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2014 Fiscal Year Final Research Report

Potential anticancer effect by inhibiting NFBD1/MDC1

Research Project

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Project/Area Number 25893292
Research Category

Grant-in-Aid for Research Activity Start-up

Allocation TypeSingle-year Grants
Research Field General medical chemistry
Research InstitutionChiba Cancer Center (Research Institute)

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)

Project Period (FY) 2013-08-30 – 2015-03-31
KeywordsNFBD1 / MDC1 / PLK1 / topoisomerase / decatenation checkpoint / neuroblastoma / CHK1 / TP53
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.

Free Research Field

がんの分子生物学

URL: 

Published: 2016-06-03  

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