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タイトル: | Id2 deletion attenuates Apc-deficient ileal tumor formation |
著者: | Biyajima, Kyoko Kakizaki, Fumihiko Shen, Xiaodong Mori, Kentaro Sugai, Manabu Taketo, M. Mark Yokota, Yoshifumi |
著者名の別形: | 柿崎, 文彦 菅井, 学 武藤, 誠 |
キーワード: | Apc C-Myc Id2 Ileal tumor initiation Mxd1 |
発行日: | 1-Jan-2015 |
出版者: | Company of Biologists Ltd |
誌名: | Biology Open |
巻: | 4 |
開始ページ: | 993 |
終了ページ: | 1001 |
抄録: | 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. |
著作権等: | © 2015. Published by The Company of Biologists Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution and reproduction in any medium provided that the original work is properly attributed. |
URI: | http://hdl.handle.net/2433/218587 |
DOI(出版社版): | 10.1242/bio.012252 |
PubMed ID: | 26163528 |
出現コレクション: | 学術雑誌掲載論文等 |
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