ArticleCell death & disease2026
Sunitinib enhances cuproptosis induced by copper ionophores via ROS-ATF3-SLC31A1 axis in thyroid Carcinoma.
Article in Cell death & disease, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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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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Who cites it
1 citing paper in PubMed.
- A cuproptosis-related lncRNAs-based risk signature for predicting prognosis and immune status in glioma.Translational cancer research · 2026Article
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Authors and funding
10 authors.
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Abstract
The clinical management of advanced thyroid carcinoma presents substantial therapeutic challenges due to non-curative surgical outcomes and resistance to both radioiodine therapy and conventional chemotherapeutic agents. Emerging evidence implicates copper dysregulation in thyroid cancer pathogenesis, yet monotherapy with copper ionophores demonstrates constrained efficacy due to tumor-intrinsic adaptive resistance mechanisms. In this study, we investigated the therapeutic potential of combining Sunitinib with copper ionophore Elesclomol as a novel strategy against thyroid carcinoma. Mechanically, we identified that Sunitinib treatment induces ROS accumulation, activating the stress-responsive transcription factor ATF3, which directly binds and transactivates the copper transporter gene SLC31A1. Clinically, TCGA analysis reveals SLC31A1 as a vulnerability in advanced thyroid cancer, with expression significantly downregulated in metastatic lesions, a deficit rescued by Sunitinib. Overall, these results demonstrate that Sunitinib and copper ionophores can induce synergistic cytotoxic effect, shedding light on therapeutic strategy for advanced thyroid carcinomas.
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