Our results suggest that miR-137 reduces stemness features of pancreatic cancer cells by Targeting KLF12-associated Wnt/β-catenin pathways and may identify new diagnostic and therapeutic targets in pancreatic cancer.
Our study suggested mechanistic relationship between miR-940 and Wnt/β-catenin in the development and progression of pancreatic carcinoma through regulation of GSK3β and sFRP1.
Our study suggests that the miR-519d-3p/RPS15A/Wnt/β-catenin regulation axis plays an important role in the progression of pancreatic cancer and may serve as potential targets for treatment of pancreatic cancer.
Our work suggests that ROBO3 may contribute to the progression of pancreatic cancer by sequestering Wnt inhibitor SFRP, which in turn leads to increased Wnt/β-catenin pathway activity.
Pretreatment with the β-catenin pathway inhibitor FH535, attenuated the cantharidin- and norcantharidin-induced repression on CD44, CD24, and EPCAM, suggesting cantharidin and its derivant repressed stemness of pancreatic cancer cells in β-catenin pathway-dependent manner.
Silencing PRMT5 induces epithelial marker E-cadherin expression and down-regulates expression of mesenchymal markers including Vimentin, collagen I and β-catenin in PaTu8988 and SW1990 cells, whereas ectopic PRMT5 re-expression partially reverses these changes, indicating that PRMT5 promotes EMT in pancreatic cancer.
This study indicated that overexpression of KL-6/MUC1 in pancreatic cancer tissues may be associated with metastasis of pancreatic cancer by regulating E-cadherin and E-cadherin/β-catenin complex expression.