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. 2020 Apr 8;11(4):225. doi: 10.1038/s41419-020-2422-3

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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. 7 — A Overexpression of ZNF703 in SMMC7721 decreased their sensitivity to sorafenib treatment, whereas depletion of ZNF703 in HCCLM3 cells increased their sensitivity to sorafenib treatment, which be rescued by ZNF703 overexpression. B The influence of silencing ZNF703 or treatment with sorafenib on the effects of colony formation in HCCLM3 cell. C The HCCLM3-shZNF703 or corresponding control cells were subcutaneously inoculated into nude mice. After subcutaneous inoculation, mice were given sorafenib (2 mg/kg) per 2 days. Then, 4 weeks after giving sorafenib, mice were harvested and xerographs were collected. Comparison of tumor weights and tumor volumes for each groups (n = 6). D Expression of ZNF703, CLDN4 and Ki67 was evaluated by immunohistochemistry in xenografts derived from HCC cells. Scale bars: 75 μm. Data are presented as mean±S.D for three independent experiments. *P < 0.05.