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. 2019 Jan 17;10(2):43. doi: 10.1038/s41419-018-1282-6

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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. 7 — Hep3B cells were treated by knocking down TP and/or adding TP enzyme inhibitor tipiracil (TPI). a TPI exhibited good binding activity to TP determined by molecular docking. b Wound healing assay was performed. Quantitative analysis showed a significant difference in the speed of migration among different treated Hep3B cells. c Invasion assay showed a significant difference in the speed of invasion among different treated Hep3B cells. d Knocking down TP and/or adding TPI inhibited tube formation as detected by three-dimensional culture assay. e Effects of knocking down TP and/or adding TPI on Hep3B xenograft tumor growth. f Number of tumor formations and lung metastasis in different groups. Images were taken at ×100 magnification. g Statistical analysis of VM formation in different treated Hep3B xenograft tumors. h Statistical analysis of VE–Cad, vascular endothelial growth factor receptor 1 (VEGFR1), and VEGFR2 expression levels in different treated Hep3B xenograft tumors. i Proposed regulatory mechanism between Twist1–TP and VM in HCC. (mean ± SD; **P < 0.01)