| Project/Area Number |
16591599
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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 | The University of Tokushima |
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Principal Investigator |
KANAYAMA Hiro-omi The University of Tokushima, Institute of Health Biosciences, Professer, 大学院・ヘルスバイオサイエンス研究部, 教授 (10214446)
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| Co-Investigator(Kenkyū-buntansha) |
FUKUMORI Tomoharu The University of Tokushima, Institute of Health Biosciences, Lecturer, 大学院・ヘルスバイオサイエンス研究部, 講師 (10314874)
NISHITANI Masaaki The University of Tokushima, Institute of Health Biosciences, Associate Professer, 大学院・ヘルスバイオサイエンス研究部, 助教授 (40304521)
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| Project Period (FY) |
2004 – 2005
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| Project Status |
Completed (Fiscal Year 2005)
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| Budget Amount *help |
¥2,800,000 (Direct Cost: ¥2,800,000)
Fiscal Year 2005: ¥900,000 (Direct Cost: ¥900,000)
Fiscal Year 2004: ¥1,900,000 (Direct Cost: ¥1,900,000)
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| Keywords | renal cell carcinoma / Apoptosis / Galectin-3 / CD8 positive T cells / ガレクチン-3 / CTL |
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| Research Abstract |
Galectin-3 is a member of the galectin gene family that is expressed at elevated levels in a variety of neoplastic cell types and has been associated with cell growth, cellular adhesion process, cell proliferation, transformation, metastasis, and apoptosis. We studied the expression of galecin-3 in renal cell carcinoma cell lines and human renal cell carcinoma tissues by RT-PCR and western blot analysis, and investigated the clinical significance and the possibility as a tumor marker. We also investigated its effect on T cell or NK cell activation. The expression of galectin-3 was identified in every renal cell carcinoma cell line we employed and was significantly higher in human renal cell carcinoma tissues than normal kidney tissues. Especially in the case with metastasis, the expression ratio was significantly high (p=0.035), which suggested that ratio could become prognostic factor of metastasis. We extracted CD8 positive T cells from human renal cell carcinoma tissues and investigated the effect of galectin-3 induced apoptosis in the cells by flow cytometry. Galectin-3 significantly induced apoptosis (p=0.039) by binding to the CD8 positive T cells, from which we concluded that galectin-3 might be involved in what is called ‘escape' from immune system of renal cell carcinoma. We have also constructed mice RCC models and metastasis models by employing Renca cells (positive and negative galectin-3 expression) and investigated anti-angiogenesis and anti-tumor effect. These results will be published shortly. To clarify the role of galectin-3 in angiogenesis or apoptosis may lead to understanding mechanism of resistance of renal cell carcinoma to various kinds of therapies. In future we plan to expand these achievements into gene therapy for renal cell carcinoma.
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