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Mechanisms and therapeutic potential of disulphidptosis in cancer
Yanhu Li1,2, Haijun Zhang1,2,3, Fengguang Yang1,2
1Lanzhou University Second Hospital, Lanzhou, PR China.
Abstract:
SLC7A11 plays a pivotal role in tumour development by facilitating cystine import to enhance glutathione synthesis and counteract oxidative stress. Disulphidptosis, an emerging form of cell death observed in cells with high expression of SLC7A11 under glucose deprivation, is regulated through reduction-oxidation reactions and disulphide bond formation. This process leads to contraction and collapse of the F-actin cytoskeleton from the plasma membrane, ultimately resulting in cellular demise. Compared to other forms of cell death, disulphidptosis exhibits distinctive characteristics and regulatory mechanisms. This mechanism provides novel insights and innovative strategies for cancer treatment while also inspiring potential therapeutic approaches for other diseases. Our review focuses on elucidating the molecular mechanism underlying disulphidptosis and its connection with the actin cytoskeleton, identifying alternative metabolic forms of cell death, as well as offering insights into disulphidptosis-based cancer therapy. A comprehensive understanding of disulphidptosis will contribute to our knowledge about fundamental cellular homeostasis and facilitate the development of groundbreaking therapies for disease treatment.
Insights
Disulphidptosis, a novel cell death pathway involving SLC7A11 and the actin cytoskeleton, offers new cancer treatment strategies. Understanding this process enhances knowledge of cellular homeostasis and disease therapy.
Area of Science:
- Cell Biology
- Biochemistry
- Oncology
Background:
- Solute carrier family 7 member 11 (SLC7A11) imports cystine, boosting glutathione synthesis and combating oxidative stress in tumors.
- High SLC7A11 expression under glucose deprivation induces disulphidptosis, a unique cell death form.
- Disulphidptosis involves redox reactions and disulphide bond formation, leading to F-actin cytoskeleton collapse and cell death.
Purpose of the Study:
- To review the molecular mechanisms of disulphidptosis.
- To explore the link between disulphidptosis and the actin cytoskeleton.
- To discuss disulphidptosis-based cancer therapy and its potential for other diseases.
Main Methods:
- Literature review of disulphidptosis.
- Analysis of redox reactions and F-actin cytoskeleton dynamics.
- Exploration of metabolic cell death pathways.
Main Results:
- Disulphidptosis is a distinct cell death mechanism regulated by SLC7A11 and redox balance.
- The F-actin cytoskeleton plays a critical role in disulphidptosis execution.
- This pathway presents novel therapeutic targets for cancer and other diseases.
Conclusions:
- Disulphidptosis offers innovative strategies for cancer treatment.
- Understanding disulphidptosis deepens fundamental knowledge of cellular homeostasis.
- Further research may yield groundbreaking therapies for various diseases.
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