Disulfidptosis and Its Emerging Relevance in Cancer and Immunity

Authors

Qidong Li
Shengrong Wu
Li Zhuang
Boyi Gan

Language

English

Publication Date

1-1-2025

Journal

Ferroptosis, Oxidative Stress, and Lipid Metabolism

DOI

10.70401/fos.2025.0004

PMID

41660164

PMCID

PMC12879491

PubMedCentral® Posted Date

2-7-2026

PubMedCentral® Full Text Version

Author MSS

Abstract

Disulfidptosis is a recently identified form of regulated cell death (RCD) triggered by disulfide stress when cystine uptake via solute carrier family 7 member 1 (SLC7A11) overwhelms the cell's reducing capacity. Unlike apoptosis or other "cell suicide" pathways, disulfidptosis likely represents a "cell sabotage" mechanism, defined by aberrant disulfide bonding and catastrophic actin cytoskeleton collapse. In this Perspective, we examine the paradoxical role of SLC7A11 as both a ferroptosis protector and a disulfidptosis trigger, and the mechanistic hallmarks of disulfidptosis. We highlight emerging therapeutic strategies to target disulfidptosis in cancer, including glucose transporter inhibition, redox-targeting agents, and nanomaterial-based approaches, and consider its dual role in immunity, where it may suppress T cell function yet act as a form of immunogenic cell death. Together, these insights position disulfidptosis as both a conceptual advance in RCD biology and a promising target for cancer therapy that warrants further mechanistic and translational exploration.

Keywords

Disulfidptosis, SLC7A11, ferroptosis, cancer therapy, immunity, cell death biomarker

Published Open-Access

yes

Recommended Citation

Li, Qidong; Wu, Shengrong; Zhuang, Li; et al., "Disulfidptosis and Its Emerging Relevance in Cancer and Immunity" (2025). Faculty, Staff and Student Publications. 5689.
https://digitalcommons.library.tmc.edu/uthgsbs_docs/5689