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Small nucleolar RNA host genes in hepatocellular carcinoma: an evidence-weighted and etiology-aware framework for mechanistic and translational interpretation

Amr Ali Mohamed Abdelgawwad El-SehrawyDiabetes, Endocrinology and Metabolism, Internal Medicine Department, Mansoura University, Mansoura, Egypt. [email protected]Yasmeen Kateb AhmedMedical Laboratory Techniques Department, College of Health and Medical Technology, University of Al-Maarif, Anbar, IraqN DjumayevaDepartment of Infectious Diseases, Samarkand State Medical University, Samarkand, UzbekistanJaafaru Sani MohammedMedical Analysis Department, Faculty of Applied Science, Tishk International University, Erbil, IraqAyesha AlmasDepartment of Basic Medical Sciences, College of Medicine, Majmaah University, majmaah 11952, Saudi Arabia. [email protected]Majid S. JabirCollege of Applied Sciences, University of Technology, Baghdad, IraqSafa HussienCentre of Research Impact and Outcome, Chitkara University, Rajpura- 140417, Punjab, IndiaAseel SmeratHourani Center for Applied Scientific Research, Al-Ahliyya Amman University, Amman 19328, JordanMaha ShakirDepartment of Medical Laboratory Technologies, College of Health and Medical Technologies, Al-Nisour University, Baghdad, IraqTina Saeed BasunduwahDiabetes, Endocrinology and Metabolism, Internal Medicine Department, Mansoura University, Mansoura, Egypt

2026en

ABI

Annotatsiya

Small nucleolar RNA host genes (SNHGs) are a distinctive subgroup of long non-coding RNAs whose loci can generate both host lncRNA transcripts and intronic small nucleolar RNAs. In hepatocellular carcinoma (HCC), dysregulated SNHGs have been linked to tumor growth, epithelial-mesenchymal transition, metastasis, stemness, immune remodeling, extracellular vesicle communication, and therapeutic resistance. However, the clinical meaning of these associations remains uneven because many reported mechanisms are based on limited cell-line experiments, retrospective cohorts, or non-stratified HCC models. This structured narrative review examines SNHG biology in HCC through an evidence-weighted and etiology-aware framework. Rather than cataloguing individual SNHG-miRNA-mRNA axes, we distinguish mechanistically stronger pathways from preliminary or hypothesis-generating findings and separate diagnostic, prognostic, predictive, and therapeutic implications. We also emphasize non-ceRNA mechanisms, including nuclear epigenetic regulation, RNA-protein interaction, protein-stability control, extracellular-vesicle signaling, and the dual-output architecture of SNHG loci. Particular attention is given to quantitative constraints of ceRNA models, differences among HBV-, HCV-, alcohol-related, and MASLD/MASH-associated HCC, and the current barriers to clinical translation. Overall, SNHGs represent promising but not yet clinically mature biomarkers or therapeutic targets. Their future value will depend on prospective validation, standardized assays, etiology-defined models, isoform-aware targeting, and integration into multi-omic and functional precision oncology frameworks.

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DOI: 10.1007/s11033-026-12203-0

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