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Causal relationship between the loss of RUNX3 expression and gastric cancer.

Runx3/Pebp2alphaC null mouse gastric mucosa exhibits hyperplasias due to stimulated proliferation and suppressed apoptosis in epithelial cells, and the cells are resistant to growth-inhibitory and apoptosis-inducing action of TGF-beta, indicating that Runx3 is a major growth regulator of gastric epithelial cells. Between 45% and 60% of human gastric cancer cells do not significantly express RUNX3 due to hemizygous deletion and hypermethylation of the RUNX3 promoter region. Tumorigenicity of human gastric cancer cell lines in nude mice was inversely related to their level of RUNX3 expression, and a mutation (R122C) occurring within the conserved Runt domain abolished the tumor-suppressive effect of RUNX3, suggesting that a lack of RUNX3 function is causally related to the genesis and progression of human gastric cancer.

Pubmed ID: 11955451


  • Li QL
  • Ito K
  • Sakakura C
  • Fukamachi H
  • Inoue Ki
  • Chi XZ
  • Lee KY
  • Nomura S
  • Lee CW
  • Han SB
  • Kim HM
  • Kim WJ
  • Yamamoto H
  • Yamashita N
  • Yano T
  • Ikeda T
  • Itohara S
  • Inazawa J
  • Abe T
  • Hagiwara A
  • Yamagishi H
  • Ooe A
  • Kaneda A
  • Sugimura T
  • Ushijima T
  • Bae SC
  • Ito Y



Publication Data

April 5, 2002

Associated Grants


Mesh Terms

  • Animals
  • Apoptosis
  • Cell Division
  • Cell Transformation, Neoplastic
  • Core Binding Factor Alpha 3 Subunit
  • DNA Methylation
  • DNA-Binding Proteins
  • Epithelium
  • Exons
  • Female
  • Gene Deletion
  • Gene Expression Regulation, Neoplastic
  • Gene Targeting
  • Humans
  • Hyperplasia
  • Male
  • Mice
  • Mice, Knockout
  • Protein Structure, Tertiary
  • Stomach
  • Stomach Neoplasms
  • Transcription Factors
  • Transforming Growth Factor beta
  • Tumor Cells, Cultured
  • Tumor Suppressor Proteins