Author/Authors :
Qing-Lin Li، نويسنده , , Kosei Ito، نويسنده , , Chohei Sakakura، نويسنده , , Hiroshi Fukamachi، نويسنده , , Ken-ichi Inoue، نويسنده , , Xin-Zi Chi، نويسنده , , Kwang Youl Lee، نويسنده , , Shintaro Nomura، نويسنده , , Chang-Woo Lee، نويسنده , , Sang-Bae Han، نويسنده , , Hwan-Mook Kim، نويسنده , , Wun-Jae Kim، نويسنده , , Hiromitsu Yamamoto، نويسنده , , Namiko Yamashita، نويسنده , , Takashi Yano، نويسنده , , Toshio Ikeda، نويسنده , , Shigeyoshi Itohara، نويسنده , , Johji Inazawa، نويسنده , , Tatsuo Abe، نويسنده , , Akeo Hagiwara، نويسنده , , et al، نويسنده ,
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.
