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. 2020 Jul 24;11(7):573. doi: 10.1038/s41419-020-02749-7

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© The Author(s) 2020

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. 3 — a Timeline of the experiments in vivo; b waterfall plot of anlotinib response after treatment in six PDX models; c there were significant differences in tumor weights between the anlotinib treatment group and the control group (0.58 ± 0.08 vs. 0.10 ± 0.01, respectively); d tumor growth curves for each PDX case; e representative hematoxylin and eosin staining of tumor tissues from PDX models, with or without anlotinib treatment; f anlotinib treatment group had substantial decreases in proliferation (PCNA) rates and increases in apoptosis (TUNEL) index numbers, compared with the control group. The expression of E-cadherin was significantly downregulated, while the expression of N-cadherin was upregulated, based on the immunohistochemistry (IHC) assay after anlotinib treatment; g expression of p-VEGFR2, p-AKT, CDK1 in PDX tumors was detected using western blot assay. *P < 0.05; **P < 0.01; ***P < 0.001. Scale bars = 100 μm.