AI Article Synopsis

  • Disulfidptosis, caused by disulfide accumulation in cells with high SLC7A11 levels under glucose starvation, is proposed as a potential cancer treatment target.
  • The study examines how gene expression and mutations relate to patient prognoses and immune cell infiltration, noting a correlation between specific gene sets and immune cell types.
  • Findings reveal that actin cytoskeleton proteins are localized in cell structures, particularly with IQGAP1 at cell junctions, indicating a role in cancer pathways and patient survival across various cancer types.

Article Abstract

Disulfidptosis was recently reported to be caused by abnormal disulfide accumulation in cells with high SLC7A11 levels subjected to glucose starvation, suggesting that targeting disulfidptosis was a potential strategy for cancer treatment. We analyzed the relationships between gene expression and mutations and prognoses of patients. In addition, the correlation between gene expression and immune cell infiltration was explored. The potential regulatory mechanisms of these genes were assessed by investigating their related signaling pathways involved in cancer, their expression patterns, and their cellular localization. Most cancer types showed a negative correlation between the gene-set variation analysis (GSVA) scores and infiltration of B cells and neutrophils, and a positive correlation between GSVA scores and infiltration of natural killer T and induced regulatory T cells. Single-cell analysis revealed that , , and were highly expressed in different bladder urothelial carcinoma subtypes, but showed a low expression. Immunofluorescence staining showed that actin cytoskeleton proteins were mainly localized in the actin filaments and plasma membrane. Notably, IQGAP1 was localized in the cell junctions. In conclusion, this study provided an overview of disulfidptosis-related actin cytoskeleton genes in pan-cancer. These genes were associated with the survival of patients and might be involved in cancer-related pathways.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC10997004PMC
http://dx.doi.org/10.1515/med-2024-0929DOI Listing

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