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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.