Elucidation of tumor regulation mechanism of galectin-3 against castration-resistant prostate cancer and clinical application

2017 Fiscal Year Final Research Report

• Project/Area Number: 15K10592
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Urology
• Research Institution: The University of Tokushima
• Principal Investigator: FUKUMORI Tomoharu 徳島大学, 病院, 講師 (10314874)
• 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)
• Project Period (FY): 2015-04-01 – 2018-03-31
• Keywords: ガレクチン-3 / 前立腺癌 / アンドロゲン受容体 / 血管新生

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.

Free Research Field

泌尿器腫瘍学