Related Experiment Video For ALG8
Updated: Jun 5, 2025
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Expression of ALG8 in hepatocellular carcinoma and its diagnostic and prognostic significance
Yang Haishen1, Feiyu Jiang2, Xinxin Si3
1Department of Hepatobiliary Surgery, Affiliated Lianyungang Hospital of Xuzhou Medical University, The First Affiliated Hospital of Kangda College of Nanjing Medical University, Lianyungang, P.R. China.
Background:
Alpha-1,3-glucosyltransferase (ALG8), a key enzyme in protein glycosylation, is implicated in the oncogenesis and progression of several human malignancies. This study aimed to define the role of ALG8 in hepatocellular carcinoma (HCC) and uncover its mechanisms of action.
Methods:
ALG8 expression in HCC and normal tissues was analyzed using the TCGA and GEO databases, validated by RT-qPCR and western blot. Survival outcomes were evaluated via Cox analyses, and ALG8's impact on HCC behavior was examined through functional assays. GO, KEGG, and GSEA identified ALG8-related pathways, validated by biochemical assays.
Results:
In bioinformatics analyses, ALG8 was overexpressed in HCC tissues (p < 0.05 for all comparisons) and correlated with poorer survival (p = 0.006 and p = 0.025, respectively), establishing its role as an independent prognostic factor. In vitro experiments showed that knockdown of ALG8 reduced HCC cell proliferation, migration, and invasion. Using the STRING platform and TCGA-LIHC dataset, we identified ALG8-interacting genes and their associated differentially expressed genes (DEGs). GO and KEGG analyses further linked ALG8 to genes involved in glycosylation, signal release, and other processes, as well as pathways including neuroactive ligand-receptor interaction and N-Glycan biosynthesis. GSEA, corroborated by western blot and immunofluorescence, points to the Wnt/β-catenin signaling cascade as a probable mechanistic pathway through which ALG8 may modulate HCC progression.
Conclusion:
Elevated ALG8 expression in HCC is linked to worse outcomes and increased tumor aggressiveness, with silencing ALG8 reducing Wnt/β-catenin signaling, highlighting ALG8 as a potential therapeutic target.
