| Project/Area Number |
18591646
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Orthopaedic surgery
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| Research Institution | Kurume University |
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Principal Investigator |
HIRAOKA Koji Kurume University, School of Medicine, Lecturer (10268914)
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| Co-Investigator(Kenkyū-buntansha) |
SYODA Takanori Kurume University, School of Medicine, Assistant (10352163)
HUJII Teruhiko Kurume University, School of Medicine, Lecturer (50199288)
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| Project Period (FY) |
2006 – 2007
|
| Project Status |
Completed (Fiscal Year 2007)
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| Budget Amount *help |
¥3,850,000 (Direct Cost: ¥3,400,000、Indirect Cost: ¥450,000)
Fiscal Year 2007: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2006: ¥1,900,000 (Direct Cost: ¥1,900,000)
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| Keywords | osteosarcoma / Cap 43 / siRNA / differentiation / vitamin D_3 / 骨転移 / 乳癌 / 転移 |
|---|
| Research Abstract |
Cap43/NDRG1 expression is induced under conditions of severe hypoxia and prolonged elevations in intracellular calcium. Recently some reports have implied that Cap43 expression is suppressed in tumor cells including prostate cancer and colorectal cancer. And these reports have suggested that Cap43 is a marker of cell differentiation and suppresses cancer metastasis by inducing cell differentiation. In this study here, we have demonstrated Cap43 expression in three osteosarcoma cell lines, MG63, U2OS, and SaOS2, under normal culture conditions. Its expression in MG63 and U2OS was enhanced by vitamin D_3 that induced production of osteocalcin in those cells. Knockdown of Cap43 using siRNA also suppressed the production of osteocalcin. Furthermore, Cap43 expression was decreased as the cells repeatedly invaded into Matrigel, paralleling cell differentiation. These data suggest that Cap43 may play an important role in cell differentiation and invasion in osteosarcoma cells.
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