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. 2023 Oct 25;23:250. doi: 10.1186/s12935-023-03099-y

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© The Author(s) 2023

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 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. 4 — CSC production was stimulated by HBV. HBx promotes AFP synthesis to stimulate the normal reprogramming of liver cells, which is essential for developing HCC progenitor/stem cells. Among the several cell lines that originate from normal hepatocytes, PreS1 upregulates the expression of CD133, CD117, and CD90. PreS1 acts as a novel oncoprotein, vital in the establishment and maintenance of CSCs during HCC’s pathogenesis