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. 2018 Jun 4;9(6):675. doi: 10.1038/s41419-018-0591-0

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© The Author(s) 2018

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as 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 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/4.0/.

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Fig. 5 — a GSEA analysis of the correlation between DDX39 levels and Wnt3A target gene signatures using TCGA data. b TOP/FOP luciferase activity assay revealed DDX39 overexpression activated Wnt/β-catenin pathway. DDX39 knockdown inhibited Wnt/β-catenin pathway. c Western blot analysis of β-catenin levels in nucleus of HCC cells with DDX39 overexpression or knockdown, EF-1α was used as the loading control. d qRT-PCR analyzed the expression of Wnt/β-catenin target genes like MYC, CD44, RUNX2, SNAIL1, and CCND1 in HCC cells with DDX39 overexpression or knockdown. Data are shown as means ± SD. *p < 0.05