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Title 

Causal relationship between the loss of RUNX3 expression and gastric cancer

Authors 

Qing Lin LiKosei ItoChohei SakakuraHiroshi FukamachiKen-ichi InoueXin-Zi ChiChang Woo LeeSang Bae HanHwan Mook KimSuk Chul Bae

Publisher 

Elsevier (Cell Press)

Issue Date 

2002

Citation 

Cell, vol. 109, no. 1, pp. 113-124

Keywords 

cancer cell culturecancer growthcancer inhibitiongene expressionstomach cancergene expression regulation, neoplastic

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

Link 

http://dx.doi.org/10.1016/S0092-8674(02)00690-6

Appears in Collections

1. Journal Articles > Journal Articles

Registered Date

2017-04-19


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