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. 2022 Nov 24;41:330. doi: 10.1186/s13046-022-02528-6

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© The Author(s) 2022

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. 2 — UBR7 inhibits HCC proliferation and tumorigenesis. A The clone formation sphere experiment analysed Huh-7 and HepG2 cells overexpressing or knocking out UBR7. B The overexpression or knockout of UBR7 cells constructs xenogeneic tumours subcutaneously in nude mice (left). Tumour volumes (mm³) (middle) and the weight (right) of mouse xenografts implanted with HepG2 cells. C The liver morphology of UBR7^WT (WT) and Alb-Cre;UBR7^fl/fl mice. D Survival analysis of UBR7^WT (n = 24) and Alb-Cre;UBR7^fl/fl mice (n = 19). E Representative H&E staining images for sections of livers in UBR7^WT and Alb-Cre;UBR7^fl/fl mice. F Quantification of tumour area (%), number, maximal size (mm) (left), and Ki67 positive cells (%) (right) in UBR7^WT and Alb-Cre;UBR7^fl/fl mice. Data are shown as mean ± SD of three independent experiments. *p < 0.05, **p < 0.01, ***p < 0.01. The scale bar in A and E was 100 μm