ArticleHuman cell2026
Integrative analysis of lncRNAs associated with disulfidptosis-related genes for prognostic risk evaluation and tumor immune microenvironment assessment in laryngeal squamous cell carcinoma.
Article in Human cell, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors.
Funding
Abstract
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.
Indexed as
Identifiers
42228246What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.