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. 2019 Aug 20;10(9):630. doi: 10.1038/s41419-019-1733-8

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© The Author(s) 2019

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. 4 — a Molecular docking scores for PPD and six potential targets. b Predicted model of PPD binding to the SH2 domain of STAT3 as shown by computational docking. The protein backbone is portrayed as a transparent green ribbon, and PPD is depicted as atom-red sticks-and-balls. c Biacore analysis results of PPD and STAT3. d, e PPD inhibited the translocation of STAT3 to the nucleus in PLC/PRF/5 cells detected by immunofluorescence and Western blot. f, g Effect of PPD on the migration and invasion of STAT3 knockdown PLC/PRF/5 and HepG2 cells. h Dual-luciferase assay results for PLC/PRF/5 and HepG2 cells suggest that Twist1 is a target gene of PPD. i Protein expression level changes of Twist1, E-cadherin, and vimentin in the PLC/PRF/5 and HepG2 cells treated with PPD. The GAPDH blot served as a loading control