ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2025
Disruption of NF-κB-Mediated Copper Homeostasis Sensitizes Breast Cancer to Cuproptosis.
Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed.
- Cuproptosis and ferroptosis: signal pathways, diseases and therapeutic targets.Signal transduction and targeted therapy · 2026Review
- Copper, cuproptosis, and cancer: biology concepts of a novel cell death.Apoptosis : an international journal on programmed cell death · 2026Review
- Cuproplasia-associated LOXL2 cooperates withJournal of gastrointestinal oncology · 2026Article
- Copper homeostasis and cuproptosis rewire the tumor microenvironment: mechanisms, immune modulation, and therapeutic opportunities.Journal of hematology & oncology · 2026Review
- Copper homeostasis and cuproptosis in cancer: mitochondrial metabolic dependency and nanomedicine-based therapeutic strategies.Apoptosis : an international journal on programmed cell death · 2026Review
- Acetylated mitochondrial MDH2 regulates CTR2 transcription to induce cuproptosis during Escherichia coli infection.Nature communications · 2026Article
- Cuproptosis: Biomarkers, Mechanisms and Treatments in Diseases.Molecules (Basel, Switzerland) · 2026Review
- Metal-based nanodrugs for cancer immunotherapy: smart nanosystems, immunomodulatory mechanisms, and translational perspectives.Frontiers in chemistry · 2026Review
- Metal Ions Within the Neuro-Immune-Tumor Axis.Journal of immunology research · 2026Review
- Disruption of NF-κB-Mediated Copper Homeostasis Sensitizes Breast Cancer to Cuproptosis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
Corrections and comments
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Authors and funding
17 authors.
Funding
Abstract
Copper plays a key role in inflammation and recent tumorigenesis. However, copper homeostasis and its role in cuproplasia and cuproptosis for cancer intervention remain incompletely explored. Here, it is unveiled that copper enhances the NF-κB pathway by directly binding to transforming growth factor β-activated kinase 1 (TAK1), thereby promoting TRAF2 interaction with and mediation of TAK1 ubiquitination and activation, leading to IκB kinase β (IKKβ) activation and mediating copper's inflammatory and oncogenic functions. Notably, copper is indispensable for TNFα/LPS-induced NF-κB activation and subsequent PD-L1 promotion. Thus, copper chelators offer protection against acute infection in murine models. Meanwhile, NF-κB represses copper uptake by negatively controlling the expression of copper transporter 1 (CTR1) transcriptionally, providing a negative feedback regulation for maintaining copper homeostasis. As a result, targeting NF-κB appears to elevate CTR1 expression, leading to excessive copper uptake and downstream MAPK and AKT activation, in turn, conferring resistance to anti-NF-κB therapies. Therefore, disruption of NF-κB not only synergizes with copper chelators to overcome drug resistance and cuproplasia, but also combines with copper ionophores to facilitate cuproptosis, providing a dual approach for combating chronic inflammation-driven cancers.
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