Journal Article

Further upregulation of β-catenin/Tcf transcription is involved in the development of macroscopic tumors in the colon of <i>Apc</i><sup>Min/+</sup> mice

Takeru Oyama, Yasuhiro Yamada, Kazuya Hata, Hiroyuki Tomita, Akihiro Hirata, HongQiang Sheng, Akira Hara, Hitomi Aoki, Takahiro Kunisada, Satoshi Yamashita and Hideki Mori

in Carcinogenesis

Volume 29, issue 3, pages 666-672
Published in print March 2008 | ISSN: 0143-3334
Published online January 2008 | e-ISSN: 1460-2180 | DOI: http://dx.doi.org/10.1093/carcin/bgn001
Further upregulation of β-catenin/Tcf transcription is involved in the development of macroscopic tumors in the colon of ApcMin/+ mice

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ApcMin/+ mouse, a mouse model for human familial adenomatosis polyposis, contains a truncating mutation in the Apc gene and spontaneously develops intestinal tumors. Our previous study revealed two distinct stages of tumorigenesis in the colon of ApcMin/+ mouse: microadenomas and macroscopic tumors. Microadenomas already have lost their remaining allele of the Apc and all microadenomas show accumulation of β-catenin, indicating that activation of the canonical Wnt pathway is an initiating event in the tumorigenesis. This study shows that expression of nuclear β-catenin in macroscopic tumors is further upregulated in comparison with that in microadenomas. Furthermore, transcriptional activity of β-catenin/T-cell factor (Tcf) signaling, assessed using β-catenin/Tcf reporter transgenic mice, is higher in the macroscopic tumors than that in microadenomas. In addition, the expression level of Dickkopf-1, which is known to be a negative modifier of the canonical Wnt pathway, was reduced only in colon tumors. These results suggest that activation of β-catenin/Tcf transcription plays a role not only in the initiation stage but also in the promotion stage of colon carcinogenesis in ApcMin/+ mice.

Journal Article.  4560 words.  Illustrated.

Subjects: Clinical Cytogenetics and Molecular Genetics

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