Elucidation of epigenome-mediated proliferation mechanism in bladder cancer and development of therapy with novel inhibitors

2017 Fiscal Year Final Research Report

• Project/Area Number: 16K20154
• Research Category: Grant-in-Aid for Young Scientists (B)
• Allocation Type: Multi-year Fund
• Research Field: Urology
• Research Institution: Nagoya City University
• Principal Investigator: Iida Keitaro 名古屋市立大学, 大学院医学研究科, 臨床研究医 (30713945)
• Research Collaborator: Yasui Takahiro 名古屋市立大学, 大学院医学研究科, 教授 (40326153) ; Suzuki Takayoshi 京都府立医科大学, 大学院医学研究科, 教授 (90372838) ; Kawai Noriyasu 名古屋市立大学, 大学院医学研究科, 准教授 (20254279) ; Ando Ryosuke 名古屋市立大学, 大学院医学研究科, 講師 (30381867) ; Naiki Taku 名古屋市立大学, 大学院医学研究科, 助教 (50551272) ; Etani Toshiki 名古屋市立大学, 大学院医学研究科, 助教 (30600754)
• Project Period (FY): 2016-04-01 – 2018-03-31
• Keywords: エピジェネティクス / ヒストン修飾 / LSD1 / 膀胱癌 / オートファジー

Outline of Final Research Achievements

We investigated therapeutic potential of a novel histone lysine demethylase 1 (LSD1) inhibitor, NCL1, in bladder cancer. Bladder cancer cell lines were treated with NCL1, and LSD1 and cell viability were assessed. Bladder cancer cells showed strong LSD1 expression, and cell viability was decreased by NCL1. In addition, autophagy was induced by NCL1 treatment. Autophagy inhibitor, chloroquine, demonstrated synergic anti-tumor effect with NCL1. In TCGA database, LSD1 RNA expression in bladder cancer was significant higher than that in normal bladder tissues. We suggest that NCL1 and autophagy inhibitor is a potential therapeutic agent for bladder cancer.

Free Research Field

医学