| Budget Amount *help |
¥4,420,000 (Direct Cost: ¥3,400,000、Indirect Cost: ¥1,020,000)
Fiscal Year 2013: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
Fiscal Year 2012: ¥2,340,000 (Direct Cost: ¥1,800,000、Indirect Cost: ¥540,000)
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| Research Abstract |
The soluble prostaglandin E2 receptor (FuEP2/Ex2) caused significant decrease of tumor growth and formation of hemorrhagic ascites in a model of intraperitoneal metastasis of ovarian cancer. In FuEP2/Ex2-expressing tumor, the number of CD31- and CD163-positive cells was significantly decreased. Secretion of VEGF, CXCL1, IL-6, and IL-8 was also suppressed in FuEP2/Ex2-expressing cells. These results suggest that suppression of angiogenesis and of immunosuppressive macrophages recruitment is taking part in the mechanism of tumor growth suppression by FuEP2/Ex2. Microarray analysis revealed that six genes were upregulated in FuEP2/Ex2-expressing-derived tumor and inhibition of TMPRSS4 activity further suppressed tumor growth. This result indicates that TMPRSS4 act as a survival factor in tumor interfered its growth by FuEP2/Ex2.
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