The basic study of molecular targeted therapy via pancreatic duct tight junctions by using a novel culture system of human pancreatic duct epithelial cells

点击翻译按钮获取中文摘要

In the present study, using normal human pancreatic duct epithelial cells and cancer cell lines. we investigated the basic study targeting tight junction molecules claudin-4, -18 and a signal molecule PKC that highly expressed in pancreatic cancer. Claudin-4 and -18 were regulated via a PKCalpha signal transduction pathway in both human pancreatic duct epithelial cells and cancer cells. The cytotoxic effects of CPE via claudin-4 are thought to be useful as a novel therapeutic tool for pancreatic cancer. The cytotoxicity was not observed at any concentration of CPE, whereas in pancreatic cancer cells, CPE had a dose-dependent cytotoxic effect. PKCalpha inhibitors represent potential therapeutic agents against human pancreatic cancer cells by the use of CPE cytotoxicity via claudin-4.