| Project/Area Number |
26461602
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Pediatrics
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| Research Institution | Chiba Cancer Center (Research Institute) |
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Principal Investigator |
Tatsumi Yasutoshi 千葉県がんセンター(研究所), がん予防センター 腫瘍ゲノム研究室, 研究員 (00450578)
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| Co-Investigator(Kenkyū-buntansha) |
中川原 章 千葉県がんセンター(研究所), その他部局等, その他 (50117181)
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| Research Collaborator |
Islam Mohammad Sazzadul 千葉大学, 大学院、医学研究院
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| Project Period (FY) |
2014-04-01 – 2017-03-31
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| Project Status |
Completed (Fiscal Year 2016)
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| Budget Amount *help |
¥4,940,000 (Direct Cost: ¥3,800,000、Indirect Cost: ¥1,140,000)
Fiscal Year 2016: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2015: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2014: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
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| Keywords | 神経芽腫 / アポトーシス / 抗癌剤耐性 / DNA損傷応答 / 細胞周期 / 自然退縮 / DNA損傷 / BMCC1 / E2F1 / 転写制御 / 細胞死 / 細胞死促進因子 |
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| Outline of Final Research Achievements |
In this study, first, we found transcriptional regulation of BMCC1 mediated by E2F1 in neuroblastoma cells. Then, we clarified a functional role of BMCC1 in apoptosis promotion of neuroblastoma cells. Furthermore, we found that reduced expression of BMCC1 may become malignant neuroblastoma by abrogating DNA damage repair and apoptosis. Molecular functions of BMCC1 uncovered in this study provide clues for defining the underlying molecular mechanism(s) that determine whether the course of neuroblastoma will be favorable or unfavorable. These results were presented at several academic conferences and also reported as academic papers (Tatsumi et al., CDDIS, 2015; Islam and Tatsumi et al., BBRC, 2016).
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