| Budget Amount *help |
¥133,640,000 (Direct Cost: ¥102,800,000、Indirect Cost: ¥30,840,000)
Fiscal Year 2014: ¥26,130,000 (Direct Cost: ¥20,100,000、Indirect Cost: ¥6,030,000)
Fiscal Year 2013: ¥27,430,000 (Direct Cost: ¥21,100,000、Indirect Cost: ¥6,330,000)
Fiscal Year 2012: ¥29,380,000 (Direct Cost: ¥22,600,000、Indirect Cost: ¥6,780,000)
Fiscal Year 2011: ¥28,990,000 (Direct Cost: ¥22,300,000、Indirect Cost: ¥6,690,000)
Fiscal Year 2010: ¥21,710,000 (Direct Cost: ¥16,700,000、Indirect Cost: ¥5,010,000)
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| Outline of Final Research Achievements |
We found that girdin and its phosphorylation play important roles in cell migration of cancer cells, endothelial cells and neuronal cells. Thus, girdin’s function influences pathophysiology of human diseases such as cancer progression and vascular disease. Girdin is an actin-binding protein and is phosphorylated at serine 1416 by Akt. In this project, we generated knock-in mice in which serine1416 in girdin was replaced with alanine. Using knock-in mice, we demonstrated that Akt-girdin signaling in cancer-associated fibroblasts contributes to tumor progression. In addition, Akt-girdin signaling in vascular smooth muscle cells was shown to be important for neointima formation after vascular injury. We also found that this signaling is crucial for growth and invasion of glioblastoma cells in vitro and in vivo. These findings suggest that Akt-giridin signaling becomes new therapeutic target for treatment of cancer and vascular disease.
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