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. 2019 Mar 12;38:126. doi: 10.1186/s13046-019-1105-3

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© The Author(s). 2019

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. 6 — KLF12 transcriptionally regulates DVL2–β-catenin signaling in pancreatic cancer cells. a TCGA analysis showing that the expression correlation of KLF12 and DVL1,DVL2,DVL3 in the TCGA pancreatic cancer data set. b RT–qPCR analysis of the expression of DVL1,DVL2,DVL3 in the indicated cells c Bioinformatics analysis showing that the DVL2 promoter contains two putative KLF12 DNA-binding motifs . d Chromatin Immunoprecipitation assays indicated that KLF12 may bind to the promoter regions of DVL2.e RT–qPCR analysis of the expression of the established downstream targets for the Wnt/β-catenin pathway in the indicated cells. e The expression of Wnt-activated /suppressed gene and nuclear β-catenin in the indicated cells, as determined by western blotting