Mechanism of Curcumin Targeting Nos3 via miR-134 to Regulate the PI3K/AKT Pathway to Inhibit the Malignant Biological Features of HCC

Background Hepatocellular carcinoma (HCC) is a highly aggressive malignancy with limited clinical treatment options. Although the natural compound curcumin has demonstrated potential anti-tumor effects, its specific regulatory mechanisms in HCC remain incompletely understood. Purpose This study aimed to investigate the molecular mechanism by which curcumin suppresses the malignant biological characteristics of HCC through microRNA (miR)-134 targeting nitric oxide synthase 3 (Nos3), thereby regulating the phosphatidylinositol 3-kinase/protein kinase B (PI3K/AKT) signaling pathway. Materials and Methods Cells were divided into a blank control group (Group A), an HCC group (Group B), and a curcumin intervention group (Group C). Group A consisted of normal human hepatocyte L-02 cells without treatment; Group B comprised human HCC BEL-7402 cells without treatment; Group C involved BEL-7402 cells treated with 50 µmol/L curcumin. Cells were cultured for 48 h. Cell proliferation was assessed using the cell counting kit-8 (CCK-8) assay, protein expression by Western blot, messenger ribonucleic acid (mRNA) levels by quantitative polymerase chain reaction (qPCR), and migration and invasion abilities by the Transwell assay. Results Compared with Group B, Group C exhibited reduced cell proliferation, decreased migration and invasion, elevated expression of apoptotic proteins (Fas, BCL2-associated X protein [Bax], Fas ligand [FasL]), and lower B-cell lymphoma 2 (Bcl-2) expression. Group C showed higher relative expression of miR-134 and Nos3 protein, while AKT and PI3K mRNA and protein levels were lower than in Group B. Conclusion Curcumin may target Nos3 via miR-134, reducing HCC cell viability, suppressing proliferation, migration, and invasion, and inducing apoptosis. Its mechanism may involve modulation of the PI3K/AKT signaling pathway.