Disulfidptosis in tumor progression.

Area of Science:

• Oncology
• Cell Death Research
• Metabolic Reprogramming

Background:

• Disulfidptosis is a regulated cell death modality triggered by cystine transporter SLC7A11, characterized by actin cytoskeleton collapse under glucose deprivation.
• It plays a critical role in tumor metabolic reprogramming, distinct from other cell death pathways.

Purpose of the Study:

• To systematically review the molecular mechanisms of disulfidptosis.
• To explore its role in tumor metabolic reprogramming and immune microenvironment.
• To discuss therapeutic strategies targeting disulfidptosis.

Main Methods:

• Systematic review of literature on disulfidptosis.
• Integration of multiomics and single-cell transcriptomics data.
• Analysis of coexpression networks of disulfidptosis-related genes (DRGs) and long noncoding RNAs (DRLs).

Main Results:

• Disulfidptosis mechanisms involve SLC7A11-mediated cystine overload and NRF2/c-Myc-regulated pentose phosphate pathway activation.
• Heterogeneous expression patterns of DRGs and their interplay with the tumor immune microenvironment were deciphered.
• Coexpression networks of DRGs and DRLs provide insights into tumor diagnosis, prognosis, and therapy.

Conclusions:

• Disulfidptosis is a crucial mechanism in tumor metabolic reprogramming with significant diagnostic and prognostic implications.
• Targeted therapies, including SLC7A11 inhibitors and glucose transporter inhibitors, show promise.
• Synergistic strategies involving natural compounds and immunotherapy offer potential for overcoming immunosuppression and advancing precision oncology.