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<p>Disulfidptosis, an emerging metabolism-associated regulated cell death pathway, involves tumor progression via the modulation of redox homeostasis. Long noncoding RNAs (lncRNAs) are promising for tumor prognostic models, but prognostic models based on lncRNAs associated with disulfidptosis-related genes remain scarce in laryngeal squamous cell carcinoma (LSCC). By utilizing TCGA-LSCC RNA sequencing datasets, this research identified differentially expressed disulfidptosis-related genes (DRGs) and lncRNAs coexpressed with these DRGs and subsequently established a 5-lncRNA prognostic signature through Pearson correlation analysis, LASSO Cox regression, and Cox regression analysis. This signature stratified LSCC patients into high-risk and low-risk subgroups with distinct survival outcomes and acceptable discriminatory performance in the analyzed TCGA-derived cohort. DUBR, a key oncogenic lncRNA in the model, correlated with poor prognosis and was functionally associated with the disulfidptosis-related gene TLN1. MeRIP-qPCR further supported that DUBR carries m6A modification, and METTL3 knockdown reduced DUBR m6A enrichment, suggesting possible METTL3-dependent m6A regulation of DUBR. DUBR silencing inhibited LSCC cell proliferation, migration, invasion, and epithelial–mesenchymal transition (EMT). Moreover, transfection with a TLN1 overexpression plasmid partially restored the proliferation inhibition induced by DUBR knockdown, supporting the potential functional involvement of TLN1 in DUBR-mediated proliferative effects. Exploratory in silico drug-response analyses identified differential predicted responses to entinostat, linsitinib, and VE-822 according to risk status and DUBR expression. This internally validated signature may support exploratory prognostic risk stratification of LSCC within the analyzed TCGA-derived cohort and may highlight DUBR as a candidate molecule for further biological investigation. Further validation in independent external cohorts and dedicated disulfidptosis functional assays is required before these findings can be considered generalizable.</p>

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Integrative analysis of lncRNAs associated with disulfidptosis-related genes for prognostic risk evaluation and tumor immune microenvironment assessment in laryngeal squamous cell carcinoma

  • 期刊论文

  • 发表日期：

    2026年6月2日

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  • Qinghua Liu,
  • Zesheng Zhang,
  • Yingli Xie,
  • Ru Tang,
  • Ge Gao,
  • Zhe Yang,
  • Duanshali Liu,
  • Yilun Zou,
  • Yongxia Zhang,
  • Mingbo Liu

摘要

Disulfidptosis, an emerging metabolism-associated regulated cell death pathway, involves tumor progression via the modulation of redox homeostasis. Long noncoding RNAs (lncRNAs) are promising for tumor prognostic models, but prognostic models based on lncRNAs associated with disulfidptosis-related genes remain scarce in laryngeal squamous cell carcinoma (LSCC). By utilizing TCGA-LSCC RNA sequencing datasets, this research identified differentially expressed disulfidptosis-related genes (DRGs) and lncRNAs coexpressed with these DRGs and subsequently established a 5-lncRNA prognostic signature through Pearson correlation analysis, LASSO Cox regression, and Cox regression analysis. This signature stratified LSCC patients into high-risk and low-risk subgroups with distinct survival outcomes and acceptable discriminatory performance in the analyzed TCGA-derived cohort. DUBR, a key oncogenic lncRNA in the model, correlated with poor prognosis and was functionally associated with the disulfidptosis-related gene TLN1. MeRIP-qPCR further supported that DUBR carries m6A modification, and METTL3 knockdown reduced DUBR m6A enrichment, suggesting possible METTL3-dependent m6A regulation of DUBR. DUBR silencing inhibited LSCC cell proliferation, migration, invasion, and epithelial–mesenchymal transition (EMT). Moreover, transfection with a TLN1 overexpression plasmid partially restored the proliferation inhibition induced by DUBR knockdown, supporting the potential functional involvement of TLN1 in DUBR-mediated proliferative effects. Exploratory in silico drug-response analyses identified differential predicted responses to entinostat, linsitinib, and VE-822 according to risk status and DUBR expression. This internally validated signature may support exploratory prognostic risk stratification of LSCC within the analyzed TCGA-derived cohort and may highlight DUBR as a candidate molecule for further biological investigation. Further validation in independent external cohorts and dedicated disulfidptosis functional assays is required before these findings can be considered generalizable.