Investigation for the methylation-promoting element in response to carcinogenesis
| Project/Area Number |
23659166
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| Research Category |
Grant-in-Aid for Challenging Exploratory Research
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| Allocation Type | Multi-year Fund |
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| Research Field |
Pathological medical chemistry
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| Research Institution | Tohoku University |
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Principal Investigator |
MOTOHASHI Hozumi 東北大学, 大学院・医学系研究科, 准教授 (00282351)
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| Project Period (FY) |
2011 – 2012
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| Project Status |
Completed (Fiscal Year 2012)
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| Budget Amount *help |
¥3,770,000 (Direct Cost: ¥2,900,000、Indirect Cost: ¥870,000)
Fiscal Year 2012: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2011: ¥2,340,000 (Direct Cost: ¥1,800,000、Indirect Cost: ¥540,000)
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| Keywords | 分子腫瘍学 / エピゲノム / がん / 予後 / DNA メチル化 / DNAメチル化 / メチル化 / 細胞増殖 |
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| Research Abstract |
The goal of this project was to clarify the molecular mechanisms underlying the selective DNA methylation during carcinogenesis. We examined glioma patients and found that expression levels of NRF2 target genes in IDH1-mutated glioma are significantly lower than IDH1 WT glioma. When we overexpress IDH1 mutant into T98 cells, one of the cell lines derived from glioma patients. IDH1-mutant cells exhibited lower expression of NRF2 target genes, decreased accumulation of NRF2 in the nucleus, and reduced expression of NRF2 gene. This study has suggested a possibility that NRF2 gene might be epigenetically silenced during the development glioma.
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Report
(3 results)
Research Products
(69 results)
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[Journal Article] Accumulation of p62/SQSTM1 is associated with poor prognosis in patients with lung adenocarcinoma2012
Author(s)
Inoue D, Suzuki T, Mitsuishi Y, Miki Y, Suzuki S, Sugawara S, Watanabe M, Sakurada A, Endo C, Uruno A, Sasano H, Nakagawa T, Satoh K, Tanaka N, Kubo H, Motohashi H, Yamamoto M
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Journal Title
Cancer Sci
Volume: 103
Issue: 4
Pages: 760-766
DOI
Related Report
Peer Reviewed
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