Causal relationship between the loss of RUNX3 expression and gastric cancer

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Title
Causal relationship between the loss of RUNX3 expression and gastric cancer
Author(s)
Qing Lin Li; Kosei Ito; Chohei Sakakura; Hiroshi Fukamachi; Ken-ichi Inoue; Xin-Zi Chi; Chang Woo Lee; Sang Bae Han; Hwan Mook Kim; Suk Chul Bae
Bibliographic Citation
Cell, vol. 109, no. 1, pp. 113-124
Publication Year
2002
Abstract
Runx3/Pebp2αC 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-β, 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.
ISSN
0092-8674
Publisher
Elsevier-Cell Press
DOI
http://dx.doi.org/10.1016/S0092-8674(02)00690-6
Type
Article
Appears in Collections:
Ochang Branch Institute > Division of Bioinfrastructure > Laboratory Animal Resource Center > 1. Journal Articles
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