Catenin delta 1 mediates epithelial–mesenchymal transition, proliferation, migration, and invasion of pancreatic cancer via the Wnt/β-catenin pathway

Abstract

Abstract Background: Catenin delta 1 (CTNND1) is upregulated in many tumors and is closely associated with poor prognosis. However, the role of CTNND1 in pancreatic cancer and its underlying mechanisms remain unclear Methods: The expression of CTNND1 in pancreatic cancer and normal tissues in the TCGA and GTEX databases was preliminarily screened and further verified by immunohistochemistry (IHC) and qPCR. Transwell, wound healing, and cell proliferation assays were used to study the effect of CTNND1 on epithelial-mesenchymal transition (EMT), proliferation, migration, and invasion of pancreatic cancer cells. Western blot experiments verified the signaling pathway mediating the effect of CTNND1 on pancreatic cancer progression. The expression of CTNND1 in the TCGA database, clinical pancreatic cancer samples, and pancreatic cancer cells was significantly upregulated. Results: We found that the silent CTNND1 in pancreatic cancer cells significantly inhibited the EMT, proliferation, migration, and invasion of pancreatic cancer cells. In addition, the silencing of CTNND1 in pancreatic cancer cells inhibited the Wnt/β-catenin signaling pathway. LiCl (a Wnt/β-catenin-specific activator) treatment partially restored the EMT, proliferation, migration, and invasion abilities of CTNND1-silenced pancreatic cancer cells. Conclusion: Our research confirmed that CTNND1 can regulate the EMT, proliferation, migration, and invasion of pancreatic cancer through the WNT/β-catenin signaling pathway.