Elucidation of mechanisms of the prostate cancer progress in consideration of AR Axis / microenvironment and the construction of the innovative treatment strategy

2016 Fiscal Year Final Research Report

• Project/Area Number: 26293350
• Research Category: Grant-in-Aid for Scientific Research (B)
• Allocation Type: Partial Multi-year Fund
• Section: 一般
• Research Field: Urology
• Research Institution: Kanazawa University
• Principal Investigator: NAMIKI Mikio 金沢大学, 医学系, 教授 (70155985)
• Co-Investigator(Kenkyū-buntansha): 溝上 敦 金沢大学, 医学系, 准教授 (50248580) ; 泉 浩二 金沢大学, 医学系, 特任助教 (80646787)
• Project Period (FY): 2014-04-01 – 2017-03-31
• Keywords: SOD3 / 前立腺癌 / 共培養 / 間質細胞

Outline of Final Research Achievements

We identified identified superoxide disumutase 3 (SOD3) which expression was decreased in prostate caner tissue compared with normal tissue. SOD3 was related with metabolism of the active oxygen and worked as a tumor inhibiting factor.
When prostate cancer cells were cocultured with derived derived from and prostate cancer and added a large quantity of testosterone into coculture, the proliferation of the prostate cancer cells was inhibited. This mechanism was involved in estrogen synthesis in stroll cells.
Furthermore, when androgen-sensitive prostate cancer cells were cocultured with andorgen-insensitive prostate cancer cells, the proliferation of androgen-sensitive prostate cancer cells in the presence of androgen was accelerated by androgen-insensitive cells. Moreover, invasion of androgen-insensitive cells was induced by androgen-sensitive cells. We synthesized flavored derivatives and confirmed anti-caner effect.

Free Research Field

泌尿器科