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Significance Drugs that cause epigenetic modification of DNA, such as 5-azacytidine (AZA), are used clinically to treat myelodysplastic syndromes and acute myeloid leukemia. In addition, AZA is being investigated for use against a range of different types of solid tumors, including lung and colorectal cancers. Treatment with AZA causes demethylation of DNA, thus increasing RNA synthesis, including the synthesis of double-stranded RNA, which is otherwise produced in virus-infected cells. We determined that cell death in response to AZA requires the antiviral enzyme RNase L. The results identify a drug target for enhancing the anticancer activity and reducing the toxicity of AZA and related drugs.

OAS-RNase L innate immune pathway mediates the cytotoxicity of a DNA-demethylating drug