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Bhalla, Kavita; Jaber, Sausan; Reagan, Kayla; Hamburg, Arielle; Underwood, Karen F; Jhajharia, Aditya; Singh, Maninder; Bhandary, Binny; Bhat, Shambhu; Nanaji, Nahid M; Hisa, Ruching; McCracken, Carrie; Creasy, Heather Huot; Lapidus, Rena G; Kingsbury, Tami; Mayer, Dirk; Polster, Brian; Gartenhaus, Ronald B
Scientific reports, 12/2020, Letnik: 10, Številka: 1Journal Article
Inactivation of Ataxia-telangiectasia mutated (ATM) gene results in an increased risk to develop cancer. We show that ATM deficiency in diffuse large B-cell lymphoma (DLBCL) significantly induce mitochondrial deacetylase sirtuin-3 (SIRT3) activity, disrupted mitochondrial structure, decreased mitochondrial respiration, and compromised TCA flux compared with DLBCL cells expressing wild type (WT)-ATM. This corresponded to enrichment of glutamate receptor and glutamine pathways in ATM deficient background compared to WT-ATM DLBCL cells. ATM DLBCL cells have decreased apoptosis in contrast to radiosensitive non-cancerous A-T cells. In vivo studies using gain and loss of SIRT3 expression showed that SIRT3 promotes growth of ATM CRISPR knockout DLBCL xenografts compared to wild-type ATM control xenografts. Importantly, screening of DLBCL patient samples identified SIRT3 as a putative therapeutic target, and validated an inverse relationship between ATM and SIRT3 expression. Our data predicts SIRT3 as an important therapeutic target for DLBCL patients with ATM null phenotype.
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JCR | SNIP | JCR | SNIP | JCR | SNIP | JCR | SNIP |
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Vir: Osebne bibliografije
in: SICRIS
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