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. 2020 May 26;20:196. doi: 10.1186/s12935-020-01265-0

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© The Author(s) 2020

Open AccessThis 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 licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence 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 licence, visit http://creativecommons.org/licenses/by/4.0/. 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 in a credit line to the data.

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Fig. 6 — FOXC2 facilitates in vivo and in vitro proliferation of HCC through Ang-2. a Representative images of NOD/SCID mice injected with FOXC2 OE and FOXC2 OE Ang-2 KD Huh-7 cells at day7, 9, 11 and 13. b Quantification analysis of bioluminescent signal of tumor-bearing mice injected with FOXC2 OE or FOXC2 OE Ang-2 KD Huh-7 cells at specified time points. Ang-2 downregulation impeded proliferation of FOXC2 OE Huh-7 cells c Tumor volume of FOXC2 OE Huh-7 cells were decreased with Ang-2 downregulation. d Tumor weight of FOXC2 OE Huh-7 cells were lightened with Ang-2 knockdown. e Ang-2 and FOXC2 expression in FOXC2 OE and FOXC2 OE Ang-2 KD tumors were analyzed through western blot. Values are presented as mean ± SEM. Significance at p < 0.01 is denoted by ‘*’ relative to control by one-way ANOVA