| Budget Amount *help |
¥16,900,000 (Direct Cost: ¥13,000,000、Indirect Cost: ¥3,900,000)
Fiscal Year 2018: ¥4,810,000 (Direct Cost: ¥3,700,000、Indirect Cost: ¥1,110,000)
Fiscal Year 2017: ¥5,720,000 (Direct Cost: ¥4,400,000、Indirect Cost: ¥1,320,000)
Fiscal Year 2016: ¥6,370,000 (Direct Cost: ¥4,900,000、Indirect Cost: ¥1,470,000)
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| Outline of Final Research Achievements |
We first examined the role of VASH2 in ovarian cancer cells. Our analyses revealed that VASH2 was involved in the expression of TGF-β type I receptor, which influenced the TGF-β-mediated epithelial-mesenchymal transition for cancer cell invasion. We then examined the role of VASH2 in pancreatic cancer by using KPC mice and cells isolated from them. Knockdown of Vash2 significantly decreased migration of KPC cells. When KPC mice were crossed with Vash2 deficient mice, metastasis was significantly decreased. Our analyses revealed that Vash2 increased tubulin detyrosination of KPC cells for their migration and invasion. We further revealed that Vash2 was involved in the expression of CXCR2 ligands and G-CSF, which were responsible for the recruitment of myeloid derived suppressor cells (MDSCs) and M2-macrophages for the evasion of tumor immunity.
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