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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. 3 — CAFs induce sorafenib resistance in HCC cells by secreting CXCL12. a The results of immunofluorescence showed that the expression of CXCL12 in CAFs in HCC tissues was significantly higher than that in paracancerous tissues (left). Statistical plot of fluorescence intensity of fibroblasts expressing α-SMA and CXCL12 in HCC tissues and paracancerous tissues (right). b ELISA showed that CAFs secreted higher level of CXCL12 than NFs. c, d Colony forming assays detected the sorafenib resistance of HCC cells (HepG2 and Huh7), after treated with the cellular supernatant of CAFs and NFs, sorafenib, and AMD3100. e, f Flow cytometry apoptosis assay detected the sorafenib resistance of HCC cells (HepG2 and Huh7), after treated with the cellular supernatant of CAFs and NFs, sorafenib, and AMD3100. g, h Western blotting was performed to detect the expression of β-actin, and Cleaved Caspase-3 in HCC cells (HepG2 and Huh7), which were treated with the cellular supernatant of CAFs, sorafenib, and AMD3100. The data presented mean ± SEM. *p < 0.01; **p < 0.001; ***p < 0.0001; ****p < 0.00001