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. 2018 Feb 27;10:26. doi: 10.1186/s13148-018-0459-2

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© The Author(s). 2018

Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

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Fig. 8 — Proposed models how DACT2 affects the β-catenin/Cdc25c pathway in nasopharyngeal carcinoma. When β-catenin/LEF1 complex is activated, it promotes the development of nasopharyngeal carcinoma by targeting its downstream genes including Cdc25c, which plays a crucial role in regulating cell cycle G2/M stage. DACT2 inhibits the activity of β-catenin/LEF1 complex by competitively binding to β-catenin and downregulates the expression of Cdc25c and its downstream genes, which can suppress nasopharyngeal carcinoma growth