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2012 Fiscal Year Final Research Report

Studies for NACC1,a pluripotent transcriptional factor, in tumorcells

Research Project

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Project/Area Number 22390071
Research Category

Grant-in-Aid for Scientific Research (B)

Allocation TypeSingle-year Grants
Section一般
Research Field Human pathology
Research InstitutionIwate Medical University

Principal Investigator

MAESAWA Chihaya  岩手医科大学, 医学部, 教授 (10326647)

Co-Investigator(Kenkyū-buntansha) NISHIDUKA Satoshi  岩手医科大学, 医学部, 講師 (50453311)
WAKABAYASI Go  岩手医科大学, 医学部, 教授 (50175064)
NONAKA Takamasa  岩手医科大学, 薬学部, 教授 (30242457)
Project Period (FY) 2010 – 2012
KeywordsNACC1 / ケミカルバイオロジー / 多能性 / 病理 / 翻訳後修飾 / 転写因子
Research Abstract

NACC1 is a member of pluripotent transcription factor, and associates with malignant phenotypes of tumor cells. The present study investigated the molecular mechanisms of NACC1 in malignant tumors. We represented that NACC1 directly bound to HDAC6, and deacetylated tubulin and cortactin. This deacetylation introduced acceleration of motility and invasion of tumor cells. NACC1 also contributed to stabilization of ERBB2 protein expression through the deacetylation of HSP90. The SUMOlylation of NACC1 introduced the binding with PML protein. Our study demonstrated that overexpression of NACC1 protein contributes to motility, invasion, proliferation activities of tumor cells, and may be a good candidate for molecular target medicine in cancer therapy.

  • Research Products

    (10 results)

All 2013 2012 2011 2010 Other

All Journal Article (6 results) (of which Peer Reviewed: 6 results) Presentation (3 results) Remarks (1 results)

  • [Journal Article] Loss of HOXD10 expression induced by upregulation of miR -10b accelerates themigration and invasion activities of ovarian cancer cells2013

    • Author(s)
      Nakayama I, Shibazaki M, Yashima-Abo A, Miura F, Sugiyama T, Masuda T, MaesawaC
    • Journal Title

      Int J Oncol

      Volume: 43(1) Pages: 63-71

    • DOI

      DOI:10.3892/ijo.2013.1935

    • Peer Reviewed
  • [Journal Article] Molecular marker identification for relapse prediction in 5-FU-based adjuvant chemotherapy in gastric and colorectal cancers.2012

    • Author(s)
      Ishida K, Nishiduka S, Chiba T, Ikeda M, Kume K, Endo F, Katagiri H, Matsuo T, Noda H, Iwaya T, Yamada N, Fujiwara H, Takahashi M, Itabashi T, Uesugi N,Maesawa C, Tamura G, Sugai T, Otsuka K, Koeda K, Wakabayashi G.
    • Journal Title

      PLoS One

      Volume: 7(8) Pages: e43236

    • DOI

      DOI:10.1371/journal.pone.0043236.

    • Peer Reviewed
  • [Journal Article] Overexpre ssion of histone deacetylase 6 contributes to accelerated migration and invasion activity of hepatocellular carcinoma cells.2012

    • Author(s)
      Kanno K, Kanno S, Nitta H, Uesugi N, Sugai T, Masuda T, Wakabayashi G , Maesawa C
    • Journal Title

      Oncol Rep.

      Volume: 28(3) Pages: 867 -73

    • DOI

      DOI:10.3892/or.2012.1898.

    • Peer Reviewed
  • [Journal Article] Sensor and effector kinases in DNAdamage checkpoint regulate capacity for homologous recombination repair offission yeast in G2 phase.2012

    • Author(s)
      Yasuhira S, Saito T, Maesawa C, Masuda T.
    • Journal Title

      DNA Repair (Amst).

      Volume: 11(8) Pages: 666-75

    • DOI

      DOI:10.1016/j.dnarep.2012.05.006.

    • Peer Reviewed
  • [Journal Article] Downregulation of cylindromatosis gene, CYLD, confers a growth advantage on malignant melanoma cells while negatively regulating their migration activity2012

    • Author(s)
      Ishikawa Y, Tsunoda K, Shibazaki M, Takahashi K, Akasaka T, Masuda T, Maesawa C.
    • Journal Title

      Int J Oncol

      Volume: 41(1) Pages: 53 -60

    • DOI

      DOI:10.3892/ijo.2012.1424

    • Peer Reviewed
  • [Journal Article] Nucleusaccumbens-associated 1 contributes to cortactin deacetylation and augments the migration of melanoma cells.2011

    • Author(s)
      Tsunoda K, Oikawa H, Tada H, Tatemichi Y, Muraoka S, Miura S, Shibazaki M,Maeda F, Takahashi K, Akasaka T, Masuda T, Maesawa C
    • Journal Title

      J Invest Dermatol.

      Volume: 131(8) Pages: 1710 -9

    • DOI

      DOI:10.1038/jid.2011.110.

    • Peer Reviewed
  • [Presentation] NACC1/HDAC6脱アセチル化機構はアクチンおよび微小間依存性の腫瘍細胞の運動能に影響を与える(NACC1/HDAC6 deacetylation system accelerates tumor cell migration via an actin - andmicrotubule-dependent process)(英語).2011

    • Author(s)
      前沢千早,多田広志,角田加奈子,柴崎晶彦,安平進士,及川弘樹,管野公徳,石川雄一,増田友之
    • Organizer
      第70回日本癌学会総会記事
    • Place of Presentation
      名古屋
    • Year and Date
      20111003-05
  • [Presentation] NACC1蛋白質のSUMO化はPML nuclear bodyへの取り込みに関連している(NACC1 recruitment within the PML nuclear body is mediated by covalent and non-covalent binding through SUMO modification)(英語).2010

    • Author(s)
      前沢 千早, 舘道 芳徳, 及川 浩樹, 増田 友之
    • Organizer
      第69日本癌学会総会記事
    • Place of Presentation
      大阪.
    • Year and Date
      20100922-24
  • [Presentation] 転写因子NACC1(nucleus accumbens associated 1)のSUMO化修飾とその生物学的意義に関する検討2010

    • Author(s)
      前沢 千早, 舘道 芳徳, 及川 浩樹, 小谷 康 慈, 増 田 友 之
    • Organizer
      第99回日本病理学会
    • Place of Presentation
      東京.
    • Year and Date
      20100427-29
  • [Remarks]

    • URL

      http//miast.jp/

URL: 

Published: 2014-08-29  

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