Trefoil Factor 2 Regulates Proliferation and Apoptosis of Pancreatic Cancer Cells and LPS-Induced Normal Pancreatic Duct Cells by β-Catenin Pathway.

INTRODUCTION

Pancreatic cancer (PC) is a malignant tumor with poor prognosis. This study aimed to determine the role of trefoil factor 2 (TFF2) in the proliferation and apoptosis of LPS-induced normal pancreatic duct cells and pancreatic cancer cells through β-catenin pathway.

METHODS

TFF2 expression in normal pancreatic duct cells, pancreatic cancer cells and LPS-induced normal pancreatic duct cells was detected by RT-qPCR analysis and Western blot analysis. The transfection effects in pancreatic cancer cells and LPS-induced normal pancreatic duct cells were analyzed by RT-qPCR analysis. After indicated transfection, proliferation, apoptosis and inflammation of these cells were respectively detected by CCK-8 assay, TUNEL assay and certain ELISA kits. Expression of β-catenin pathway-related proteins was analyzed by Western blot analysis. Co-immunoprecipitation assay determined the combination of TFF2 and β-catenin.

RESULTS

TFF2 expression was increased in pancreatic cancer cells and LPS-induced HPDE cells compared with HPDE cells. According to TFF2 expression in these cells, PanC-1 cells and 5 μg/mL LPS were selected. In addition, TFF2 interference decreased the proliferation and promoted the apoptosis of PanC-1 cells and LPS-induced HPDE cells. However, TFF2 interference did not obviously change the levels of TNF-α, IL-1β and IL-6 in PanC-1 cells and LPS-induced HPDE cells. Furthermore, TFF2 interference suppressed the expression of β-catenin, c-Myc, Cyclin D1 and BIRC5 in PanC-1 cells and LPS-induced HPDE cells. TFF2 was demonstrated to combine with β-catenin.

DISCUSSION

TFF2 interference inhibits proliferation and promotes apoptosis of PanC-1 cells and LPS-induced HPDE cells by suppressing β-catenin pathway.