Establishment of the new strategy with REIC/Dkk-3 against androgen independent prostate cancer.

2017 Fiscal Year Final Research Report

• Project/Area Number: 15K07754
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Veterinary medical science
• Research Institution: Nippon Veterinary and Life Science University
• Principal Investigator: Ochiai Kazuhiko 日本獣医生命科学大学, 獣医学部, 准教授 (30550488)
• Co-Investigator(Kenkyū-buntansha): 呰上 大吾 日本獣医生命科学大学, 獣医学部, 准教授 (80453934)
• Project Period (FY): 2015-04-01 – 2018-03-31
• Keywords: 前立腺がん / REIC/Dkk-3 / SGTA / イヌ / ホルモン療法抵抗性 / ARシグナル伝達

Outline of Final Research Achievements

The pathological condition of canine prostate cancer resembles that of human androgen-independent prostate cancer. Both canine and human androgen receptor (AR) signalling are inhibited by overexpression of the dimerized co-chaperone SGTA, which is considered to cause the development of androgen-independency. REIC interferes with SGTA dimerization and rescues AR signalling. This study aimed to assess the effects of REIC and SGTA interactions on AR signalling in the canine androgen-independent prostate cancer cell line CHP-1.
MTH and Halo-tag PD assays showed that canine REIC interacted with SGTA and interfered with SGTA dimerization. Additionally, reporter assays revealed that canine REIC restored AR signalling. Therefore, we confirmed the interaction between canine SGTA and REIC, as well as their role in AR signalling. Our results suggest that this interaction might contribute to the development of a novel strategy for androgen-independent prostate cancer treatment.

Free Research Field

基礎獣医学