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

By Qing Li, Kosei Ito, C. Sakakura, H. Fukamachi, Ken-ichi Inoue, X. Chi, Kwang-Youl Lee, S. Nomura, C. Lee, Sang-bae Han and 17 more. Cell, 2002

1,069 citations recorded by the source corpus.

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.

Subfields: Epidemiology, Hematology, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/ccad34e1df4d54f1d60e8c3b6cdf1c1e29632fee

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In Hematology

1. Ross A. Gagliano
2. Daniel G. Tenen

In Molecular Biology

1. T. Ozaki
2. Dan R. Littman
3. Ross A. Gagliano
4. T. Komori
5. A. Nakagawara
6. Daniel G. Tenen

Citations in the corpus

• Review of (2006, background): “However, they are reported to mediate distinct biological functions in vivo (Okuda et al., 1996; Speck and Gilliland, 2002; Ducy et al., 1997; Levanon et al., 2002; Li et al., 2002).”
• Role of p53 in Cell Death and Human Cancers (2011, background): “RUNX3 is one of Runt-related (RUNX) gene family members and has been considered to be a candidate tumor suppressor for human gastric cancer [123,124], however, it remains unclear how RUNX3 exerts its tumor suppressor function.”
• Differential requirements for Runx proteins in CD4 repression and epigenetic silencing during T lymphocyte development. (2002, background): “This observation suggests thatlethality (Komori et al., 1997; Li et al., 2002), we analyzed positive selection favors thymocytes with intact expres-T cells in Rag2 mutant host mice, deficient for mature sion of Runx1, and it is hence difficult to determine if thisT lymphocytes, that had been…”
• Disruption of differentiation in human cancer: AML shows the way (2003, background): “However, a recent study has implicated another AML1 family member, RUNX3, in gastric carcinoma”