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

ABSTRACT:

ORGANISM(S): Homo Sapiens

TISSUE(S): Lymphoma Cells

DISEASE(S): Cancer

PROVIDER: ST001429 | MetabolomicsWorkbench |

REPOSITORIES: MetabolomicsWorkbench

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

Project description: Not available

| S-EPMC7793627 | biostudies-literature

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

Project description: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-factor—Host Cell Factor (HCF)-1—contributes to MYC activity in a Burkitt lymphoma setting. We identify high-confidence direct targets of the MYC–HCF-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 MYC–HCF-1 interaction is essential for tumor maintenance in vivo. This work highlights the MYC–HCF-1 interaction as a focal point for development of novel anti-cancer therapies.

2021-01-11 | GSE152385 | GEO

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

Project 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.'

2021-02-17 | MSV000086896 | GNPS