MiR-424-5p Acts as an Oncogene in Hep3B Cells by Activating the PI3K/AKT Signaling Pathway
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. Overall design: This dataset supports comparative transcriptomic research between normal and cancerous human liver cells, which is fundamental for understanding hepatocellular carcinoma (HCC) pathogenesis. The project includes RNA-seq data from 6 cell line samples in total, comprising 3 biological replicates of the normal human hepatocyte cell line L02 and 3 biological replicates of the human hepatocellular carcinoma cell line Hep3B. All samples were processed under consistent baseline conditions, such as standard culture, and the dataset provides raw sequencing data in FASTQ files along with a processed gene expression matrix, for example, FPKM or TPM counts. This resource is suitable for applications like identifying differentially expressed genes and pathways, exploring oncogenic mechanisms, and serving as a control or reference in studies of liver disease models, drug screening, or functional genomics.