ArticleFrontiers in oncology2025
MiR-424-5p acts as an oncogene in Hep3B cells by activating the PI3K/AKT signaling pathway.
Article in Frontiers in oncology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Hepatocellular carcinoma (HCC) remains a global health challenge with high morbidity and mortality. MicroRNAs (miRNAs) play pivotal roles in cancer progression, yet their context-dependent functions in HBV-HCC are unclear. This study demonstrates that miR-424-5p is significantly upregulated in HBV positive Hep3B cells, correlating with poor patient prognosis. Integrated bioinformatic analysis predicted that the target genes of miR-424-5p are significantly enriched in the PI3K/AKT signaling pathway. Functional experiments showed that knockdown of miR-424-5p suppressed cell proliferation, migration, and colony formation. Mechanistically, miR-424-5p knockdown led to the upregulation of PTEN and downregulation of phosphorylated PI3K/AKT, indicating inhibition of this pathway. These findings unveil an oncogenic role of miR-424-5p in HBV-HCC, suggesting its function is driven by viral specific dysregulation of the PI3K/AKT pathway, with PTEN involvement. Our study highlights miR-424-5p as a potential therapeutic target and provides insights into etiology-specific miRNA regulatory networks.
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