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Inducing disulfidptosis in tumors:potential pathways and significance
Tao Mi1,2, Xiangpan Kong1,2, Meiling Chen1,2
1Department of Urology Children's Hospital of Chongqing Medical University National Clinical Research Center for Child Health and Disorders Ministry of Education Key Laboratory of Child Development and Disorders Chongqing P.R. China.
Abstract:
Regulated cell death (RCD) is crucial for the elimination of abnormal cells. In recent years, strategies aimed at inducing RCD, particularly apoptosis, have become increasingly important in cancer therapy. However, the ability of tumor cells to evade apoptosis has led to treatment resistance and relapse, prompting extensive research into alternative death processes in cancer cells. A recent study identified a novel form of RCD known as disulfidptosis, which is linked to disulfide stress. Cancer cells import cystine from the extracellular environment via solute carrier family 7 member 11 (SLC7A11) and convert it to cysteine using nicotinamide adenine dinucleotide phosphate (NADPH). When NADPH is deficient or its utilization is impaired, cystine accumulates, leading to the formation of disulfide bonds in the actin cytoskeleton, triggering disulfidptosis. Disulfidptosis reveals a metabolic vulnerability in tumors, offering new insights into cancer therapy strategies. This review provides a detailed overview of the mechanisms underlying disulfidptosis, the current research progress, and limitations. It also highlights innovative strategies for inducing disulfidptosis and explores the potential of combining these approaches with traditional cancer therapies, particularly immunotherapy, to expedite clinical translation.
Insights
Discovered disulfidptosis, a novel regulated cell death (RCD) pathway triggered by disulfide stress and linked to cancer metabolism. This new RCD mechanism offers innovative therapeutic strategies for cancer treatment.
Area of Science:
- Oncology
- Cell Biology
- Metabolic Pathways
Background:
- Regulated cell death (RCD) is vital for eliminating abnormal cells, with apoptosis being a key target in cancer therapy.
- Tumor cells frequently evade apoptosis, leading to treatment resistance and disease relapse.
- Research is exploring alternative RCD pathways to overcome therapeutic resistance.
Purpose of the Study:
- To introduce and explain disulfidptosis, a novel RCD pathway.
- To elucidate the underlying mechanisms of disulfidptosis.
- To explore its potential as a cancer therapeutic strategy.
Main Methods:
- Review of existing literature on regulated cell death and cancer metabolism.
- Detailed examination of the molecular mechanisms linking cystine import, NADPH levels, and disulfide stress.
- Analysis of the role of solute carrier family 7 member 11 (SLC7A11) in disulfidptosis.
Main Results:
- Disulfidptosis is induced by the accumulation of extracellular cystine due to impaired nicotinamide adenine dinucleotide phosphate (NADPH) utilization.
- Cystine accumulation leads to disulfide bond formation in the actin cytoskeleton, triggering this novel cell death.
- This process highlights a metabolic vulnerability exploitable in tumor cells.
Conclusions:
- Disulfidptosis represents a new form of RCD linked to metabolic dysfunction and disulfide stress.
- Targeting disulfidptosis offers a promising avenue for novel cancer therapies.
- Combining disulfidptosis induction with immunotherapy may enhance treatment efficacy and expedite clinical translation.
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