A new strategy for improving the efficacy of the conventional therapy of pancreatic cancer by remodeling its microenvironment

2014 Fiscal Year Final Research Report

• Project/Area Number: 25670586
• Research Category: Grant-in-Aid for Challenging Exploratory Research
• Allocation Type: Multi-year Fund
• Research Field: Digestive surgery
• Research Institution: Kyushu University
• Principal Investigator: TANAKA Masao 九州大学, 医学(系)研究科(研究院), 教授 (30163570)
• Co-Investigator(Kenkyū-buntansha): TAKAHATA Shunichi 九州大学, 大学病院, 講師 (50437779) ; UEDA Junji 佐賀大学, 医学部, 准教授 (90529801) ; MANABE Tatsuya 九州大学, 医学研究院, 助教 (60546464) ; SHIRAHANE Kengo 九州大学, 医学研究院, 共同研究員 (10529803) ; OHUCHIDA Kenoki 九州大学, 大学病院, 助教 (20452708)
• Project Period (FY): 2013-04-01 – 2015-03-31
• Keywords: 膵癌 / 膵星細胞 / 癌微小環境 / リモデリング

Outline of Final Research Achievements

In genetically engineered mouse model of pancreatic cancer, the histopathological findings, including pancreatic intraepithelial neoplasia and a lot of fibrous tissue in the tumor stroma, were similar to those of human.
Integrin alpha v was widely expressed in the stroma of pancreatic cancer. Knockdown of integrin alpha v in pancreatic stellate cells decreased the production of extracellular matrix such as collagenⅠand fibronectin. PDGFA, a growth factor related to cancer-stromal interaction, and CTGF, a profibrotic growth factor, were also down-regulated by knockdown of integrin alpha v. When pancreatic cancer cells and pancreatic stellate cells were co-transplanted subcutaneously into nude mice, knockdown of integrin alpha v in pancreatic stellate cells decreased the tumor growth as compared with the control.

Free Research Field

医歯薬学