DOI: https://doi.org/10.36347/sajb.2026.v14i11.003

Pages: 766-772

Objective: To investigate the effects of miR-199a-5p on the proliferation and migration of hepatocellular carcinoma (HCC) cells and to characterize changes in DEPDC1B and Wnt/β-catenin-related proteins. Methods: Hep3B and MHCC-97H cells were used to establish miR-199a-5p overexpression and DEPDC1B rescue models. The experimental groups were miR-NC, miR-199a-5p, miR-199a-5p + vector, and miR-199a-5p + DEPDC1B. Expression of miR-199a-5p and DEPDC1B mRNA was measured by quantitative reverse-transcription PCR (qRT-PCR). Cell viability activity was assessed using the CCK-8 assay at 24, 48, 72, 96, and 120 h. Cell migration was evaluated using Transwell assays. Western blotting was used to assess DEPDC1B, E-cadherin, N-cadherin, vimentin, Wnt3a, β-catenin, cyclin D1, and c-Myc protein levels. Results: Compared with the miR-NC group, transfection with miR-199a-5p significantly increased miR-199a-5p expression and reduced DEPDC1B mRNA and protein levels in both Hep3B and MHCC-97H cells. CCK-8 growth curves showed an overall reduction in OD450 values following miR-199a-5p overexpression, consistent with suppressed cell viability activity. Transwell assays showed fewer migrating cells in the miR-199a-5p and miR-199a-5p + vector groups than in the miR-NC group (P < 0.01, as indicated in the figure); cell counts showed a trend toward recovery after DEPDC1B re-expression. Western blotting showed that miR-199a-5p overexpression was accompanied by lower levels of DEPDC1B, Wnt3a, cyclin D1, and c-Myc, as well as reduced levels of the mesenchymal phenotype-associated proteins N-cadherin and vimentin. Conclusion: miR-199a-5p overexpression suppressed HCC cell proliferation and migration-associated phenotypes, potentially at least in part through downregulation of DEPDC1B and attenuation of Wnt/β-catenin-related signaling. DEPDC1B re-expression partially restored the malignant phenotype, suggesting that the miR-199a-5p–DEPDC1B axis may participate in HCC progression.