Study of regulatory mechanism controlling cancer cell reprogramming

2016 Fiscal Year Final Research Report

• Project/Area Number: 25290048
• Research Category: Grant-in-Aid for Scientific Research (B)
• Allocation Type: Partial Multi-year Fund
• Section: 一般
• Research Field: Tumor biology
• Research Institution: Nagoya City University (2014-2016); 愛知県がんセンター(研究所) (2013)
• 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): Natsume Atsushi 名古屋大学, 医学系研究科, 准教授 (30362255) ; Shinjo Keiko 名古屋市立大学, 大学院医学研究科, 助教 (40641618) ; Katsushima Keisuke 名古屋市立大学, 大学院医学研究科, 助教 (00754053)
• Project Period (FY): 2013-04-01 – 2017-03-31
• Keywords: エピジェネティクス / 非翻訳RNA / がん / がん治療

Outline of Final Research Achievements

Plastic epigenetic regulation might be linked to the morphological and lineage heterogeneity. However, knowledge about how epigenome is altered specifically at certain loci and how this affects the phenotypes of tumor is largely unknown. In the current project, we found that the notch-regulated long non-coding RNA, TUG1, promotes self-renewal by quenching microRNA in the cytoplasm and recruiting polycomb to repress differentiation genes in the nucleus. Intravenous treatment with antisense oligonucleotides targeting TUG1 coupled with drug delivery system induces glioma cell differentiation and efficiently represses glioma cell growth in vivo. Our data provide a strong rationale for targeting TUG1 as a specific and potent therapeutic approach to eliminate the glioma cells.

Free Research Field

分子腫瘍学