ArticleTranslational cancer research2026
Selenium metabolism-related gene
Article in Translational cancer research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Background: Selenium metabolism is implicated in redox regulation and tumor progression, yet its role in oral squamous cell carcinoma (OSCC) remains elusive. Thioredoxin reductase 1 (TXNRD1), a core selenoprotein, has been linked to malignant phenotypes, but its clinical relevance and biological functions in OSCC require further elucidation. Therefore, this study aimed to systematically investigate the prognostic value and biological functions of TXNRD1 in OSCC through multi-omics analysis and experimental validation. Methods: We integrated multi-omics data from The Cancer Genome Atlas (TCGA) and Molecular Signatures Database (MSigDB) to systematically screen selenium metabolism-related prognostic genes. Least absolute shrinkage and selection operator (LASSO) regression, single-cell transcriptomics GSE103322, and immune infiltration analyses were applied to evaluate the clinical value and microenvironmental features of TXNRD1. Furthermore, we established stable TXNRD1-knockdown OSCC cell lines HSC-2 using lentiviral-mediated short hairpin RNA (shRNA), and performed Cell Counting Kit-8 (CCK-8) proliferation assays, colony formation assays, and flow cytometry to validate its functional roles Results: TXNRD1 was identified as a key selenium-related risk gene. It was significantly overexpressed in OSCC tissues and strongly correlated with poor overall survival area under the curve [area under the curve (AUC) =0.750]. Functional enrichment and single-cell analyses revealed that TXNRD1-high cancer cells were enriched in cell-cycle pathways (E2F targets, G2M checkpoint) and exhibited enhanced intercellular communication via MIF, LAMININ, and SPP1 pathways, along with associations with immune checkpoint genes PDCD1 and LAG3. Critically, our Conclusions: TXNRD1 drives OSCC progression through a dual mechanism-facilitating S-phase progression and suppressing apoptosis-and represents a promising prognostic biomarker and therapeutic target in OSCC.
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