ArticleDiscover oncology2025
Construction of a novel disulfidptosis and cuproptosis-related lncRNA signature for predicting the clinical outcome and immune response in stomach adenocarcinoma.
Article in Discover oncology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- Development and validation of a novel disulfidptosis-associated LncRNA model for risk stratification and targeted therapy guidance in gastric adenocarcinoma.American journal of cancer research · 2026Article
- Epigenetic modification of cuproptosis by non-coding RNAs in cancer drug resistance.Molecular cancer · 2025Review
- The role of cuproptosis in the occurrence and development of gastric cancer.Frontiers in pharmacology · 2025Review
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4 authors.
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Abstract
backgroundDisulfidptosis, a newly discovered form of cell death resulting from disulfide stress, remains unclear in its role in stomach adenocarcinoma (STAD). This study aimed to establish a novel disulfidptosis and cuproptosis-related lncRNAs (DCRLs) signature for STAD.
methodsWe sourced RNA-seq data for STAD from the The Cancer Genome Atlas (TCGA) repository. STAD samples underwent nonnegative matrix factorization (NMF) clustering to identify distinct molecular subgroups, followed by Lasso-Cox regression to construct a prognostic model for DCRLs. Subsequently, the model's clinical predictive capacity was evaluated using a nomogram. The expression of risk lncRNAs was validated via quantitative reverse transcription polymerase chain reaction (qRT-PCR).
resultsThe samples were classified into three molecular subtypes based on DCRLs, with the C1 subtype demonstrating the worst prognosis. We identified four independent prognostic lncRNAs (AC016394.2, NUTM2A-AS1, OIP5-AS1, and LIMS1-AS1) and constructed a prognostic risk model. Survival analysis revealed that high-risk patients had a poorer prognosis. The model's risk score was strongly correlated with the tumor mutational burden (TMB), microsatellite instability (MSI), immune subtypes, and tumor-infiltrating immune cells (TIICs) in the tumor microenvironment (TME). Analysis utilizing the Tumor Immune Dysfunction and Exclusion (TIDE) revealed a higher risk of tumor immune evasion among high-risk patients. Moreover, the expression levels of four risk lncRNAs were higher in the majority of gastric cancer cell lines compared to normal cell lines.
conclusionOur study establishes a risk model that effectively predicts clinical outcomes and immune response in STAD.
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