Development of new treatment strategy targeting CAVEOLIN-1 and 2 related signaling axis

2017 Fiscal Year Final Research Report

• Project/Area Number: 15K10597
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Urology
• Research Institution: University of Miyazaki
• Principal Investigator: Kamoto Toshiyuki 宮崎大学, 医学部, 教授 (00281098)
• Co-Investigator(Kenkyū-buntansha): 杉江 悟 宮崎大学, 医学部, その他 (50626140) ; 向井 尚一郎 宮崎大学, 医学部, 准教授 (10315369) ; 月野 浩昌 宮崎大学, 医学部, 講師 (60433059) ; 山崎 浩司 宮崎大学, 医学部, 医員 (30777355)
• Project Period (FY): 2015-04-01 – 2018-03-31
• Keywords: 前立腺癌 / 去勢抵抗性前立腺癌 / カベオリン-1 / カベオリン-2

Outline of Final Research Achievements

We evaluated that plasma concentration of Caveolin (CAV)1 and CAV2 was increased in castration resistant prostate cancer (CRPC) patients compared with androgen sensitive prostate cancer patients. Next, we introduced CAV1 and CAV2 specific small interfering into PC3 cell line (CRPC) to knock-down (KD) both molecules. We performed cell migration assay using PC3 prostate cancer cells and compared the results between CAV1-KD, CAV2-KD and negative control PC3 cells. In addition, we performed real-time quantitative PCR (RT-qPCR) and RT2 Profiler PCR Array analysis to identify factors that influence migration. As a result, we observed significant downregulation in cell motility of CAV1-KD and CAV2-KD PC3 cells compared with negative control. RT-qPCR revealed that the expression of vimentin and N-cadherin were downregulated in CAV1-KD PC3 cells. In addition, PCR array revealed decreased expression of MGAT5, MMP13, MYCL in CAV1-KD PC3, and ETV4, FGFR4 and SRC in CAV2-KD PC3.

Free Research Field

泌尿器科