2018 Fiscal Year Final Research Report
Development of low molecular weight compounds switching transcription activity for abnormal epigenetic regulation in glioma
| Project/Area Number |
17K19724
|
|---|
| Research Category |
Grant-in-Aid for Challenging Research (Exploratory)
|
| Allocation Type | Multi-year Fund |
|---|
| Research Field |
Surgery related to the biological and sensory functions and related fields
|
|---|
| Research Institution | Kyoto University |
|---|
Principal Investigator |
|
|---|
| Co-Investigator(Kenkyū-buntansha) |
荒川 芳輝 京都大学, 医学研究科, 特定講師 (20378649)
上久保 靖彦 京都大学, 医学研究科, 特定教授 (60548527)
|
|---|
| Research Collaborator |
Terada Yukinori
Matsui Yasuzumi
Makino Yasuhide
Hattori Etsuko
Hattori Etsuko
|
|---|
| Project Period (FY) |
2017-06-30 – 2019-03-31
|
| Keywords | グリオーマ / RUNX1 / 悪性転化 / Mesenchymal型転換 / 転写スイッチ / 低分子化合物 / コンセンサス配列 / 転写ネットワーク |
|---|
| Outline of Final Research Achievements |
Chb-M', alkylating agent-conjugated consensus sequence binding compound (alkylating agent－conjugated pyrrole－imidazole polyamide) disturbed cell growth of various types of glioma cell lines. Its main mechanism was apoptosis induction. Using mRNA array and phosphorylated protein array, a group of genes controlled by Chb-M 'administration was identified, which showed the inhibition of cell survival signal transduction. These results suggest that Chb-M 'targeting abnormal transcription network may become a drug for treatment of glioma.
|
| Free Research Field |
脳神経外科
|
| Academic Significance and Societal Importance of the Research Achievements |
悪性グリオーマは、予後不良の悪性脳腫瘍である。グリオーマ悪性転化に関わるメカニズムを標的にした薬剤の開発を行った。コンセンサス配列結合阻害化合物Chb－M’が、複数のタイプのグリオーマ細胞株でアポトーシス誘導を行い、腫瘍増殖抑制を示した。これらの結果から、Chb－M’がグリオーマ治療薬として有望であることが明らかとなった。
|
