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In vitro RNA interference against beta-catenin inhibiting the proliferation of pediatric hepatic tumors

Research Project

Project/Area Number 16591785
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeSingle-year Grants
Section一般
Research Field Pediatric surgery
Research InstitutionOsaka University

Principal Investigator

KUSAFUKA Takeshi  Osaka University, Graduate School of Medicine, Assistant, 医学系研究科, 助手 (70263267)

Co-Investigator(Kenkyū-buntansha) YONEDA Akihiro  Osaka University, Graduate School of Medicine, Assistant, 医学系研究科, 助手 (30372618)
FUKUZAWA Masahiro  Osaka University, Graduate School of Medicine, Professor, 医学系研究科, 教授 (60165272)
Project Period (FY) 2004 – 2005
Project Status Completed (Fiscal Year 2005)
Budget Amount *help
¥3,500,000 (Direct Cost: ¥3,500,000)
Fiscal Year 2005: ¥1,400,000 (Direct Cost: ¥1,400,000)
Fiscal Year 2004: ¥2,100,000 (Direct Cost: ¥2,100,000)
Keywordshepatoblastoma / HepG2 / Huh-6 / beta-catenin / RNA interference / pediatric
Research Abstract

To address beta-catenin's capacity in maintaining the malignant phenotype in established pediatric hepatoblastoma and hepatocellular carcinoma cell lines, HuH-6,and HepG2,harboring mutated and overexpressed beta-catenin, we carried out a series of in vitro analyses through a transfection of short interfering RNAs to generate a loss of function model. HuH-7,another hepatoblastoma cell line derived from a pediatric patient without a stabilizing mutation was used for comparison. RNA interference successfully manipulated the degradation of overexpressed beta-catenin. In all cell lines, beta-catenin mRNA was suppressed by 80-90 % after 48 h of transfection, and a reduction of its protein expression was demonstrated. In HuH-6 and HepG2,the pre-existing beta-catenin nuclear accumulation disappeared and reductions of beta-catenin downstream target genes, c-myc and cyclinD1,were also evidenced after treatment. The in vitro proliferation of both cell lines was transiently inhibited. In contrast, the suppression of beta-catenin in HuH-7 did not lead to a significant change in the expression of target genes or cellular proliferation. Our data indicate that beta-catenin can be considered a specific target for gene therapy in pediatric hepatic tumors with mutations and overexpression of this gene.

Report

(3 results)
  • 2005 Annual Research Report   Final Research Report Summary
  • 2004 Annual Research Report
  • Research Products

    (3 results)

All 2006 2004

All Journal Article (3 results)

  • [Journal Article] In vitro RNA interference against beta-catenin inhibits the proliferation of pediatric hepatic tumors2006

    • Author(s)
      Sangkhathat S, Kusafuka T, et al.
    • Journal Title

      Int J Oncol 28(3)

      Pages: 715-722

    • Description
      「研究成果報告書概要(和文)」より
    • Related Report
      2005 Annual Research Report 2005 Final Research Report Summary
  • [Journal Article] In vitro RNA interference against beta-catenin inhibits the proliferation of pediatric hepatic tumors2006

    • Author(s)
      Sangkhathat S, Kusafuka T, et al.
    • Journal Title

      Int J Oncol. 28

      Pages: 715-722

    • Description
      「研究成果報告書概要(欧文)」より
    • Related Report
      2005 Final Research Report Summary
  • [Journal Article] Novel germ-line deletion of SNF5/INI1/SMARCB1 gene in neonate presenting with congenital malignant rhabdoid tumor of kidney and brain primitive neuroectodermal tumor.2004

    • Author(s)
      Kusafuka T. et al.
    • Journal Title

      Genes Chromosomes Cancer 40(2)

      Pages: 133-139

    • Related Report
      2004 Annual Research Report

URL: 

Published: 2004-04-01   Modified: 2016-04-21  

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