Identification of a novel tumor-associated protein in gliomagenesis and chemicals targeting its function.
Project/Area Number |
26640088
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Research Category |
Grant-in-Aid for Challenging Exploratory Research
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Allocation Type | Multi-year Fund |
Research Field |
Tumor biology
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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)
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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)
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Project Period (FY) |
2014-04-01 – 2016-03-31
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Project Status |
Completed (Fiscal Year 2015)
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Budget Amount *help |
¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000)
Fiscal Year 2015: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2014: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
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Keywords | グリオブラストーマ / エピジェネティクス / 治療 / 膠芽腫 / エピゲノム / 癌治療 / ヒストン修飾 / 遺伝子変異 |
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.
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Report
(3 results)
Research Products
(30 results)
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[Journal Article] Aberrant TET1 Methylation Closely Associated with CpG Island Methylator Phenotype in Colorectal Cancer.2015
Author(s)
5.Ichimura N, Shinjo K, An B, Shimizu Y, Yamao K, Ohka F, Katsushima K, Hatanaka A, Tojo M, Yamamoto E, Suzuki H, Ueda M, Kondo Y
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Journal Title
Cancer Prev Res (Phila)
Volume: 10
Issue: 8
Pages: 702-11
DOI
Related Report
Peer Reviewed / Int'l Joint Research
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[Journal Article] Regulation of AURKC expression by CpG island methylation in human cancer cells.2015
Author(s)
Fujii S, Srivastava V, Hegde A, Kondo Y, Shen L, Hoshino K, Gonzalez Y, Wang J, Sasai K, Ma X, Katayama H, Estecio MR, Hamilton SR, Wistuba I, Issa JP, Sen S.
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Journal Title
Tumour Biol
Volume: 36
Issue: 10
Pages: 8147-58
DOI
Related Report
Peer Reviewed / Int'l Joint Research
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[Journal Article] Long-Term Pancreatic Beta Cell Exposure to High Levels of Glucose but Not Palmitate Induces DNA Methylation within the Insulin Gene Promoter and Represses Transcriptional Activity.2015
Author(s)
Ishikawa K, Tsunekawa S, Ikeniwa M, Izumoto T, Iida A, Ogata H, Uenishi E, Seino Y, Ozaki N, Sugimura Y, Hamada Y, Kuroda A, Shinjo K, Kondo Y, Oiso Y.
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Journal Title
PLoS One
Volume: 10(2)
Issue: 2
Pages: e0115350-e0115350
DOI
NAID
Related Report
Peer Reviewed / Open Access / Acknowledgement Compliant
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[Journal Article] miR-615-5p is epigenetically inactivated and functions as a tumor suppressor in pancreatic ductal adenocarcinoma.2015
Author(s)
Gao W, Gu Y, Li Z, Cai H, Peng Q, Tu M, Kondo Y, Shinjo K, Zhu Y, Zhang J, Sekido Y, Han B, Qian Z, Miao Y.
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Journal Title
Oncogene
Volume: 34
Issue: 13
Pages: 1629-40
DOI
Related Report
Peer Reviewed
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[Book] Cancer Science2014
Author(s)
Kondo Y, Katsushima K, Ohka F, Natsume A, Shinjo K.
Total Pages
7
Publisher
The official journal of the Japanese Cancer Association
Related Report
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