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Gene amplification-associated overexpression of the RNA editing enzyme ADAR1 enhances human lung tumorigenesis

AutorAnadón, C.; Guil, S.; Simó-Riudalbas, L.; Moutinho, C.; Setien, F.; Martínez-Cardús, A.; Moran, S.; Villanueva, A.; Calaf, M.; Vidal, August; Lazo, Pedro A. ; Zondervan, I.; Savola, S.; Kohno, T.; Yokota, J.; Pouplana, L. R. de; Esteller, M.
Fecha de publicación2016
EditorNature Publishing Group
CitaciónOncogene 35(33): 4407-4413 (2016)
ResumenThe introduction of new therapies against particular genetic mutations in non-small-cell lung cancer is a promising avenue for improving patient survival, but the target population is small. There is a need to discover new potential actionable genetic lesions, to which end, non-conventional cancer pathways, such as RNA editing, are worth exploring. Herein we show that the adenosine-toinosine editing enzyme ADAR1 undergoes gene amplification in non-small cancer cell lines and primary tumors in association with higher levels of the corresponding mRNA and protein. From a growth and invasion standpoint, the depletion of ADAR1 expression in amplified cells reduces their tumorigenic potential in cell culture and mouse models, whereas its overexpression has the opposite effects. From a functional perspective, ADAR1 overexpression enhances the editing frequencies of target transcripts such as NEIL1 and miR-381. In the clinical setting, patients with early-stage lung cancer, but harboring ADAR1 gene amplification, have poor outcomes. Overall, our results indicate a role for ADAR1 as a lung cancer oncogene undergoing gene amplification-associated activation that affects downstream RNA editing patterns and patient prognosis.
Versión del editorhttps://doi.org/10.1038/onc.2015.469
Identificadoresdoi: 10.1038/onc.2015.469
issn: 0950-9232
e-issn: 1476-5594
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