Contribution of glucocorticoid receptor in the mechanism of castration resistancy of prostate cancers

Research Project

Project/Area Number	25460426
Research Category	Grant-in-Aid for Scientific Research (C)
Allocation Type	Multi-year Fund
Section	一般
Research Field	Human pathology
Research Institution	National Cancer Center Japan
Principal Investigator	Kuwata Takeshi 国立研究開発法人国立がん研究センター, 東病院, 科長 (00327321)
Project Period (FY)	2013-04-01 – 2016-03-31
Project Status	Completed (Fiscal Year 2015)
Budget Amount *help	¥4,940,000 (Direct Cost: ¥3,800,000、Indirect Cost: ¥1,140,000) Fiscal Year 2015: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000) Fiscal Year 2014: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000) Fiscal Year 2013: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Keywords	前立腺癌 / 抗アンドロゲン療法 / アンドロゲン受容体 / グルココルチコイド受容体 / アンドロゲン
Outline of Final Research Achievements	In this study, the role of glucocorticoid receptor (GR) in castration resistancy of androgen-receptor(AR)-positive prostate cancer. In a human prostate cancer cell line, LNCap, expresses GR in addition to AR. Dexamethasone could activate androgen-receptor-respose-element and induces PSA in LNCap-GR, constitutively expressing GR. LNCap-GR could also subcutaneous-transplantable in SICD mice, while parental LNCap could not.

Report

(4 results)