| Budget Amount *help |
¥5,200,000 (Direct Cost: ¥4,000,000、Indirect Cost: ¥1,200,000)
Fiscal Year 2013: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
Fiscal Year 2012: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2011: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
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| Research Abstract |
The sphingosine-1-phosphate receptor S1PR2 is the first G protein-coupled receptor that negatively regulates cell migration through inhibition of Rac downstream of G12/13-Rho. S1PR2 expressed in tumor cells mediates inhibition of cell migration and invasion in vitro and hematogenous metastasis in vivo. S1PR2 expressed in host vascular endothelial cells and bone marrow-derived myeloid cells together mediate inhibition of tumor angiogenesis and tumor growth in vivo. We studied the roles of host S1PR2 in metastasis and post-ischemic angiogenesis and found interesting results. We also tested a widely accepted concept that sphingosine kinase 1 (SphK1), a major S1P synthesizing enzyme, plays an causative role in cancer development, by comparing incidence of malignancies between SphK1 transgenic mice and their littermates. We found no difference in incidence of either spontaneous or ENU (a mutagen)-induced tumor development between SphK1 transgenic and littermate wild type mice.
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