2013 Fiscal Year Final Research Report

Elucidation of the mechanism of Epithelial-Mesenchymal Transition in peritoneal environment of gastric cancer

Research Project

Project/Area Number	24791402
Research Category	Grant-in-Aid for Young Scientists (B)
Allocation Type	Multi-year Fund
Research Field	Digestive surgery
Research Institution	Kanazawa University
Principal Investigator	KINOSHITA Jun 金沢大学, 医学系, 協力研究員 (90584855)
Project Period (FY)	2012-04-01 – 2014-03-31
Keywords	胃癌 / 腹膜播種 / 上皮間葉転換
Research Abstract	In this study, we evaluated the mechanism of EMT of Human PeritonealMesothelial Cell(HPMC) in in peritoneal environment of gastric cancer. We also investigated the inhibitory effect of PSK on the TGF/Smad signalling pathway and TGFb induced EMT in human HPMCs and gastric cancer cells. In vitro, TGFb increased the expression of E cadherin and decreased the expression of mesenchymal markers in HPMCs and which was suppressed by PSK. PSK suppressed TGFb induced phosphorylation of Smad2 in HPMCs in western blot analysis.In mouse subctaneous xenograft models, PSK inhibited the tumor fibrosis induced by co-inoculation of gastric cancer cells and HPMCs. PSK might have the potential to reduce TGFb induced activation of HPMCs in the peritoneal microenvironment of gastric cancer.