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Notarangelo, Giulia; Spinelli, Jessica B; Perez, Elizabeth M; Baker, Gregory J; Kurmi, Kiran; Elia, Ilaria; Stopka, Sylwia A; Baquer, Gerard; Lin, Jia-Ren; Golby, Alexandra J; Joshi, Shakchhi; Baron, Heide F; Drijvers, Jefte M; Georgiev, Peter; Ringel, Alison E; Zaganjor, Elma; McBrayer, Samuel K; Sorger, Peter K; Sharpe, Arlene H; Wucherpfennig, Kai W; Santagata, Sandro; Agar, Nathalie Y R; Suvà, Mario L; Haigis, Marcia C
Science, 09/2022, Letnik: 377, Številka: 6614Journal Article
Gain-of-function mutations in isocitrate dehydrogenase (IDH) in human cancers result in the production of d-2-hydroxyglutarate (d-2HG), an oncometabolite that promotes tumorigenesis through epigenetic alterations. The cancer cell-intrinsic effects of d-2HG are well understood, but its tumor cell-nonautonomous roles remain poorly explored. We compared the oncometabolite d-2HG with its enantiomer, l-2HG, and found that tumor-derived d-2HG was taken up by CD8 T cells and altered their metabolism and antitumor functions in an acute and reversible fashion. We identified the glycolytic enzyme lactate dehydrogenase (LDH) as a molecular target of d-2HG. d-2HG and inhibition of LDH drive a metabolic program and immune CD8 T cell signature marked by decreased cytotoxicity and impaired interferon-γ signaling that was recapitulated in clinical samples from human patients with mutant gliomas.
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JCR | SNIP | JCR | SNIP | JCR | SNIP | JCR | SNIP |
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Povezave do osebnih bibliografij avtorjev | Povezave do podatkov o raziskovalcih v sistemu SICRIS |
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Vir: Osebne bibliografije
in: SICRIS
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