Potential anticancer effect by inhibiting NFBD1/MDC1
| Project/Area Number |
25893292
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| Research Category |
Grant-in-Aid for Research Activity Start-up
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| Allocation Type | Single-year Grants |
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| Research Field |
General medical chemistry
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| Research Institution | Chiba Cancer Center (Research Institute) |
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Principal Investigator |
ANDO KIYOHIRO 千葉県がんセンター(研究所), がん治療開発グループ, 客員研究員 (10455389)
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| Project Period (FY) |
2013-08-30 – 2015-03-31
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| Project Status |
Completed (Fiscal Year 2014)
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| Budget Amount *help |
¥2,730,000 (Direct Cost: ¥2,100,000、Indirect Cost: ¥630,000)
Fiscal Year 2014: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2013: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
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| Keywords | NFBD1 / MDC1 / PLK1 / topoisomerase / decatenation checkpoint / neuroblastoma / CHK1 / TP53 / 癌 / 遺伝子 / キナーゼ阻害 / アポトーシス / TOPOIIalpha / ICRF-193 |
|---|
| Outline of Final Research Achievements |
It has been reported that functional inhibition of NFBD1/MDC1 potentiates anticancer effect. However, the molecular mechanism and biomarker that predicts its sensitivity have been still unclear. In this study, we clarified that NFBD1 is phosphorylated by PLK1 and allows cell to enter mitosis by recovering decatenation checkpoint that is mediated a physical interaction of NFBD1 and TOPOIIα. These results indicated that the precocious M phase entry by inhibiting NFBD1 might increase sensitivity of a genotoxic agent and radiation. Furthermore, our microarray analysis suggested that possible candidates of biomarker related to the sensitivity were TP53 and its downstream genes.
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Report
(3 results)
Research Products
(3 results)
