ReviewAmerican journal of cancer research2025
Research progress and potential therapeutic targets of a novel disulfide stress-driven cell death-disulfidptosis in gynecological tumors and other gynecological disorders.
Review in American journal of cancer research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
1 citing paper in PubMed.
- Disulfidptosis and androgenic cancers: from molecular mechanisms to clinical applications and future translational research.Frontiers in endocrinology · 2026Review
Corrections and comments
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Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Disulfidptosis is a novel Nicotinamide Adenine Dinucleotide Phosphate (NADPH) deficiency-driven cell death pathway characterized by cystine overload and aberrant disulfide bond formation in actin cytoskeletal proteins, distinct from apoptosis, ferroptosis, and other programmed cell death modalities. In gynecological tumors (ovarian, cervical, and endometrial cancers), this process is orchestrated by dysregulated SLC7A11 expression, impaired thioredoxin system function, and Rac-WRC-Arp2/3-mediated actin network collapse. Bioinformatic analyses of The Cancer Genome Atlas (TCGA)/Gene Expression Omnibus (GEO) datasets have revealed that disulfidptosis-related genes (e.g., SLC7A11, GYS1, NCKAP1) and lncRNAs (e.g., PRDX6-AS1, EMSLR) correlate with patient prognosis, chemoresistance, and tumor immune microenvironment (TME) remodeling. Therapeutic strategies to induce disulfidptosis include glucose deprivation to limit NADPH supply, inhibition of NADPH-generating enzymes (e.g., G6PD inhibition), and nanodelivery systems (e.g., FeOOH@Fe-Ap@Au) that synchronize disulfidptosis with ferroptosis. Preliminary evidence proposes that disulfidptosis inducers may synergize with immune checkpoint inhibitors (ICIs) through TME modulation, though experimental validation remains ongoing. Beyond malignancies, disulfidptosis-related pathways have been implicated in endometriosis, where disulfidptosis-related genes (DRGs; e.g., PDLIM1, ACTB) regulate ectopic lesion progression via immune-metabolic crosstalk. This review comprehensively summarizes the molecular mechanisms, disease associations, and translational potential of disulfidptosis in gynecological disorders, proposing targeted therapeutic paradigms and future research directions.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.