Isocitrate dehydrogenase 1 primes group-3 medulloblastomas for cuproptosis

异柠檬酸脱氢酶 1 启动 3 组髓母细胞瘤发生铜凋亡

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作者:Derek Dang ,Akash Deogharkar ,John McKolay ,Kyle S Smith ,Pooja Panwalkar ,Simon Hoffman ,Wentao Tian ,Sunjong Ji ,Ana P Azambuja ,Siva Kumar Natarajan ,Joanna Lum ,Jill Bayliss ,Katie Manzeck ,Stefan R Sweha ,Erin Hamanishi ,Matthew Pun ,Diya Patel ,Sagar Rau ,Olamide Animasahun ,Abhinav Achreja ,Martin P Ogrodzinski ,Jutta Diessl ,Jennifer Cotter ,Debra Hawes ,Fusheng Yang ,Robert Doherty ,Andrea T Franson ,Allison R Hanaford ,Charles G Eberhart ,Eric H Raabe ,Brent A Orr ,Robert J Wechsler-Reya ,Brandon Chen ,Costas A Lyssiotis ,Yatrik M Shah ,Sophia Y Lunt ,Ruma Banerjee ,Alexander R Judkins ,John R Prensner ,Carl Koschmann ,Sebastian M Waszak ,Deepak Nagrath ,Marcos Simoes-Costa ,Paul A Northcott ,Sriram Venneti
MYC-driven group-3 medulloblastomas (MBs) are malignant pediatric brain cancers without cures. To define actionable metabolic dependencies, we identify upregulation of dihydrolipoyl transacetylase (DLAT), the E2-subunit of pyruvate dehydrogenase complex (PDC) in a subset of group-3 MB with poor prognosis. DLAT is induced by c-MYC and targeting DLAT lowers TCA cycle metabolism and glutathione synthesis. We also note upregulation of isocitrate dehydrogenase 1 (IDH1) gene expression in group-3 MB patient tumors and suppression of IDH1 epigenetically reduces c-MYC and downstream DLAT levels in multiple c-MYC amplified cancers. DLAT is a central regulator of cuproptosis (copper-dependent cell death) induced by the copper ionophore elesclomol. DLAT expression in group-3 MB cells correlates with increased sensitivity to cuproptosis. Elesclomol is brain-penetrant and suppresses tumor growth in vivo in multiple group-3 MB animal models. Our data uncover an IDH1/c-MYC dependent vulnerability that regulates DLAT levels and can be targeted to kill group-3 MB by cuproptosis.

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