| Project/Area Number |
15591687
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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 |
Urology
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| Research Institution | Kobe University |
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Principal Investigator |
HARA Isao Kobe University, Graduate School of Medicine, Associate Professor, 大学院医学系研究科, 助教授 (10263378)
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| Project Period (FY) |
2003 – 2006
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| Project Status |
Completed (Fiscal Year 2006)
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| Budget Amount *help |
¥3,300,000 (Direct Cost: ¥3,300,000)
Fiscal Year 2006: ¥600,000 (Direct Cost: ¥600,000)
Fiscal Year 2005: ¥500,000 (Direct Cost: ¥500,000)
Fiscal Year 2004: ¥700,000 (Direct Cost: ¥700,000)
Fiscal Year 2003: ¥1,500,000 (Direct Cost: ¥1,500,000)
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| Keywords | bladder cancer / CD44 / adhesion molecule / 接着分子 / 浸潤能 |
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| Research Abstract |
We evaluated the effects of the over expression of CD44v8-10, one of the high molecular form of CD44, on the malignant potential of UM-UC-3 human bladder cancer cells in vitro and in vivo. We introduced CD44v8-10 complementary DNA into UM-UC-3 cells, which do not express detectable level of CD44v8-10 protein, and generated the CD44v8-10 over expressing cell line UM-UC-3/v8-10 and the vector only transfected cell line UM-UC-3/C. The effects of the introduction of CD44v8-10 into UM-UC-3 cells on the ability to bind hyaluronic acid (HA) were analyzed by the cell adhesion assay and the cell migration assay. We then evaluated tumor progression of UM-UC-3 sublines after subcutaneous and orthotopic injection into athymic nude mice. There were no significant differences in in vitro growth rates. UM-UC-3/v8-10 cells showed significantly decreased binding and migration ability to HA but not to other extracellular matrix proteins. Furthermore, UM-UC-3/v8-10 cells demonstrated significantly increased tumor growth after subcutaneous as well as orthotopic injection into athymic nude mice and enhanced lymph node metastasis after orthotopic injection compared with UM-UC-3/C cells. In conclusions, these findings suggest that CD44v8-10 over expression in human bladder cancer cells decreases their interaction with HA and potentiates their malignant progression.
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