Fig. 3
The Tumor-Suppressive Function of miR-29c-5p in Pancreatic Cancer and Its Regulatory Mechanism with H19. (A) The expression levels of miR-29c-5p in diverse pancreatic cell lines: In contrast to normal pancreatic ductal epithelial cells (HPDE), the expression of miR-29c-5p was conspicuously downregulated in pancreatic cancer cell lines (HPAF-II, MIA PaCa-2), *p < 0.05, **p < 0.01, ***p < 0.001. (B) The regulation of cell proliferation by miR-29c-5p: Transfection with miR-29c-5p mimics markedly inhibited cell proliferation (with a decreased OD450 value), while the inhibitor promoted proliferation (data presented as mean ± standard deviation, n = 3, *p < 0.05, **p < 0.01, ***p < 0.001.) (C) Transwell migration assay: The migration rate of the miR-29c-5p mimics group was approximately 60% lower than that of the negative control (NC) group, while the migration rate of the inhibitor group increased by approximately 80% (quantitative analysis by ImageJ, *p < 0.05, **p < 0.01, ***p < 0.001.) (D) The targeted interaction between miR-29c-5p and H19, prediction of the binding sites and secondary structure alignment (via RNAhybrid algorithm); the dual-luciferase reporter gene assay affirmed that the wild-type H19 (H19-WT) could suppress luciferase activity, while the mutant binding site (H19-MUT) abolished this effect, *p < 0.05, **p < 0.01, ***p < 0.001.) (E) Clinical survival analysis: Data from the TCGA database indicated that pancreatic cancer patients with a high expression of miR-29c-5p had a significantly longer overall survival than those with a low expression (HR = 0.56, p = 0.006, log-rank test).
