2014 Fiscal Year Final Research Report
The tumor control mechanism of galectin-3 in prostate cancer bone metastasis
| Project/Area Number |
24592394
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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) |
KANAYAMA Hiro-omi 徳島大学, 大学院ヘルスバイオサイエンス研究部, 教授 (10214446)
TAKAHASHI Masayuki 徳島大学, 大学院ヘルスバイオサイエンス研究部, 准教授 (50325255)
NAKATSUJI Hiroyoshi 徳島大学, 大学院ヘルスバイオサイエンス研究部, 非常勤講師 (50437638)
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| Project Period (FY) |
2012-04-01 – 2015-03-31
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| Keywords | 前立腺癌 / ガレクチン-3 / 破骨細胞 / 骨芽細胞 |
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| Outline of Final Research Achievements |
We generated continuous galectin-3-overexpressed LNCaP cells and galectin-3-downregulated PC-3 cells using siRNA. Overexpression of galectin-3 in LNCaP cells promoted invasion and migration of tumor cells comparing with control LNCaP cells. Downregulation of galectin-3 in PC-3 cells suppressed invasion and migration comparing with control PC-3 cells. Galectin-3 significantly suppressed anti-androgen effect induced by enzalutamide or bicalutamide in LNCaP comparing with controls by activating androgen transcriptional activity of AR. Galectin-3 has been shown to promote activation of osteoclasts because TRAP-positive cells of the osteoclast was significantly increased 1.7-fold by the addition of recombinant galectin-3. These data indicate that galectin-3 is involved in the tumor progression and anti-androgen drug resistance of CRPC by regulating invasion, migration, transcriptional activity of AR, and osteoclast activity.
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| Free Research Field |
医歯薬学
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