Project/Area Number |
26462422
|
Research Category |
Grant-in-Aid for Scientific Research (C)
|
Allocation Type | Multi-year Fund |
Section | 一般 |
Research Field |
Urology
|
Research Institution | Nagoya City University |
Principal Investigator |
NAIKI Taku 名古屋市立大学, 大学院医学研究科, 助教 (50551272)
|
Co-Investigator(Kenkyū-buntansha) |
河合 憲康 名古屋市立大学, 大学院医学研究科, 講師 (20254279)
内木 綾 名古屋市立大学, 大学院医学研究科, 講師 (20509236)
安藤 亮介 名古屋市立大学, 大学院医学研究科, 助教 (30381867)
惠谷 俊紀 名古屋市立大学, 大学院医学研究科, 研究員 (30600754)
飯田 啓太郎 名古屋市立大学, 大学院医学研究科, 臨床研究医 (30713945)
|
Project Period (FY) |
2014-04-01 – 2017-03-31
|
Project Status |
Completed (Fiscal Year 2016)
|
Budget Amount *help |
¥4,940,000 (Direct Cost: ¥3,800,000、Indirect Cost: ¥1,140,000)
Fiscal Year 2016: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2015: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2014: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
|
Keywords | 去勢抵抗性前立腺癌 / 細胞間連絡能 / 細胞間連絡機構 / コネキシン |
Outline of Final Research Achievements |
Prostate cancer growth is androgen sensitive, therefore, the first-line therapy of prostate cancer is androgen deprivation therapy like castration. However, the therapeutic efficacy is limited. Chemotherapy including taxane derivatives is next strategy in castration resistant prostate cancer (CRPC), however, the distribution of derivatives is various. Connexin 43 (Cx43) is a major gap junction (GJ) protein, and intracellular communication by using low molecular substances is normally performed through GJ. We previously established new CRPC animal models, and present study, cDNA microarray analyses revealed that Cx43 was suppressed in CRPC. Moreover, Cx43 regulates apoptotic signaling in castrated condition in new established Cx43 overexpressed prostate cancer cells. Therefore, GJ may play important roles in preventing castration resistant growth.
|