2017 Fiscal Year Final Research Report
The elucidation on androgen signaling pathway in prostate cancer and development of its targeting drug
Project/Area Number |
15K10610
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Research Category |
Grant-in-Aid for Scientific Research (C)
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Allocation Type | Multi-year Fund |
Section | 一般 |
Research Field |
Urology
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Research Institution | Nihon University |
Principal Investigator |
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Co-Investigator(Kenkyū-buntansha) |
山口 健哉 日本大学, 医学部, 准教授 (00297813)
浦野 友彦 国際医療福祉大学, 医学部, 主任教授 (20334386)
福田 昇 日本大学, 総合科学研究所, 教授 (40267050)
藤原 恭子 日本大学, 医学部, 助教 (40595708)
芦苅 大作 日本大学, 医学部, 助手 (70748053)
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Co-Investigator(Renkei-kenkyūsha) |
INOUE Satoshi 東京都健康長寿医療センター, 研究所, 研究部長 (40251251)
TAKAYAMA Kenichi 東京都健康長寿医療センター, 研究所, 研究員 (50508075)
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Project Period (FY) |
2015-04-01 – 2018-03-31
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Keywords | 前立腺癌 / アンドロゲン受容体 / アンドロゲン応答遺伝子 / PIポリアミド |
Outline of Final Research Achievements |
Since androgen receptor (AR) signaling pathway has crucial role in genesis and development of prostate cancer (PCa), androgen deprivation therapy (ADT) is the first-line treatment for prostate cancer (PC). However, long term treatment with ADT often results in the recurrence of lethal castration resistant PC (CRPC), which remains a large unmet medical need. To develop effective curatives for CRPC, we have tried to identify new androgen responsive genes and AR collaborator, which regulate AR activity. In the present study, we conducted the functional analyses of these candidate genes, and examined the efficacy of pyrrole-imidazole polyamides (PIPs) targeting them. Our current data clearly indicated that the candidate genes ABHD2, G3BP2, ACSL3 could be induced by androgen, and have tumor promoting function for PC cells. In addition, we found that PIP, which could recognize OCT1 binding site had anti-tumor function in vitro and in vivo.
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Free Research Field |
前立腺癌
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