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Analysis of ovarian tumourigenesis due to activators for histone deacetylases(HDACs) that are highly overexpressed in cancers

Research Project

Project/Area Number 21592129
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeSingle-year Grants
Section一般
Research Field Obstetrics and gynecology
Research InstitutionKyoto University

Principal Investigator

HIGASHITSUJI Hisako  京都大学, 医学研究科, 助教 (20402852)

Project Period (FY) 2009 – 2011
Project Status Completed (Fiscal Year 2011)
Budget Amount *help
¥4,550,000 (Direct Cost: ¥3,500,000、Indirect Cost: ¥1,050,000)
Fiscal Year 2011: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2010: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2009: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Keywordsガンキリン / HSCO / ヒストン脱アセチル化酵素 / 卵巣癌 / 活性化因子 / HDAC1 / SIRT1 / がん抑制遺伝子 / ヒストン / 脱アセチル化酵素
Research Abstract

Protooncogene Gankyrin is overexpressed in ovarian cancer. Gankyrin accelerates to degrade pRb protein. Gankyrin inhibits the interaction of p16INK4a with cdk4. Gankyrin enhances to degrade p53 protein by MDM2. Gankyrin suppresses the activity of NFkappaB, partly due to recruitment of SIRT1 histone deacetylase to NFkappaB protein. HSCO gene is overexpressed in ovarian cancer. HSCO inhibits the activity of p53 due to recruitment of HDAC1 histone deacetylase to p53 protein. Gankyrin and HSCO activate the activity of HDACs. These enhanced activities of HDACs accelerate to grow cancer cells more aggressively. The activities of invasion and metastasis are enhanced due to these activated HDACs. Nicotinamide suppresses SIRT1 activity. TSA(Trichostatin A) inhibits HDAC1 activity. These HDAC inhibitors suppress the growth, invasion, and metastasis of cancer cells.

Report

(4 results)
  • 2011 Annual Research Report   Final Research Report ( PDF )
  • 2010 Annual Research Report
  • 2009 Annual Research Report
  • Research Products

    (12 results)

All 2011 2010 2009 2008

All Journal Article (6 results) (of which Peer Reviewed: 5 results) Presentation (6 results)

  • [Journal Article] Adriamycin enhances proteasome-mediated generation of the proapoptotic processed form of MAGE-A4 in hepatoma cells2011

    • Author(s)
      Sakurai T, Kudo M, Itoh K, Ryu U, Higashitsuji H, Fujita J.
    • Journal Title

      Oncology

      Volume: 81 Issue: Suppl. 1 Pages: 30-5

    • DOI

      10.1159/000334307

    • Related Report
      2011 Final Research Report
  • [Journal Article] Adriamycin enhances proteasome-mediated generation of the proapoptotic processed form of MAGEA-4 in hepatoma cells2011

    • Author(s)
      Sakurai T., et al
    • Journal Title

      Oncology

      Volume: 81 Pages: 30-35

    • Related Report
      2011 Annual Research Report
    • Peer Reviewed
  • [Journal Article] MDM2 is a novel E3 ligase for HIV-1 Vif2009

    • Author(s)
      Izumi T, Takaori-Kondo A, Shirakawa K, Higashitsuji H, Itoh K, Io K, Matsui M, Iwai K, Kondoh H, Sato T, Tomonaga M, Ikeda S, Akari H, Koyanagi Y, Fujita J, Uchiyama T.
    • Journal Title

      Retrovirology

      Volume: 6 Issue: 1 Pages: 1-10

    • DOI

      10.1186/1742-4690-6-1

    • Related Report
      2011 Final Research Report
    • Peer Reviewed
  • [Journal Article] MDM2 is a novel E3 ligase for HIV-1 Vif.2009

    • Author(s)
      Izumi T
    • Journal Title

      Retrovirology 6

      Pages: 1-10

    • Related Report
      2009 Annual Research Report
    • Peer Reviewed
  • [Journal Article] Association of gankyrin protein expression with early clinical stages and IGFBP-5 expression in human hepatocellular carcinoma2008

    • Author(s)
      Umemura A, Itoh Y, Itoh K, Yamaguchi K, Nakajima T, Higashitsuji H, Onoue H, Fukumoto M, Okanoue T, Fujita J.
    • Journal Title

      Hepatology

      Volume: 47(2) Issue: 2 Pages: 493-502

    • DOI

      10.1002/hep.22027

    • Related Report
      2011 Final Research Report
    • Peer Reviewed
  • [Journal Article] Gankyrin oncoprotein overexpression as a critical factor for tumor growth in human esophageal squamous cell carcinoma and its clinical significance2008

    • Author(s)
      Ortiz CM, Ito T, Tanaka E, Tsunoda S, Nagayama S, Sakai Y, Higashitsuji H, Fujita J, Shimada Y.
    • Journal Title

      Int J Cancer

      Volume: 122 Issue: 2 Pages: 325-332

    • DOI

      10.1002/ijc.23106

    • Related Report
      2011 Final Research Report
    • Peer Reviewed
  • [Presentation] CIRP(cold-inducible RNA binding protein)は癌細胞の浸潤能、転移能を亢進する2011

    • Author(s)
      東辻久子
    • Organizer
      第63回日本産科婦人科学会学術講演会
    • Place of Presentation
      リーガロイヤルホテル大阪、大阪市
    • Year and Date
      2011-08-30
    • Related Report
      2011 Final Research Report
  • [Presentation] CIRP (cold-inducible RNA binding protein)は癌細胞の浸潤能、転移能を亢進する2011

    • Author(s)
      東辻久子
    • Organizer
      第63回日本産科婦人科学会学術講演会
    • Place of Presentation
      大阪市、リーガロイヤルホテル大阪
    • Year and Date
      2011-08-30
    • Related Report
      2011 Annual Research Report
  • [Presentation] がん遺伝子CIRP(cold-inducible RNA binding protein)は癌細胞の浸潤能と転移能を亢進させる2010

    • Author(s)
      東辻久子
    • Organizer
      第52回日本消化器病学会大会
    • Place of Presentation
      パシフィコ横浜、横浜市
    • Year and Date
      2010-10-14
    • Related Report
      2011 Final Research Report
  • [Presentation] がん遺伝子CIRP(cold-inducible RNA binding protein)は癌細胞の浸潤能と転移能を亢進させる2010

    • Author(s)
      東辻久子
    • Organizer
      JDDW2010第52回日本消化器病学会大会
    • Place of Presentation
      横浜市パシフィコ横浜
    • Year and Date
      2010-10-14
    • Related Report
      2010 Annual Research Report
  • [Presentation] 卵巣癌で過剰発現するがん遺伝子ガンキリンはNFkappaB(RelA)と結合しその転写活性化能を抑制する2009

    • Author(s)
      東辻久子
    • Organizer
      第61回日本産科婦人科学会学術講演会
    • Place of Presentation
      国立京都国際会館、京都市
    • Year and Date
      2009-04-05
    • Related Report
      2011 Final Research Report
  • [Presentation] 卵巣癌で過剰発現する癌遣伝子産物ガンキリンはNFkappaB(RelA)と結合しその転写活性化能を抑制する。2009

    • Author(s)
      東辻久子
    • Organizer
      第61回日本産科婦人科学会学術講演会
    • Place of Presentation
      国立京都国際会館、京都市
    • Year and Date
      2009-04-05
    • Related Report
      2009 Annual Research Report

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Published: 2009-04-01   Modified: 2016-04-21  

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