Therapeutic Potential of miR-384 in Gastric Cancer: Dual Regulation of Epithelial-Mesenchymal Transition and Cell Proliferation Through Direct Targeting of CTNNB1.

Emerging evidence highlights the pivotal involvement of microRNAs (miRNAs) in modulating epithelial-mesenchymal transition (EMT) processes during gastric carcinogenesis. The present study specifically explored the functional significance of miR-384 and its molecular mechanisms in gastric cancer (GC) progression. Comparative analysis of miR-384 expression profiles between GC specimens and adjacent normal tissues was performed using RT-qPCR. Functional characterization was achieved through gain-of-function and loss-of-function approaches by transfecting GC cells with miR-384 mimics or inhibitors, followed by evaluation of proliferative capacity, invasive potential and EMT markers. Potential mRNA targets were predicted via bioinformatics algorithms, with subsequent validation through rescue experiments demonstrating miR-384's direct binding to CTNNB1. Complementary in vivo studies were conducted to assess the tumor-suppressive effects of miR-384. A marked reduction in miR-384 expression was observed in both clinical GC samples and cultured cell lines relative to normal counterparts. Ectopic miR-384 expression significantly attenuated malignant phenotypes, suppressing cellular proliferation and motility while inducing apoptotic pathways. Computational prediction coupled with experimental verification identified CTNNB1 as a direct downstream target, through which miR-384 exerts its inhibitory effects on nuclear translocation and subsequent modulation of EMT and proliferative pathways. Importantly, the miR-384/CTNNB1 axis was shown to effectively constrain tumor growth in animal models. miR-384 exerts tumor-suppressive effects in GC by inhibiting cellular proliferation and EMT, while promoting apoptosis through downregulation of CTNNB1.