Causal relationship between the loss of RUNX3 expression and gastric cancer - PubMed (original) (raw)

. 2002 Apr 5;109(1):113-24.

doi: 10.1016/s0092-8674(02)00690-6.

Kosei Ito, Chohei Sakakura, Hiroshi Fukamachi, Ken ichi Inoue, Xin Zi Chi, Kwang Youl Lee, Shintaro Nomura, Chang Woo Lee, Sang Bae Han, Hwan Mook Kim, Wun Jae Kim, Hiromitsu Yamamoto, Namiko Yamashita, Takashi Yano, Toshio Ikeda, Shigeyoshi Itohara, Johji Inazawa, Tatsuo Abe, Akeo Hagiwara, Hisakazu Yamagishi, Asako Ooe, Atsushi Kaneda, Takashi Sugimura, Toshikazu Ushijima, Suk Chul Bae, Yoshiaki Ito

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• PMID: 11955451
• DOI: 10.1016/s0092-8674(02)00690-6

Free article

Causal relationship between the loss of RUNX3 expression and gastric cancer

Qing Lin Li et al. Cell. 2002.

Free article

Abstract

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.

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Comment in

• RUNX 3, apoptosis 0: a new gastric tumour suppressor.
  Moss SF. Moss SF. Gut. 2003 Jan;52(1):12-3. doi: 10.1136/gut.52.1.12. Gut. 2003. PMID: 12477750 Free PMC article. No abstract available.

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