ArticleCellular & molecular biology letters2025
FLNA, a disulfidptosis-related gene, modulates tumor immunity and progression in colorectal cancer.
Article in Cellular & molecular biology letters, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed.
- Disulfidptosis: molecular mechanisms and therapeutic targets.Signal transduction and targeted therapy · 2026Review
- Disulfidptosis: Mechanisms, evidence boundaries, and translational opportunities.Redox biology · 2026Review
- Surface Proteomics of Cancer-Derived Extracellular Vesicles Reveals Universal Heat Shock Proteins and Cancer Signatures.Molecular & cellular proteomics : MCP · 2026Article
- The emerging role of disulfidptosis in metabolic synergistic death and cancer immunotherapy.Oncogenesis · 2026Review
- Solute carrier transporters as metabolic gatekeepers in tumor-microenvironment crosstalk.Acta pharmacologica Sinica · 2026Review
- Targeting cell death: a promising approach for colorectal cancer therapy.Cancer cell international · 2026Review
- The role of disulfidptosis-driven tumor microenvironment remodeling in pancreatic cancer progression.Frontiers in immunology · 2026Article
- Disulfidptosis as an immunometabolic rheostat in gastrointestinal cancers: tuning the balance between T Cell exhaustion and immunogenic cell death.Frontiers in cell and developmental biology · 2026Review
- Disulfidptosis: A Metabolic Cell Death Mechanism with Therapeutic Potential in Cancer.Oncology research · 2026Review
- Biological Performance and Molecular Mechanisms of Mesyl MicroRNA-Targeted Oligonucleotides in Colorectal Cancer Cells.International journal of molecular sciences · 2025Article
- Quantitative proteomic analysis reveals potential serum diagnostic markers for colorectal adenoma.Frontiers in molecular biosciences · 2025Article
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Authors and funding
13 authors.
Funding
Abstract
backgroundDisulfidptosis represents a novel type of regulated cell death induced by excessively high intracellular levels of cystine. Targeting disulfide imbalance is considered a promising treatment approach for colorectal cancer (CRC). However, the involvement of disulfidptosis in CRC immunotherapy is undefined.
methodsUnsupervised clustering was applied to The Cancer Genome Atlas (TCGA) datasets to classify disulfidptosis-related phenotypes. The tumor microenvironment (TME) was characterized using diverse bioinformatics algorithms, including gene set variation analysis (GSVA) for pathway enrichment analysis and CIBERSORT for immune cell profiling. A disulfidptosis-related gene (DRG) signature was generated for stratifying CRC cases, and univariate Cox regression was utilized for identifying prognostic DRGs. Filamin A (FLNA) was pinpointed as a pivotal regulator of disulfidptosis, and its functional impacts on tumor progression and immunotherapy response were further investigated.
resultsTwo different groups were determined on the basis of the built disulfidptosis-related signature (DRS), showing distinct clinical outcomes, as well as different pathway activation, drug sensitivity, and immune infiltration patterns. The high-DRS subgroup correlated with poorer prognosis, elevated immunosuppressive cell activity, and reduced cytotoxic immune cell infiltration. FLNA emerged as a critical mediator of disulfidptosis in CRC, with its knockdown suppressing tumor cell migration and invasion in vitro. The FLNA inhibitor PTI-125 attenuated tumor growth and epithelial-mesenchymal transition (EMT), while FLNA depletion reversed glucose-driven metastasis. Notably, combined glucose transporter 1 (GLUT1) inhibition and anti-programmed cell death protein 1 (PD-1) therapy enhanced CD8
conclusionsThis study elucidates the interplay between disulfidptosis and the CRC immune landscape, highlighting FLNA as a therapeutic target. These findings suggest that modulating disulfidptosis in conjunction with immunotherapy may offer a novel treatment paradigm for CRC.
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