2016 Fiscal Year Final Research Report
Elucidation of mechanisms of the prostate cancer progress in consideration of AR Axis / microenvironment and the construction of the innovative treatment strategy
Project/Area Number |
26293350
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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
|