iCAF: Cancer associated fibroblast derived from iPS cells and its surface glycan as a target of cancer therapy.

2017 Fiscal Year Final Research Report

• Project/Area Number: 15H04924
• Research Category: Grant-in-Aid for Scientific Research (B)
• Allocation Type: Single-year Grants
• Section: 一般
• Research Field: Digestive surgery
• Research Institution: University of Tsukuba
• Principal Investigator: Tatsuya ODA 筑波大学, 医学医療系, 教授 (20282353)
• Co-Investigator(Kenkyū-buntansha): 木田 泰之 国立研究開発法人産業技術総合研究所, 生命工学領域, 研究グループ長 (20396526) ; 舘野 浩章 国立研究開発法人産業技術総合研究所, 生命工学領域, 上級主任研究員 (30450670)
• Co-Investigator(Renkei-kenkyūsha): HIRABAYASHI Jun 国立研究開発法人・産業技術総合研究所, 幹細胞工学研究センター・糖鎖レクチン工学研究チーム, 主席研究員・研究チーム長 (40156691) ; ISHII Genichirou 独立行政法人・国立がん研究センター, 臨床腫瘍病理部, 室長 (00270869) ; OHKOHCHI Nobuhiro 筑波大学, 医学医療系, 教授 (40213673)
• Project Period (FY): 2015-04-01 – 2018-03-31
• Keywords: 膵癌 / 癌ー間質相互作用 / CAF (がん関連線維芽細胞） / 糖鎖 / レクチン / ドラッグデリバリー

Outline of Final Research Achievements

We comprehensively analyzed glyacan expression of clinical pancreatic cancer stem cell-like cell line (CSCL-1), and identified that H type 3 sugar chain was specifically expressed, and that rBC2 lectin binds to it. In addition, we have studied application of rBC2 lectin as a therapeutic carrier targeting direct cancer stem cells.
In addition, when mesenchymal stem cells are co-cultured with CSCL-1 and transplanted subcutaneously into mice, CAF boosted tumor growth. When the CAF was isolated as the first generation (F1), F2 the tumor growth capacity gradually weakened as the generation progress (i.e. F0, F1, F2 ), while the CAF marker showed a tendency to become higher.

Free Research Field

腫瘍治療学