ArticleBiochemistry and biophysics reports2026
ATM inhibition restores IFN-γ sensitivity and induces ferroptosis in NSCLC via DNA damage response.
Article in Biochemistry and biophysics 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
Cancer immunotherapy has demonstrated remarkable clinical success across diverse tumor types. Nevertheless, durable responses occur in only a subset of patients, and both primary and acquired resistance remain major challenges. Interferon-γ (IFN-γ), a key effector cytokine in anti-tumor immunity, is often neutralized by tumor cells through mechanisms that attenuate its activity. In this study, we examined the regulation of IFN-γ responsiveness in two human NSCLC cell lines, PC-9 and A549. PC-9 cells exhibited greater resistance to IFN-γ treatment compared with A549 cells. Transcriptomic analysis revealed that IFN-γ-resistant PC-9 cells were enriched in genes associated with the homologous recombination (HR) DNA repair pathway following exposure to IFN-γ. Given the critical role of the serine/threonine kinase ataxia telangiectasia mutated (ATM) in detecting DNA double-strand breaks and coordinating HR repair, we investigated whether ATM contributes to IFN-γ resistance by using the ATM inhibitor KU-55933. Inhibition of ATM restored IFN-γ sensitivity by inducing ferroptosis in NSCLCs. Mechanistically, the combination of IFN-γ treatment and ATM inhibition elicited a robust DNA damage response and disrupted glutathione metabolism, reducing the GSH/GSSG ratio and thereby promoting ferroptosis through increased susceptibility to oxidative stress. These findings highlight the pivotal role of DNA damage response pathways in mediating the anti-tumor effects of IFN-γ.
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