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Cuproptosis: p53-regulated metabolic cell death?
Chen Xiong1,2, Hong Ling2,3,4, Qian Hao5,6
1Fudan University Shanghai Cancer Center and Institutes of Biomedical Sciences, Fudan University, Shanghai, 200032, China.
Cell Death and Differentiation
|February 9, 2023
Summary
Cuproptosis, a novel cell death pathway, is triggered by copper binding to metabolic proteins. Cancer cells resist cuproptosis via glycolysis, but the tumor suppressor p53 may regulate this process.
Area of Science:
- Biochemistry
- Cell Biology
- Cancer Metabolism
Background:
- Cuproptosis is a copper-induced cell death mechanism impacting oxidative phosphorylation.
- Cancer cells often resist cuproptosis by favoring glycolysis (Warburg effect).
- The tumor suppressor p53 influences metabolism, iron-sulfur cluster, and glutathione biosynthesis.
Purpose of the Study:
- To review the mechanism of cuproptosis.
- To explore the role of p53 in regulating cuproptosis.
- To propose mechanisms for p53-mediated cuproptosis regulation in cancer.
Main Methods:
- Literature review of cuproptosis mechanisms.
- Analysis of p53's role in metabolic regulation.
- Investigation of p53's influence on iron-sulfur cluster and glutathione pathways.
Main Results:
- Copper binding to lipoylated proteins induces proteotoxic stress, leading to cuproptosis.
- Cancer cells' reliance on glycolysis confers resistance to cuproptosis.
- p53's metabolic regulatory functions and involvement in key cuproptosis components suggest a regulatory role.
Conclusions:
- Cuproptosis is a distinct cell death pathway linked to cellular metabolism.
- p53 may act as a key regulator of cuproptosis, potentially offering therapeutic avenues.
- Understanding p53's interaction with cuproptosis is crucial for cancer research.
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