ArticleScientific reports2026
Mitochondrial protein COXFA4L3 (C15ORF48) confers resistance to DNA-damaging anticancer agents by repressing mitochondrial DNA damage responses.
Article in Scientific reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
DNA-damaging anticancer agents selectively kill highly proliferative cancer cells by inducing DNA damage, such as DNA double- or single-strand breaks, and by inhibiting DNA replication and transcription. These agents have been used for cancer chemotherapy for a long time; however, acquired resistance remains a serious problem that limits their effectiveness. Although mitochondria have their own DNA, which is distinct from nuclear DNA, the involvement of mitochondria and mitochondrial DNA (mtDNA) in resistance to DNA-damaging anticancer agents remains largely unknown. In this study, we found that the mitochondrial small protein cytochrome c oxidase-associated subunit FA4-like 3 (COXFA4L3), formerly known as C15ORF48, confers resistance to DNA-damaging anticancer agents. Mechanistically, DNA-damaging anticancer agents damage mtDNA and induce the cytosolic release of TFAM-unbound mtDNA via the mitochondrial permeability transition pore (mPTP), thereby promoting cell death via activation of the innate immune signalling cGAS-STING pathway. COXFA4L3 inhibits the cytosolic release of mtDNA by repressing mtDNA damage and mPTP opening. These results suggest that mitochondria affect sensitivity to DNA-damaging anticancer agents through COXFA4L3-mediated repression of mtDNA damage responses.
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