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. 2020 Dec 15;40(6):1147–1161. doi: 10.1038/s41388-020-01593-5

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© The Author(s) 2020, corrected publication 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. 7 — A The cell proliferation ability of Ct-HBx was eliminated by the introduction of TXNIP in both MIHA and LO2 cells as indicated by XTT assay. B Overexpression of TXNIP abrogated the increased colony formation rate and size induced by Ct-HBx in both MIHA and LO2 cells. C Re-introduction of TXNIP induced the tumor growth arrest after subcutaneous injection of both LO2 and MIHA cells. D Schematic diagram demonstrating the oncogenic role and mechanism of Ct-HBx and TXNIP in HBV-related HCC. Basically, Ct-HBx downregulates the expression of TXNIP by transactivation through NFATC2. Downregulated TXNIP promotes hepatocarcinogenesis by inducing metabolic reprogramming to aerobic glycolysis in a mTORC1-dependent and independent manner.