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Significance APOBEC3B (A3B) is overexpressed in multiple tumor types and a major source of mutation by converting DNA cytosines to uracils. A3B-positive tumors are often more heterogenous and result in poor clinical outcomes. We show that a proportion of A3B-catalyzed uracil lesions is repaired by uracil DNA glycosylase 2 (UNG)-driven base excision repair and that rendering cells UNG-defective leads to cytotoxicity. This cell death mechanism requires uracil processing by mismatch repair proteins and functional p53. Our results indicate that UNG inhibition could be a strategy to kill a subset of A3B-positive tumors.

The deaminase APOBEC3B triggers the death of cells lacking uracil DNA glycosylase