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Title: Id2 deletion attenuates Apc-deficient ileal tumor formation
Authors: Biyajima, Kyoko
Kakizaki, Fumihiko  kyouindb  KAKEN_id
Shen, Xiaodong
Mori, Kentaro
Sugai, Manabu
Taketo, M. Mark
Yokota, Yoshifumi
Author's alias: 柿崎, 文彦
菅井, 学
武藤, 誠
Keywords: Apc
Ileal tumor initiation
Issue Date: 1-Jan-2015
Publisher: Company of Biologists Ltd
Journal title: Biology Open
Volume: 4
Start page: 993
End page: 1001
Abstract: The expression level of inhibitor of DNA binding 2 (Id2) is increased in colorectal carcinomas and is positively correlated with poor prognosis. However, the functional significance of Id2 in intestinal tumorigenesis has not been fully defined using genetic approaches. Here, we show that Id2 promotes ileal tumor initiation in Apc-deficient mice. Expression of Id2 was stimulated by Wnt signaling through the enhancer region of the Id2 promoter at the early stage of tumorigenesis in Apc+/Δ716 (ApcΔ716 ) mice. Genetic depletion of Id2 in ApcΔ716 mice caused ?80% reduction in the number of ileal polyps, but had little effect on tumor size. Notably, the lack of Id2 increased the number of apoptotic cells in the normal crypt epithelium of the mice. Furthermore, DNA microarray analysis revealed that the expression level of Max dimerization protein 1 (Mxd1), known as a c-Myc antagonist, was specifically increased by Id2 deletion in the ileal intestinal epithelium of ApcΔ716 mice. In contrast, the protein level of c-Myc, but not the mRNA level, was decreased by loss of Id2 in these mice. These results indicate that loss of Id2 inhibits tumor initiation by up-regulation of Mxd1 and down-regulation of c-Myc in ApcΔ716 mice.
Rights: © 2015. Published by The Company of Biologists Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (, which permits unrestricted use, distribution and reproduction in any medium provided that the original work is properly attributed.
DOI(Published Version): 10.1242/bio.012252
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