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Pubmed ID: 35945217
Publication Date: 2022/08/09

MYC sensitises cells to apoptosis by driving energetic demand.


The MYC oncogene is a potent driver of growth and proliferation but also sensitises cells to apoptosis, which limits its oncogenic potential. MYC induces several biosynthetic programmes and primary cells overexpressing MYC are highly sensitive to glutamine withdrawal suggesting that MYC-induced sensitisation to apoptosis may be due to imbalance of metabolic/energetic supply and demand. Here we show that MYC elevates global transcription and translation, even in the absence of glutamine, revealing metabolic demand without corresponding supply. Glutamine withdrawal from MRC-5 fibroblasts depletes key tricarboxylic acid (TCA) cycle metabolites and, in combination with MYC activation, leads to AMP accumulation and nucleotide catabolism indicative of energetic stress. Further analyses reveal that glutamine supports viability through TCA cycle energetics rather than asparagine biosynthesis and that TCA cycle inhibition confers tumour suppression on MYC-driven lymphoma in vivo. In summary, glutamine supports the viability of MYC-overexpressing cells through an energetic rather than a biosynthetic mechanism.
Authors: Edwards-Hicks Joy , Su Huizhong , Mangolini Maurizio , Yoneten Kubra K , Wills Jimi , Rodriguez-Blanco Giovanny , Young Christine , Cho Kevin , Barker Heather , Muir Morwenna , Guerrieri Ania Naila , Li Xue-Feng , White Rachel , Manasterski Piotr , Mandrou Elena , Wills Karen , Chen Jingyu , Abraham Emily , Sateri Kianoosh , Qian Bin-Zhi , Bankhead Peter , Arends Mark , Gammoh Noor , von Kriegsheim Alex , Patti Gary J , Sims Andrew H , Acosta Juan Carlos , Brunton Valerie , Kranc Kamil R , Christophorou Maria , Pearce Erika L , Ringshausen Ingo , Finch Andrew J ,

Reference:

  1. ncbi.nlm.nih.gov. [Last access 2022/08/09].

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