TRIM29 and pancreatic neoplasm: Moreover, overexpressed miR-185 was shown to inhibit TRIM29 at both the transcriptional and protein levels in MGC803 cells [75,76] Additionally, TRIM29 was discovered to increase Dvl2 stability in pancreatic cancer, thus leading to increased β-catenin to trigger the Wnt/β-catenin pathway, as shown by in vitro experiments in human pancreatic cancer cells Panc1 and BxPC3 and in vivo using a subcutaneous xenograft model in NOD/SCID mice [77].