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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. 2 — Compared with NFs, CAFs significantly promoted sorafenib resistance in HCC cells. a CAFs were isolated from HCC tissues. Meanwhile, paracancerous normal fibroblasts (NFs) were isolated from non-tumor tissues adjacent to HCC (upper). Statistical plot of fluorescence intensity of fibroblasts expressing α-SMA in HCC tissues and paracancerous tissues (below). b Colony forming assays of HCC cells (HepG2 and Huh7), which were treated with the cellular supernatant of CAFs and NFs, and sorafenib. c, d Cell viability assay: compared with NFs, CAFs significantly enhanced sorafenib resistance in HCC cells (HepG2 and Huh7). The data presented mean ± SEM. ***p < 0.0001; ****p < 0.00001