Tumor suppressor function of BMCC1 in neuroblastoma
| Project/Area Number |
17K10132
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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, 上席研究員 (00450578)
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| Project Period (FY) |
2017-04-01 – 2020-03-31
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| Project Status |
Completed (Fiscal Year 2019)
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| Budget Amount *help |
¥4,680,000 (Direct Cost: ¥3,600,000、Indirect Cost: ¥1,080,000)
Fiscal Year 2019: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2018: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2017: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
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| Keywords | 神経芽腫 / BMCC１ / アポトーシス / DNA損傷応答 / BMCC1 / ミトコンドリア / ゲノム安定性 / DNA損傷 / 転写制御 / タンパク分解制御 / ゲノム不安定性 / 染色体不安定性 / DNA傷害 / 悪性化 |
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| Outline of Final Research Achievements |
In this study, we aimed to elucidate the molecular basis of BMCC1, a favorable prognostic factor for neuroblastoma, in repression of malignant transformation of neuroblastoma. As part of our results, we found that BMCC1, which acts as a brake for Akt-survival signal and induces mitochondrial cell death, was rapidly transcribed in an ATM-E2F1-dependent manner in response to DNA damage with cisplatin. We also found that BMCC1 was cleaved and degraded by caspase 9-dependent mechanism at the later stage of apoptotic cell death in mitochondrial pathway. We reported these findings in BMC Cancer.
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| Academic Significance and Societal Importance of the Research Achievements |
本研究の成果として、ミトコンドリア細胞死におけるBMCC1の発現プロファイルおよびその制御機構を明らかにした。BMCC1の時期特異的な発現プロファイルは、抗癌剤感受性およびゲノムの安定維持に関わるDNA損傷からミトコンドリア細胞死に至る過程におけるBMCC1の機能を理解する重要な手がかりとなる点で学術的に意義深い。BMCC1の発現制御メカニズムは、難治性となった神経芽腫の有効な治療法の開発への応用が期待できる点で、社会的に意義深い。
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Report
(4 results)
Research Products
(18 results)
