Molecular analysis of platelet-dependent tumor cell proliferation

2014 Fiscal Year Final Research Report

• Project/Area Number: 25830125
• Research Category: Grant-in-Aid for Young Scientists (B)
• Allocation Type: Multi-year Fund
• Research Field: Tumor therapeutics
• Research Institution: Japanese Foundation for Cancer Research
• Principal Investigator: TAKAGI Satoshi 公益財団法人がん研究会, がん化学療法センター, 研究員 (20582240)
• Research Collaborator: SATO Shigeo ; OH-HARA Tomoko ; TAKAMI Miho ; NODA Sachie
• Project Period (FY): 2013-04-01 – 2015-03-31
• Keywords: 骨肉腫 / 血小板 / 血小板凝集 / PDGF / Akt

Outline of Final Research Achievements

In this study, we clarified the signal transduction pathway which was activated in cancer cells by the interaction with platelets and investigated the efficacy of inhibitors which target the identified pathway. We found that osteosarcoma cells could activate platelets via the direct cell-cell interaction and the PDGF-BB released by activated-platelets activated PDGFR-Akt axis in the osteosarcoma cells. Furthermore, we found that Sunitinib, a PDGFR inhibitor, and LY294002, a PI3K inhibitor, suppressed platelet-dependent sarcoma cells proliferation. These findings suggest that these inhibitors targeting PI3K-Akt axis and/or anti-platelet agents might be the anti-tumor drugs.

Free Research Field

細胞生物学