ArticleVirology journal2025
Human endogenous retrovirus ERVK3-1 characterizes a metabolically active and immunosuppressive subtype of liver cancer.
Article in Virology journal, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed.
- Activation of endogenous retroviruses in tumor cells and their immunomodulatory mechanisms: from molecular basis to clinical translation.Frontiers in oncology · 2026Review
- Endogenous retroviruses and response to immune checkpoint inhibitors: mechanisms, clinical evidence, and therapeutic implications.Frontiers in immunology · 2026Review
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7 authors.
Funding
Abstract
backgroundHuman endogenous retroviruses (HERVs), particularly the HERV-K family, are increasingly recognized for their roles in cancer biology, yet the function of ERVK3-1 (HERVK_3p21.31) in liver hepatocellular carcinoma (LIHC) remains largely unexplored.
methodsWe analyzed transcriptomic data from the TCGA-LIHC cohort to identify differentially expressed genes (DEGs) between high and low ERVK3-1 expression groups, followed by functional enrichment analyses (GO, KEGG, GSEA), protein-protein interaction (PPI) network construction, and hub gene identification. The immunological relevance of ERVK3-1 was assessed through TIP immune cycle analysis, single-cell RNA sequencing datasets, and correlation with immune checkpoint expression. Immunotherapy responsiveness was evaluated using TIDE and TCIA databases.
resultsHigh ERVK3-1 expression was associated with enrichment in metabolic and oxidative stress-related pathways, while low expression correlated with cell cycle and DNA replication. PPI analysis revealed mitosis-related hub genes (e.g., CCNB1, CDK1). ERVK3-1 expression promoted early immune cell recruitment but was inversely correlated with later stages of the cancer immunity cycle, including immune infiltration and T-cell killing. Single-cell data showed high ERVK3-1 expression in immunosuppressive subsets, alongside positive associations with inhibitory immune checkpoints (e.g., PD-1, CTLA-4, TIM-3). High ERVK3-1 expression also correlated with greater immune evasion and reduced immunotherapy responsiveness.
conclusionsERVK3-1 plays a multifaceted role in LIHC progression, contributing to metabolic reprogramming, immune suppression, and resistance to immunotherapy. These findings highlight ERVK3-1 as a potential prognostic biomarker and therapeutic target in liver cancer.
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