# Disulfidptosis and its emerging relevance in cancer and immunity

## TL;DR

Disulfidptosis is a new type of cell death linked to disulfide stress, with potential roles in cancer and immune responses.

## Contribution

The paper introduces disulfidptosis as a novel regulated cell death mechanism and explores its therapeutic potential in cancer.

## Key findings

- Disulfidptosis is triggered by disulfide stress and involves actin cytoskeleton collapse.
- SLC7A11 plays a dual role in both protecting against ferroptosis and triggering disulfidptosis.
- Therapeutic strategies targeting disulfidptosis include glucose transporter inhibition and redox-targeting agents.

## 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.