analysis in function of androgen in testcular germ cell tumor

2017 Fiscal Year Final Research Report

• Project/Area Number: 16K15695
• Research Category: Grant-in-Aid for Challenging Exploratory Research
• Allocation Type: Multi-year Fund
• Research Field: Urology
• Research Institution: Kyoto Prefectural University of Medicine
• Principal Investigator: Ueda Takashi 京都府立医科大学, 医学(系)研究科(研究院), 客員講師 (50601598)
• Co-Investigator(Kenkyū-buntansha): 中村 晃和 京都府立医科大学, 医学(系)研究科(研究院), 客員教授 (10381964) ; 浮村 理 京都府立医科大学, 医学(系)研究科(研究院), 教授 (70275220) ; 大石 正勝 京都府立医科大学, 医学(系)研究科(研究院), 客員講師 (90405316) ; 上田 紗弥 (伊藤紗弥) 京都府立医科大学, 医学(系)研究科(研究院), 博士研究員 (90534511) ; 本郷 文弥 京都府立医科大学, 医学(系)研究科(研究院), 准教授 (80291798) ; 金沢 元洪 京都府立医科大学, 医学(系)研究科(研究院), 助教 (00468266) ; 藤原 敦子 京都府立医科大学, 医学(系)研究科(研究院), 講師 (20457980)
• Project Period (FY): 2016-04-01 – 2018-03-31
• Keywords: アンドロゲン / 精巣腫瘍 / セミノーマ / TPH1 / セロトニン

Outline of Final Research Achievements

Epidemiological findings suggest that andorogen/AR signal has a role in semioma progression. However, the role of androgen/AR signal in seminoma progression remains unclear.
Additon of androgen in seminoma cell line (TCam-2) suppressed cell growth and suppression of androgen/AR signal in xenograft model mouse promoted cell growth of TCam-2.Activation of androgen/AR signaling in TCam-2 cells reduced the expression of TPH1 in SE cells, followed by the reduction of serotonin secretion in cell culture supernatant. These results suggested that silencing of androgen/AR signaling may cause initiation and progression of seminoma through increase in TPH1 gene expression level.

Free Research Field

泌尿器科腫瘍学