Utility of arachidonic acid metabolism-related molecules as a novel target to anti-tumor strategy

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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.