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Dynamically Reprograms Mitochondrial Respiration to Augment Cuproptosis in Cancer Therapy
Haohan Zhou1, Ruijue Wang2,3, Fang Zhu4
1Department of Orthopedic Oncology, Changzheng Hospital, Naval Medical University, Shanghai, China.
Small (Weinheim an Der Bergstrasse, Germany)
|February 7, 2026
Summary
This study introduces a novel nanoparticle that delivers lactate oxidase to reprogram cancer cell metabolism, enhancing copper-induced cell death (cuproptosis) and promoting antitumor effects.
Area of Science:
- Biochemistry
- Cell Biology
- Oncology
Background:
- Cuproptosis is a newly identified regulated cell death pathway dependent on copper ions and mitochondrial respiration.
- Metabolic reprogramming is a key strategy in cancer therapy.
- Lactate oxidase plays a role in modulating cellular energy metabolism.
Purpose of the Study:
- To investigate the role of lactate oxidase in cuproptosis.
- To develop a nanoparticle for targeted delivery of lactate oxidase into cancer cells.
- To explore the potential of metabolic reprogramming for cancer treatment.
Main Methods:
- Development of copper-coordinated polymer nanoparticles for lactate oxidase delivery.
- Assessment of nanoparticle effects on cancer cell metabolism, including pyruvate dehydrogenase and pyruvate kinase activity.
- Evaluation of nanoparticle-induced cuproptosis and ferroptosis.
- In vivo antitumor efficacy studies.
Main Results:
- Nanoparticles efficiently delivered lactate oxidase into cancer cells, reprogramming energy metabolism by converting lactate to pyruvate.
- Metabolic reprogramming boosted mitochondrial function, promoting cuproptosis via DLAT oligomerization and TCA cycle disruption.
- Nanoparticles induced both cuproptosis and ferroptosis through distinct mechanisms.
- Significant in vivo antitumor efficacy was observed.
Conclusions:
- Lactate oxidase delivery via nanoparticles effectively reprograms cancer cell metabolism to induce cuproptosis.
- This approach offers a novel therapeutic strategy by exploiting metabolic vulnerabilities for cancer treatment.
- The dual induction of cuproptosis and ferroptosis presents a promising avenue for enhanced antitumor activity.
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