ArticleFrontiers in pharmacology2026
Ferumoxytol potentiates ferroptotic radiosensitization through NCOA4-associated iron mobilization in brain-metastatic lung cancer cells.
Article in Frontiers in pharmacology, 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
Background: Brain metastasis remains a major cause of mortality in patients with advanced non-small cell lung cancer, whereas effective radiosensitization strategies are constrained by heterogeneous tumor responses and the tolerance of normal brain tissue. Ferumoxytol, a clinically used iron oxide nanoparticle formulation, has emerging translational potential as an iron-modulating agent. However, whether Ferumoxytol enhances radiosensitivity in brain-metastatic lung cancer cells and the mechanisms underlying this effect remain unclear. Methods: PC-9 lung adenocarcinoma cells and NCI-H1915 brain-metastatic lung adenocarcinoma cells were used to evaluate ferumoxytol under basal and irradiated conditions. Ferroptosis-associated phenotypes, oxidative stress, clonogenic survival, and cell-cycle distribution were assessed. TMT-based proteomics and public single-cell and spatial transcriptomic analyses were used for candidate prioritization and disease-context support. NCOA4 was evaluated by siRNA-mediated loss of function, single-dose clonogenic assays, time-resolved NCOA4/FTH1 immunoblotting, bafilomycin A1-based autophagic-flux analysis, and endogenous NCOA4-FTH1 co-immunoprecipitation. Results: Ferumoxytol induced mitochondrial, biochemical, and molecular changes consistent with ferroptosis and enhanced irradiation-associated ROS accumulation, lipid peroxidation, and loss of clonogenic survival. Proteomic analysis prioritized NCOA4, while public transcriptomic analyses provided associative disease-context support. In H1915 cells, NCOA4 silencing attenuated combined-treatment Fe Conclusion: Ferumoxytol enhances ferroptosis-associated oxidative injury and radiosensitivity in the tested lung cancer cell models. The combined loss-of-function, autophagic-flux, and protein-interaction data support the involvement of NCOA4-associated ferritin handling and iron mobilization. However, the observed FTH1 accumulation and the absence of iron-chelator rescue, cargo-specific lysosomal tracking, and
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