ncRNA-Mediated Upregulation of AURKA Promotes Hepatocellular Carcinoma Progression and Alters the Immune Microenvironment.
Hepatocellular carcinoma (HCC) remains a major cause of cancer-related mortality worldwide.
APA
Chen Z, Chu T, et al. (2026). ncRNA-Mediated Upregulation of AURKA Promotes Hepatocellular Carcinoma Progression and Alters the Immune Microenvironment.. Bioinformatics and biology insights, 20, 11779322261435461. https://doi.org/10.1177/11779322261435461
MLA
Chen Z, et al.. "ncRNA-Mediated Upregulation of AURKA Promotes Hepatocellular Carcinoma Progression and Alters the Immune Microenvironment.." Bioinformatics and biology insights, vol. 20, 2026, pp. 11779322261435461.
PMID
41908244
Abstract
Hepatocellular carcinoma (HCC) remains a major cause of cancer-related mortality worldwide. Aurora kinase A (AURKA), a critical regulator of mitosis and spindle assembly, has been implicated in tumorigenesis, yet its clinical relevance and immune associations in HCC require further clarification. Here, we performed integrated bioinformatic analyses using TCGA/GTEx-derived datasets and public platforms (including TIMER and GEPIA2) to characterize AURKA expression patterns, prognostic significance, and functional pathways in HCC. Potential upstream noncoding RNA (ncRNA) interactions were explored using ENCORI and miRNet 2.0, and immune microenvironment correlations were assessed via TIMER/GEPIA2 and TISIDB. We found that AURKA was significantly overexpressed in HCC and associated with unfavorable prognosis and more advanced clinicopathological features. A putative ncRNA regulatory axis involving DUXAP8 and hsa-miR-490-3p was identified as being associated with AURKA expression. Moreover, AURKA expression correlated with immune cell infiltration and immune-related features, suggesting a relationship with the tumor immune microenvironment. Collectively, our analyses suggest that a putative DUXAP8/hsa-miR-490-3p/AURKA regulatory network may be associated with HCC progression and correlates with features of the tumor immune microenvironment. These findings offer insight into potential biomarkers and therapeutic targets for personalized HCC treatment.
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