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. 2021 Jul 16;10(7):52. doi: 10.1038/s41389-021-00338-7

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© The Author(s) 2021

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. 6 — a–c Xenotransplanted HCC is re-sensitized to Sorafenib treatment upon depletion of USP29. Sorafenib-resistant SNU398 cells expressing either a control shRNA (shLuc) or a shRNA against USP29 (shUSP29) were implanted into the flanks of immunodeficient NSG mice and treated with vehicle solution or Sorafenib, respectively. Tumor growth curves over time (a) and tumor weights at the time of sacrifice (b) were determined, N = 4. Images of the tumors at the time of sacrifice are shown in (c). ns not significant; **P < 0.01; ***P < 0.001; Two-way ANOVA. d, e USP29-deficient tumors exhibit higher rates of apoptosis upon Sorafenib treatment. Histological sections of the tumors described in (a–c) were immunostained for USP29 and HIF1α (d). Immunostaining for cleaved Caspase 3 was used to quantify apoptosis (d, e). f Sorafenib-resistant PDX tumors present high USP29, HIF1α, and GLUT1 protein levels. Tumor pieces of HCC patient-derived xenotransplanted (PDX) mice which have been previously classified as Sorafenib-responsive or Sorafenib-resistant were analyzed by immunoblotting for the expression of HIF1α, USP29, and GLUT1. Immunoblotting for β-Tubulin was used as loading control. Results represent three independent experiments.