| Project/Area Number |
15K10592
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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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 |
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| Co-Investigator(Kenkyū-buntansha) |
金山 博臣 徳島大学, 大学院医歯薬学研究部(医学系), 教授 (10214446)
高橋 正幸 徳島大学, 大学院医歯薬学研究部(医学系), 准教授 (50325255)
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| Project Period (FY) |
2015-04-01 – 2018-03-31
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| Project Status |
Completed (Fiscal Year 2017)
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| Budget Amount *help |
¥4,810,000 (Direct Cost: ¥3,700,000、Indirect Cost: ¥1,110,000)
Fiscal Year 2017: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2016: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2015: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Keywords | ガレクチン-3 / 前立腺癌 / アンドロゲン受容体 / 血管新生 / 破骨細胞 / 骨芽細胞 |
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| Outline of Final Research Achievements |
Castration-resistant prostate cancer is resistant to hormone therapy and chemotherapy. Therefore, establishing a treatment for castration-resistant prostate cancer is one of the most important task. In this study, we demonstrated that galectin-3 significantly promoted the expression of androgen receptor-related genes and PSA transcriptional activity of prostate cancer cells, resulting that galectin-3 involved in the resistance of antiandrogen agents. In addition, it was proved that the microvessel density was significantly higher in the galectin-3-expressing prostate cancer cells and the expression of the angiogenic factor VEGFB was significantly increased. From the above, it has been proved that galectin-3 is a molecule involved in the resistance to treatment by controlling the androgen receptor and angiogenesis of prostate cancer cells, and it plays an important role in the treatment of castration-resistant prostate cancer.
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