ArticleBiomolecules & therapeutics2025
IFI16 Enhances Chemosensitivity of Breast Cancer Cells by Inhibiting DNA Damage Response.
Article in Biomolecules & therapeutics, 2025. 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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4 authors.
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Abstract
Many chemotherapeutic agents exert their cytotoxic effects primarily by inducing DNA damage. In response to DNA damage, cells activate a signaling cascade known as DNA damage response (DDR) to repair the damage and promote cell survival. Accordingly, the capacity of the DDR in cancer cells is a critical factor that influences their sensitivity to chemotherapy. Here, we identified a role for interferon γ-inducible protein 16 (IFI16) in modulating the DDR and chemosensitivity of breast cancer cells. Depletion of IFI16 in MDA-MB-231 cells conferred resistance to the DNA-damaging agents doxorubicin and 5-fluorouracil, as evidenced by increased cell viability and reduced caspase-3 cleavage compared to control cells. Mechanistically, IFI16 interacted with the MRE11-RAD50-NBS1 complex and disrupted the interaction between NBS1 and ataxia telangiectasia mutated (ATM), a critical step for ATM activation.
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