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PARP inhibition induced DNA demethylation through downregulation of Dnmt3.

Research Project

Project/Area Number 25840015
Research Category

Grant-in-Aid for Young Scientists (B)

Allocation TypeMulti-year Fund
Research Field Molecular biology
Research InstitutionNational Cancer Center Japan

Principal Investigator

HIROAKI Fujimori  独立行政法人国立がん研究センター, 研究所, 研究員 (00590043)

Project Period (FY) 2013-04-01 – 2015-03-31
Project Status Completed (Fiscal Year 2014)
Budget Amount *help
¥4,550,000 (Direct Cost: ¥3,500,000、Indirect Cost: ¥1,050,000)
Fiscal Year 2014: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2013: ¥2,600,000 (Direct Cost: ¥2,000,000、Indirect Cost: ¥600,000)
KeywordsPARP阻害剤 / PARP / Dnmt3 / DNAメチル化
Outline of Final Research Achievements

Epigenetic factors are recently noticed as significant targets for anti-cancer therapy, in which the utility of DNMT 3 inhibition has been demonstrated. It is because DNMT3 overexpressing in several tumors inactivated multiple tumor suppressor genes in methylation-dependent manner and DNMT3 dysfunction in these cancer cells induced cancer cell death through recovering expression of tumor suppressor genes. However, specific DNMT3 inhibitor is now under development. In this study, we demonstrated that Parp-1 is required for Dnmt3 expression in vitro and in vivo and that PARP inhibition suppressed A549 proliferation through reduction of the DNMT3B expression. Since PARP inhibitor demonstrated the significant anti-tumor effect to BRCA-/- cancers with few side effect, enlarged application of the inhibitor with other clinical protocols is hoped. Our current study shows the possibility that PARP inhibitor works as an epigenetic anti-cancer drug for DNMT3 overexpressing tumor.

Report

(3 results)
  • 2014 Annual Research Report   Final Research Report ( PDF )
  • 2013 Research-status Report
  • Research Products

    (5 results)

All 2014 2013

All Presentation (5 results)

  • [Presentation] PARP is required for Dnmt3 transcription and protects ES cells and cancer cells from transcriptional activation of silenced genes.2014

    • Author(s)
      Hiroaki Fujimori
    • Organizer
      2014年度 がん若手ワークショップ
    • Place of Presentation
      蓼科グランドホテル滝の湯
    • Year and Date
      2014-09-03 – 2014-09-06
    • Related Report
      2014 Annual Research Report
  • [Presentation] Parp-1 has a novel role as Dnmt3 regulator.2014

    • Author(s)
      Hiroaki Fujimori
    • Organizer
      The PARP Family & Friends
    • Place of Presentation
      Cold Spring Harbor, USA
    • Year and Date
      2014-04-09 – 2014-04-12
    • Related Report
      2014 Annual Research Report
  • [Presentation] PARP-1はDNMT3の発現を維持する新規調節因子である。2013

    • Author(s)
      藤森浩彰、向井大晃、益谷美都子
    • Organizer
      発がん病理研究会
    • Place of Presentation
      ユインチホテル南城(沖縄県那覇市)
    • Related Report
      2013 Research-status Report
  • [Presentation] Parp-1 has a novel role as Dnmt3 regulator and PARP inhibitor acts as a epigenetic drug recovering silenced expression of tumor-suppressor genes.2013

    • Author(s)
      Hiroaki Fujimori, Hideki Ogino, Hiroaki Mukai, Yasufumi Murakami, Mitsuko Masutani
    • Organizer
      PARP2013
    • Place of Presentation
      CHLU research Center (Canada, Quebec city)
    • Related Report
      2013 Research-status Report
  • [Presentation] Poly(ADP-ribose) polymerase-1 maintains gene silencing through regulation of DNA methyltransferases.2013

    • Author(s)
      Hiroaki Fujimori,Hiroaki Mukai, Yasufumi Murakami, MitsukoMasutani
    • Organizer
      日本分子生物学会
    • Place of Presentation
      ポートピアホテル(兵庫県神戸市)
    • Related Report
      2013 Research-status Report

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Published: 2014-07-25   Modified: 2019-07-29  

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