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Disulfidoptosis: A New Key to Unlocking Cancer Treatment
Xue Li1, Shujun Xu1, Liwei Jia1
1School of Pharmacy, Heilongjiang University of Chinese Medicine, Harbin, China.
Abstract:
The metabolic properties of disulfidoptosis targeting cancer cells have become a new key to unlocking cancer treatment's lock. Conventional cancer therapies aim to kill tumor cells through apoptosis, but cell death is carried out by a network of cascading enzymes. Malignant cells can evade the death process by downregulating key enzymes or inhibiting death-inducing triggers, leading to cancer persistence and recurrence of cancer cells that are resistant to conventional therapies and immune escape, which has compelled researchers to explore new therapeutic avenues. Disulfidoptosis is triggered by the accumulation of excessive intracellular disulfides in cells with high expression of solute carrier family 7 member 11 (SLC7A11) under glucose starvation conditions, which simultaneously induces the breakage of intracellular disulfide bonds and leads to protein malfunction, thereby triggering cancer cell death. However, there is no comprehensive account of disulfidoptosis application in cancer therapy. This review comprehensively summarizes the mechanism of disulfidoptosis for cancer treatment, which provides new ideas for cancer treatment.
Insights
Disulfidoptosis, a novel cancer cell death pathway, offers a new therapeutic strategy by targeting cancer cells with high SLC7A11 expression under glucose starvation. This approach overcomes resistance to conventional apoptosis-based treatments.
Area of Science:
- Oncology
- Molecular Biology
- Biochemistry
Background:
- Conventional cancer therapies often fail due to malignant cells evading apoptosis.
- Cancer cell resistance and immune escape necessitate exploration of alternative therapeutic strategies.
- Disulfidoptosis presents a promising new avenue for cancer treatment.
Purpose of the Study:
- To comprehensively review the mechanism of disulfidoptosis in cancer treatment.
- To highlight disulfidoptosis as a novel therapeutic target.
- To provide new insights into cancer therapy development.
Main Methods:
- Literature review of disulfidoptosis mechanisms.
- Analysis of solute carrier family 7 member 11 (SLC7A11) role.
- Investigation of glucose starvation effects on cancer cells.
Main Results:
- Disulfidoptosis is induced by excessive intracellular disulfides in SLC7A11-high cells under glucose starvation.
- This process leads to protein malfunction and cancer cell death.
- It offers a potential alternative to apoptosis-resistant cancer treatments.
Conclusions:
- Disulfidoptosis represents a distinct cancer cell death pathway.
- Targeting disulfidoptosis, particularly in SLC7A11-expressing tumors, is a viable therapeutic strategy.
- This review provides a foundation for future research and clinical applications of disulfidoptosis in oncology.
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