ST001429 - GNPS MYC regulates ribosome biogenesis and mitochondrial gene expression programs through its interaction with Host Cell Factor-1

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Description

b'MYC is an oncoprotein transcription factor that is overexpressed in the majority cancers. Although MYC itself is considered undruggable, it may be possible to inhibit MYC by targeting the co-factors it uses to drive oncogenic gene expression patterns. Here, we use loss- and gain- of function approaches to interrogate how one MYC co-factorHost Cell Factor (HCF)-1contributes to MYC activity in a Burkitt lymphoma setting. We identify high-confidence direct targets of the MYCHCF-1 interaction that are regulated through a recruitment-independent mechanism, including genes that control mitochondrial function and rate-limiting steps for ribosome biogenesis and translation. We describe how these gene expression events impact cell growth and metabolism, and demonstrate that the MYCHCF-1 interaction is essential for tumor maintenance in vivo. This work highlights the MYCHCF-1 interaction as a focal point for development of novel anti-cancer therapies.' [doi:10.25345/C5FJ6B] [dataset license: CC0 1.0 Universal (CC0 1.0)]

Keywords: GNPS ; Metabolomics ; Metabolomics Workbench

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Principal Investigators:
(in alphabetical order) 		Simona Codreanu, Vanderbilt University, N/A
Submitting User: mwang87
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