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Gannon, Hugh S; Zou, Tao; Kiessling, Michael K; Gao, Galen F; Cai, Diana; Choi, Peter S; Ivan, Alexandru P; Buchumenski, Ilana; Berger, Ashton C; Goldstein, Jonathan T; Cherniack, Andrew D; Vazquez, Francisca; Tsherniak, Aviad; Levanon, Erez Y; Hahn, William C; Meyerson, Matthew
Nature communications, 12/2018, Letnik: 9, Številka: 1Journal Article
Systematic exploration of cancer cell vulnerabilities can inform the development of novel cancer therapeutics. Here, through analysis of genome-scale loss-of-function datasets, we identify adenosine deaminase acting on RNA (ADAR or ADAR1) as an essential gene for the survival of a subset of cancer cell lines. ADAR1-dependent cell lines display increased expression of interferon-stimulated genes. Activation of type I interferon signaling in the context of ADAR1 deficiency can induce cell lethality in non-ADAR1-dependent cell lines. ADAR deletion causes activation of the double-stranded RNA sensor, protein kinase R (PKR). Disruption of PKR signaling, through inactivation of PKR or overexpression of either a wildtype or catalytically inactive mutant version of the p150 isoform of ADAR1, partially rescues cell lethality after ADAR1 loss, suggesting that both catalytic and non-enzymatic functions of ADAR1 may contribute to preventing PKR-mediated cell lethality. Together, these data nominate ADAR1 as a potential therapeutic target in a subset of cancers.
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in: SICRIS
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