| Budget Amount *help |
¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000)
Fiscal Year 2016: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
Fiscal Year 2015: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
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| Outline of Final Research Achievements |
Lamellipodia are formed at the leading edge of migrating cells, and the formation is regulated by the metabolism of PI(4,5)P2, an inositol phospholipid, into PI(3,4,5)P3. Phospholipase C (PLC)-related but catalytically inactive protein (PRIP) has high homology to PLC-δ1 and binds to PI(4,5)P2 at the pleckstrin homology (PH) domain. However, the functions of PRIP in the regulation of phosphoinositide signaling have not been determined.
In this study, we examined the potential role and mechanisms of PRIP in controlling phosphoinositide metabolism and migration activity of cancer cells. PRIP overexpression in MCF-7 and BT-549 human breast cancer cells inhibited cell migration in vitro and metastasis development in vivo. PI(3,4,5)P3 production was decreased in Prip-overexpressing MCF-7 and BT-549 cells. Collectively, the suppressor activity of PRIP in PI(4,5)P2 metabolism regulates the tumour migration, suggesting PRIP as a promising target for protection against metastatic progression.
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