Disulfidptosis in tumor progression DOI Creative Commons

Senlin Wan,

Cong Liang,

Chunfeng Wu

et al.

Cell Death Discovery, Journal Year: 2025, Volume and Issue: 11(1)

Published: April 28, 2025

Abstract Disulfidptosis, a regulated cell death modality driven by the cystine transporter solute carrier family 7 member 11 (SLC7A11), is characterized actin cytoskeleton collapse under glucose starvation. This review systematically elucidates pivotal role of disulfidptosis in tumor metabolic reprogramming, with focus on its molecular mechanisms and distinctions from other pathways. The core include SLC7A11-mediated overload NRF2/c-Myc-regulated pentose phosphate pathway activation. By integrating multiomics data single-cell transcriptomics, we comprehensively decipher heterogeneous expression patterns disulfidptosis-related genes (DRGs) their dynamic interplay immune microenvironment remodeling. Furthermore, coexpression networks DRGs long noncoding RNAs (DRLs) offer novel insights into diagnosis, prognosis, targeted therapy. Therapeutically, SLC7A11 inhibitors (e.g., HG106) BAY-876) demonstrate efficacy exploiting vulnerabilities, whereas natural compounds synergizing checkpoint blockade provide strategies to counteract immunosuppressive microenvironments. Through interdisciplinary collaboration clinical translation, research holds transformative potential redefining precision oncology.

Language: Английский

Identification of disulfidptosis in esophageal squamous cell carcinoma based on single-cell and bulk RNA-seq data to predict prognosis and treatment response DOI Creative Commons
Xiaodan Zhang, Jianting Du, Xiao Lin

et al.

Frontiers in Immunology, Journal Year: 2025, Volume and Issue: 16

Published: April 15, 2025

Purpose Our study aims to identify the molecular subtypes of genes associated with disulfidptosis in esophageal squamous cell carcinoma(ESCC), develop a prognostic model, and potential therapeutic targets. Methods Based on GSE53625 expression profile data, we identified significant survival differences through consensus cluster analysis. Subsequently, univariate Cox, multivariate LASSO-Cox regression analysis were used establish risk stratification models. The transcriptome data TCGA-ESCC cohort GSE160269 single-cell sequencing dataset integrated verify biological significance further analyze heterogeneity tumor immune microenvironment, explore intercellular communication network, screen targeted drugs, providing theoretical basis for subsequent translational research. Results We two distinct patterns overall survival. Then, constructed signature disulfidptosis, results showed patients high score had worse prognosis. Univariate Cox demonstrated that was an independent factor validated validation set. subgroups differed proportion infiltration related signaling pathways ESCC. exploration immunotherapy confirmed our also certain predictive power immunotherapy. Drug screening suggested AZD8186 JQ1 as therapies high-score patients. Conclusion This provides new ESCC, explores targets, support personalized treatment.

Language: Английский

Citations

0

Disulfidptosis in tumor progression DOI Creative Commons

Senlin Wan,

Cong Liang,

Chunfeng Wu

et al.

Cell Death Discovery, Journal Year: 2025, Volume and Issue: 11(1)

Published: April 28, 2025

Abstract Disulfidptosis, a regulated cell death modality driven by the cystine transporter solute carrier family 7 member 11 (SLC7A11), is characterized actin cytoskeleton collapse under glucose starvation. This review systematically elucidates pivotal role of disulfidptosis in tumor metabolic reprogramming, with focus on its molecular mechanisms and distinctions from other pathways. The core include SLC7A11-mediated overload NRF2/c-Myc-regulated pentose phosphate pathway activation. By integrating multiomics data single-cell transcriptomics, we comprehensively decipher heterogeneous expression patterns disulfidptosis-related genes (DRGs) their dynamic interplay immune microenvironment remodeling. Furthermore, coexpression networks DRGs long noncoding RNAs (DRLs) offer novel insights into diagnosis, prognosis, targeted therapy. Therapeutically, SLC7A11 inhibitors (e.g., HG106) BAY-876) demonstrate efficacy exploiting vulnerabilities, whereas natural compounds synergizing checkpoint blockade provide strategies to counteract immunosuppressive microenvironments. Through interdisciplinary collaboration clinical translation, research holds transformative potential redefining precision oncology.

Language: Английский

Citations

0