Phosphorylation of the gastric tumor suppressor RUNX3 following H. pylori infection results in its localization to the cytoplasm
- Authors
- Cinghu, Senthilkumar; Goh, Yun-Mi; Oh, Byung-Chul; Lee, You-Soub; Lee, Ok-Jun; Devaraj, Halagowder; Bae, Suk-Chul
- Issue Date
- Mar-2012
- Publisher
- WILEY-BLACKWELL
- Citation
- JOURNAL OF CELLULAR PHYSIOLOGY, v.227, no.3, pp.1071 - 1080
- Journal Title
- JOURNAL OF CELLULAR PHYSIOLOGY
- Volume
- 227
- Number
- 3
- Start Page
- 1071
- End Page
- 1080
- URI
- https://scholarworks.bwise.kr/gachon/handle/2020.sw.gachon/16525
- DOI
- 10.1002/jcp.22820
- ISSN
- 0021-9541
- Abstract
- As H. pylori infection progresses, intestinal metaplasia (IM), a key event in gastric carcinogenesis, develops in the stomach. The mechanism by which H. pylori infection causes the trans-differentiation of gastric cells to intestinal-type cells remains an important question. In the current study, we found that RUNX3 is deregulated in all human IM specimens examined by either down regulation or mislocalization; Aberrant localization of a gastric tumor suppressor RUNX3 is observed in most human cases of IM with concurrent H. pylori infection, and RUNX3 is down-regulated in most cases of IM without H. pylori-infection. The cytoplasmic mislocalization of a RUNX3 was associated with H. pylori-induced c-Src activation and RUNX tyrosine phosphorylation. Moreover, gastric epithelial cells of Runx3-/- mice expressed the intestinal markers Muc2 and Li-Cadherin, which suggests that the deregulation of Runx3 is a key event in the intestinalization of the gastric epithelium. Collectively, the results of the current study suggest that RUNX3 deregulation is associated with H. pylori-induced pathogenesis and the development of IM. J. Cell. Physiol. 227: 10711080, 2012. (C) 2011 Wiley Periodicals, Inc.
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