Molecular Info® Copy Right © 2001
Institute of Molecular Development LLC
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Causal Relationship between the Loss of RUNX3 Expression and Gastric Cancer
Qing-Lin Li, et.al.
The Cell, April 2002, 109: 113-124.
Runx3/Pebp2aC 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-B, 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
related to the progression of human gastric cancer.
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