ArticleJournal of bone oncology2026
Lapatinib induces ferroptosis in osteosarcoma via the SLC1A5-GPX4 axis.
Article in Journal of bone oncology, 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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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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6 authors.
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Abstract
Background: Osteosarcoma (OS) continues to have a poor prognosis, underscoring the urgent need for novel therapeutic strategies. Ferroptosis, an iron-dependent form of regulated cell death, offers a promising alternative to circumvent apoptosis resistance. Lapatinib (Lap), a well-known EGFR/HER2 inhibitor, exhibits potential beyond its canonical targets. Methods: The anti-OS effects of Lap were evaluated in U2OS and HOS cell lines using CCK-8, colony formation, Transwell, and flow cytometry assays. Its potential target was identified through molecular docking, molecular dynamics simulations, CETSA, and DARTS. Ferroptosis induction was assessed by measuring key markers (MDA, GSH, Fe Results: Lap significantly inhibited OS cell proliferation, migration, and invasion, and induced cell death predominantly via ferroptosis. It elevated lipid peroxidation and triggered characteristic ferroptotic events (Fe Conclusion: This study reveals a novel mechanism by which lapatinib inhibits OS via the SLC1A5-GPX4 axis to induce ferroptosis, providing a preclinical rationale for further evaluation of lapatinib repurposing in osteosarcoma.
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