The cell permeable peptide inhibits pancreatic ductal adenocarcinoma cell proliferations and can be used as the molecular targeting dru

• Project/Area Number: 25461969
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: General surgery
• Research Institution: Hokkaido University
• Principal Investigator: Nakamura Toru 北海道大学, 医学(系)研究科(研究院), 助教 (70645796)
• Co-Investigator(Kenkyū-buntansha): HIRANO SATOSHI 北海道大学, 医学(系)研究科(研究院), 教授 (50322813) ; TSUCHIKAWA TAKAHIRO 北海道大学, 大学病院, 講師 (50507572) ; TANAKA EIICHI 北海道大学, 医学(系)研究科(研究院), 客員研究員 (60374279)
• Project Period (FY): 2013-04-01 – 2016-03-31
• Project Status: Completed (Fiscal Year 2015)
• Budget Amount: ¥4,940,000 (Direct Cost: ¥3,800,000、Indirect Cost: ¥1,140,000); Fiscal Year 2015: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000); Fiscal Year 2014: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000); Fiscal Year 2013: ¥2,470,000 (Direct Cost: ¥1,900,000、Indirect Cost: ¥570,000)
• Keywords: 膵癌新規分子標的治療薬 / 膵癌バイオマーカー / 膵癌新規分子標的治療 / 細胞膜透過性ペプチド治療

Outline of Final Research Achievements

Calcineurin binding pancreatic cancer invasion (CBPCI) was found in pancreatic ductal adenocarcinoma (PDAC) tissue, and was correlated with cancer cell proliferations and patients’ prognosis. We established PDAC orthotopic xenograft model mice and treated them with the molecular target peptide for CBPCI which could inhibit PDAC cell proliferations via inhibition of binding with calcineurin (PPP3CA). The side effects of the peptide treatment was not severe than FK506. The m-TOR pathway was suggested as a signal pathway of the CBPCI growth effect. E-cadherin was also suggested as an invasion factor for the CBPCI.