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. 2018 Mar 22;37(26):3485–3500. doi: 10.1038/s41388-018-0161-z

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© The Author(s) 2018

Open Access This article is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License, which permits any non-commercial use, sharing, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, and provide a link to the Creative Commons license. You do not have permission under this license to share adapted material derived from this article or parts of it. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by-nc-nd/4.0/.

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Fig. 5 — CREPT regulated Wnt/β-catenin signaling pathway in CRC cells. a KEGG analysis based on RNA-sequencing data of HCT116 cells stably overexpressing CREPT or control cells. b Ectopic expression of CREPT in DLD-1 cell line enhanced TopFlash luciferase reporter activity but not FopFlash reporter (b1), while depletion of CREPT reduced dual-luciferase reporter assays in SW480 cells (b2). TopFlash, a classic Wnt-response luciferase reporter containing 3xTCF4 binding site. FopFlash, a negative reporter of which TCF4 binding site is mutant. c The mRNA expression of Wnt downstream targets CCND1, c-MYC, and AXIN2 were enhanced in the presence of CREPT in DLD-1 cells and HCT116 cells. d The mRNA expression of CCND1, c-MYC, and AXIN2 was diminished under CREPT knockdown in HT29 and SW480 cells. e The protein expression of β-catenin, c-MYC, CYCLIN D1, and AXIN2 was increased upon ectopic expression of CREPT in DLD1, HCT116 (e1), HCEC 1CT, and 2CT cells (e2), while decreased in CREPT knockdown HT29 and SW480 cells (e3).