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. 2023 Dec 6;23:1198. doi: 10.1186/s12885-023-11613-8

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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. 5 — CAFs enhance sorafenib resistance of HCC cells through CXCL12 in vivo. a Representative images of tumors in mice of CAFs + AMD3100 group, CAFs group, and NFs group after different treatments. b The tumor volume in different treatment groups. c The tumor proliferation trend in different treatment groups. d Pathological validation of tumors under a microscope (40X), after H&E staining and Immunohistochemistry in tumor tissues. The immunohistochemistry staining to detect the expression of Cleaved Caspase-3 in different treatment groups from the tumor tissues of mice. e The expression level of Cleaved Caspase-3 in different treatment groups from the tumors of mice. The data presented mean ± SEM. **p < 0.001; ***p < 0.0001; ****p < 0.00001