Disulfidptosis mechanisms and therapeutic implications in cancer metabolic reprogramming and future perspectives

Ronghui Chen1, Jianhang You2, Suxia Weng3

  • 1Clinical Oncology School of Fujian Medical University, Fujian Cancer Hospital (Fujian Branch of Fudan University Shanghai Cancer Center), Fuzhou, 350000, China.

Discover Oncology
|October 3, 2025
PubMed

Insights

Disulfidptosis, a novel cell death pathway, shows promise in cancer therapy by inducing disulfide bond stress to inhibit tumor growth. Understanding its role in the tumor microenvironment is key for developing new oncology treatments.

Area of Science:

  • Oncology
  • Cell Death Mechanisms
  • Cancer Therapeutics

Background:

  • Regulatory cell death offers unique advantages for cancer treatment.
  • Disulfidptosis, a specific type of cell death, inhibits tumor growth by creating disulfide bond stress.
  • Genes involved in disulfidptosis influence cancer cell survival and proliferation.

Purpose of the Study:

  • To review the regulatory cell death mechanism known as disulfidptosis.
  • To examine the mechanisms of disulfidptosis and its associated genes in cancer.
  • To analyze the impact of disulfidptosis on the tumor microenvironment and explore therapeutic prospects.

Main Methods:

  • Literature review of disulfidptosis mechanisms.
  • Analysis of gene associations with cancer survival and proliferation.
  • Examination of the tumor microenvironment's role in disulfidptosis.
  • Exploration of emerging therapeutic strategies targeting disulfidptosis.

Main Results:

  • Disulfidptosis effectively inhibits tumor growth through disulfide bond stress.
  • Disulfidptosis-related genes are crucial for cancer cell survival and proliferation.
  • Disulfidptosis influences cancer's metabolic reprogramming and antioxidant response within the tumor microenvironment.
  • Disulfidptosis presents significant potential for cancer treatment.

Conclusions:

  • Disulfidptosis is a promising regulatory cell death pathway for cancer therapy.
  • Further research into disulfidptosis mechanisms and its interaction with the tumor microenvironment is warranted.
  • Targeting disulfidptosis offers novel therapeutic avenues for oncology.

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