Disulfidptosis and androgenic cancers: from molecular mechanisms to clinical applications and future translational research

TL;DR

This paper explores how disulfidptosis, a new type of cell death, could help treat androgenic cancers like prostate and bladder cancer by targeting protein disulfide bonds.

Contribution

The paper systematically reviews disulfidptosis mechanisms and its potential as a novel therapeutic target in male cancers.

Findings

Disulfidptosis regulates tumor cell survival through protein disulfide bonds.

It shows potential as a therapeutic target in prostate, testicular, and bladder cancers.

The paper highlights key regulatory genes and clinical application challenges.

Abstract

Disulfidptosis, a newly discovered form of programmed cell death, has garnered significant attention in tumor biology and reproductive system research in recent years, particularly demonstrating importance in urological cancer studies. Prostate cancer, testicular cancer, and bladder cancer are highly prevalent malignant tumors among men globally. Modern medical research reveals their complex pathogenesis and the limited efficacy of traditional treatments, necessitating the identification of novel therapeutic targets. Disulfidptosis influences tumor cell survival and death by regulating the formation and cleavage of intracellular protein disulfide bonds, highlighting its pivotal role in tumorigenesis and progression. This paper systematically reviews the molecular mechanisms of disulfidptosis, elucidates its regulatory role in male cancer cells—including key regulatory genes and therapeutic target potential—and discusses its application value and challenges as a potential therapeutic target based on clinical research. It aims to deepen understanding of disulfidptosis regulation, provide new insights and strategies for future precision treatment and clinical translation of male cancers, and drive innovation in related therapeutic approaches.

Figures