Please use this identifier to cite or link to this item: https://doi.org/10.1016/j.bbrc.2004.06.099
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dc.titleRunx3-/-gastric epithelial cells differentiate into intestinal type cells
dc.contributor.authorFukamachi, H.
dc.contributor.authorIto, K.
dc.contributor.authorIto, Y.
dc.date.accessioned2011-11-29T09:23:41Z
dc.date.available2011-11-29T09:23:41Z
dc.date.issued2004
dc.identifier.citationFukamachi, H., Ito, K., Ito, Y. (2004). Runx3-/-gastric epithelial cells differentiate into intestinal type cells. Biochemical and Biophysical Research Communications 321 (1) : 58-64. ScholarBank@NUS Repository. https://doi.org/10.1016/j.bbrc.2004.06.099
dc.identifier.issn0006291X
dc.identifier.urihttp://scholarbank.nus.edu.sg/handle/10635/29056
dc.description.abstractWe have previously reported that Runx3, a runt domain transcription factor, is a major growth regulator of gastric epithelial cells, that a lack of RUNX3 function is causally related to the genesis and progression of human gastric cancer, and that expression of RUNX3 is greatly reduced in intestinal metaplasias in human stomachs. Here we examined the differentiation of Runx3-/- mouse gastric epithelial cells and found that some cells differentiated into intestinal type cells, which expressed Cdx2, a transcription factor that has been shown to induce intestinal metaplasia in transgenic mice. Differentiation of intestinal type cells was not found in culture of Runx3 +/+ gastric epithelial cells. These results suggest that gastric epithelial cells can differentiate into intestinal type cells, probably due to expression of Cdx2 in them when the function of Runx3 is impaired. The relationship between loss of function of Runx3, formation of intestinal metaplasia, and gastric cancer was discussed. © 2004 Elsevier Inc.
dc.description.urihttp://libproxy1.nus.edu.sg/login?url=http://dx.doi.org/10.1016/j.bbrc.2004.06.099
dc.sourceScopus
dc.subjectCdx2
dc.subjectGastric cancer
dc.subjectIntestinal metaplasia
dc.subjectRunx3
dc.subjectTransdifferentiation
dc.typeArticle
dc.contributor.departmentNATIONAL UNIVERSITY MEDICAL INSTITUTES
dc.contributor.departmentMEDICINE
dc.description.doi10.1016/j.bbrc.2004.06.099
dc.description.sourcetitleBiochemical and Biophysical Research Communications
dc.description.volume321
dc.description.issue1
dc.description.page58-64
dc.description.codenBBRCA
dc.identifier.isiut000223032800010
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