Identification of a novel tumor-associated protein in gliomagenesis and chemicals targeting its function.

2015 Fiscal Year Final Research Report

• Project/Area Number: 26640088
• Research Category: Grant-in-Aid for Challenging Exploratory Research
• Allocation Type: Multi-year Fund
• Research Field: Tumor biology
• Research Institution: Nagoya City University
• Principal Investigator: Kondo Yutaka 名古屋市立大学, 医学(系)研究科(研究院), 教授 (00419897)
• Co-Investigator(Renkei-kenkyūsha): SHINJO Keiko 名古屋市立大学, 大学院医学研究科, 助教 (40641618) ; NATSUME Atsushi 名古屋大学, 大学院医学研究科, 准教授 (30362255) ; SUZUKI Takayoshi 京都府立医科大学, 大学院医学研究科, 教授 (90372838)
• Project Period (FY): 2014-04-01 – 2016-03-31
• Keywords: グリオブラストーマ / エピジェネティクス / 治療

Outline of Final Research Achievements

In the current project, using mouse model (Tp53 and Nf1 loss), which spontaneously develops proneural GBM, we found that a certain specific gene locus is commonly (100%) amplified in multiple mice (n=5). In addition, although HMT-1 is not located in the amplified locus, it was overexpressed from early stage of gliomagenesis in this model. Intriguingly, among the genes located in commonly amplified locus, we identified HMT-2, which forms aberrant complex with HMT-1 in the tumor cells. Inhibition of HMT-1 and/or HMT-2 by a small molecules or siRNA system efficiently suppressed the tumor growth both in vitro and in vivo. Our data indicate that targeting these molecules (HMT-1 and HMT-2) may be a novel and potent therapeutic strategy for GBMs, especially proneural subtype.

Free Research Field

がんエピジェネティクス