ArticleMedicina (Kaunas, Lithuania)2022
Comparative RNA-Sequencing Analysis Reveals High Complexity and Heterogeneity of Transcriptomic and Immune Profiles in Hepatocellular Carcinoma Tumors of Viral (HBV, HCV) and Non-Viral Etiology.
Article in Medicina (Kaunas, Lithuania), 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 8 citations in OpenAlex.
- An integrative transcriptomic analysis for prognosis and tumor microenvironment in HBV/HCV-associated hepatocellular carcinoma.Molecular therapy. Oncology · 2026Article
- Network pharmacology and molecular docking reveal antiviral mechanisms of silver nanoparticles synthesized by Oscillatoria sp. against HCV pathogenesis.Scientific reports · 2025Article
- An Update of Immunohistochemistry in Hepatocellular Carcinoma.Diagnostics (Basel, Switzerland) · 2025Review
- HCV-related hepatocellular carcinoma: gene signatures associated with TERT promoter mutations and sex.Journal of translational medicine · 2025Article
- Betulonic Acid Inhibits Type-2 Porcine Reproductive and Respiratory Syndrome Virus Replication by Downregulating Cellular ATP Production.International journal of molecular sciences · 2024Article
- Multiomics profiling of buffy coat and plasma unveils etiology-specific signatures in hepatocellular carcinoma.Clinical and molecular hepatology · 2024Article
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Authors and funding
11 authors at 3 institutions in 2 countries.
Funding
Abstract
Background and Objectives: Hepatocellular carcinoma (HCC), the most common type of primary liver cancer, is the leading cause of cancer-related mortality. It arises and progresses against fibrotic or cirrhotic backgrounds mainly due to infection with hepatitis viruses B (HBV) or C (HCV) or non-viral causes that lead to chronic inflammation and genomic changes. A better understanding of molecular and immune mechanisms in HCC subtypes is needed. Materials and Methods: To identify transcriptional changes in primary HCC tumors with or without hepatitis viral etiology, we analyzed the transcriptomes of 24 patients by next-generation sequencing. Results: We identified common and unique differentially expressed genes for each etiological tumor group and analyzed the expression of SLC, ATP binding cassette, cytochrome 450, cancer testis, and heat shock protein genes. Metascape functional enrichment analysis showed mainly upregulated cell-cycle pathways in HBV and HCV and upregulated cell response to stress in non-viral infection. GeneWalk analysis identified regulator, hub, and moonlighting genes and highlighted CCNB1, ACTN2, BRCA1, IGF1, CDK1, AURKA, AURKB, and TOP2A in the HCV group and HSF1, HSPA1A, HSP90AA1, HSPB1, HSPA5, PTK2, and AURKB in the group without viral infection as hub genes. Immune infiltrate analysis showed that T cell, cytotoxic, and natural killer cell markers were significantly more highly expressed in HCV than in non-viral tumors. Genes associated with monocyte activation had the highest expression levels in HBV, while high expression of genes involved in primary adaptive immune response and complement receptor activity characterized tumors without viral infection. Conclusions: Our comprehensive study underlines the high degree of complexity of immune profiles in the analyzed groups, which adds to the heterogeneous HCC genomic landscape. The biomarkers identified in each HCC group might serve as therapeutic targets.
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