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ncRNA-Mediated Upregulation of AURKA Promotes Hepatocellular Carcinoma Progression and Alters the Immune Microenvironment

Title: ncRNA-Mediated Upregulation of AURKA Promotes Hepatocellular Carcinoma Progression and Alters the Immune Microenvironment
Authors: Chen, Zhitao; Chu, Tianshu; Ding, Chenchen; Gu, Yangjun; Li, Qiyong
Source: Bioinformatics and Biology Insights ; volume 20 ; ISSN 1177-9322 1177-9322
Publisher Information: SAGE Publications
Publication Year: 2026
Description: 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.
Document Type: article in journal/newspaper
Language: English
DOI: 10.1177/11779322261435461
Availability: https://doi.org/10.1177/11779322261435461; https://journals.sagepub.com/doi/pdf/10.1177/11779322261435461; https://journals.sagepub.com/doi/full-xml/10.1177/11779322261435461
Rights: https://creativecommons.org/licenses/by-nc/4.0/ ; https://journals.sagepub.com/page/policies/text-and-data-mining-license
Accession Number: edsbas.89B7EC18
Database: BASE