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AKT1 Phosphorylates FDX1 to Promote Cuproptosis Resistance in Triple‐Negative Breast Cancer
https://orcid.org/0000-0003-1232-3248
AbstractCuproptosis, a recently defined copper‐dependent cell death pathway, remains largely unexplored in tumor therapies, particularly in breast cancer. This study demonstrates that triple‐negative breast cancer (TNBC) bears a relatively elevated copper levels and exhibits resistance to cuproptosis. Mechanistically, copper activates the AKT signaling pathway, which inhibits ferredoxin‐1 (FDX1), a key regulator of cuproptosis. AKT1‐mediated FDX1 phosphorylation not only abrogates FDX1‐induced cuproptosis and aerobic respiration but also promotes glycolysis. Consequently, the combination of AKT1 inhibitors and the copper ionophores synergistically alleviate TNBC tumorigenesis both in vitro and in vivo. In summary, the findings reveal a crucial mechanism underlying TNBC resistance to cuproptosis and suggest a potential therapeutic approach for TNBC.
AKT1 Phosphorylates FDX1 to Promote Cuproptosis Resistance in Triple‐Negative Breast Cancer
https://orcid.org/0000-0003-1232-3248
AbstractCuproptosis, a recently defined copper‐dependent cell death pathway, remains largely unexplored in tumor therapies, particularly in breast cancer. This study demonstrates that triple‐negative breast cancer (TNBC) bears a relatively elevated copper levels and exhibits resistance to cuproptosis. Mechanistically, copper activates the AKT signaling pathway, which inhibits ferredoxin‐1 (FDX1), a key regulator of cuproptosis. AKT1‐mediated FDX1 phosphorylation not only abrogates FDX1‐induced cuproptosis and aerobic respiration but also promotes glycolysis. Consequently, the combination of AKT1 inhibitors and the copper ionophores synergistically alleviate TNBC tumorigenesis both in vitro and in vivo. In summary, the findings reveal a crucial mechanism underlying TNBC resistance to cuproptosis and suggest a potential therapeutic approach for TNBC.
AKT1 Phosphorylates FDX1 to Promote Cuproptosis Resistance in Triple‐Negative Breast Cancer
https://orcid.org/0000-0003-1232-3248
AbstractCuproptosis, a recently defined copper‐dependent cell death pathway, remains largely unexplored in tumor therapies, particularly in breast cancer. This study demonstrates that triple‐negative breast cancer (TNBC) bears a relatively elevated copper levels and exhibits resistance to cuproptosis. Mechanistically, copper activates the AKT signaling pathway, which inhibits ferredoxin‐1 (FDX1), a key regulator of cuproptosis. AKT1‐mediated FDX1 phosphorylation not only abrogates FDX1‐induced cuproptosis and aerobic respiration but also promotes glycolysis. Consequently, the combination of AKT1 inhibitors and the copper ionophores synergistically alleviate TNBC tumorigenesis both in vitro and in vivo. In summary, the findings reveal a crucial mechanism underlying TNBC resistance to cuproptosis and suggest a potential therapeutic approach for TNBC.
AKT1 Phosphorylates FDX1 to Promote Cuproptosis Resistance in Triple‐Negative Breast Cancer
Advanced Science
Sun, Zicheng (Autor:in) / Xu, Huazhen (Autor:in) / Lu, Guanming (Autor:in) / Yang, Ciqiu (Autor:in) / Gao, Xinya (Autor:in) / Zhang, Jing (Autor:in) / Liu, Xin (Autor:in) / Chen, Yongcheng (Autor:in) / Wang, Kun (Autor:in) / Guo, Jianping (Autor:in)
20.02.2025
Aufsatz (Zeitschrift)
Elektronische Ressource
Englisch
Nanoparticles Synergize Ferroptosis and Cuproptosis to Potentiate Cancer Immunotherapy
| Wiley | 2024
Nanoparticles Synergize Ferroptosis and Cuproptosis to Potentiate Cancer Immunotherapy
| Wiley | 2024