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. 2018 Mar 1;8:3891. doi: 10.1038/s41598-018-22113-2

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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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Bufalin blocks HCC cell proliferation and transformation through CCRK-mediated β-catenin/TCF signaling. (A) CCRK knockdown attenuated the effect of bufalin on suppressing cell proliferation. Stably CCRK-depriving PLC5 cells or parental cells were treated with indicated concentrations of bufalin or vehicle. Cell growths were detected using CCK-8 assay. Inhibitory rates were plotted as the percentage of viable cells treated with vehicle. (B) CCRK expression promoted bufalin-induced cell suppression. Stable CCRK-expressing LO2 cells or parental cells were treated with indicated concentrations of bufalin or vehicle followed by the detection of cell growths in CCK-8 assay. (C and D) Bufalin abrogated CCRK-induced anchorage-dependent (C) or -independent cell growth (D) detected by colony formation or soft agar assays, respectively. Representative images of colonies formed are shown. Original magnification ×100. (E) Bufalin impeded CCRK-induced G1/S cell cycle progression. (F) Bufalin suppressed CCRK-induced β-catenin/TCF signaling activity. Protein expressions of CCRK, active and total β-catenin, CCND1, EGFR and PCNA were detected and β-actin was used as a loading control. **P < 0.01; ***P < 0.001.