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. 2019 May 27;121(1):22–33. doi: 10.1038/s41416-019-0482-x

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© The Author(s) 2019

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. 5 — M2 macrophages confer sorafenib resistance by activation of ERK/MAPK and PI3K/AKT pathways through HGF/c-Met signalling. a Treatment with sorafenib, M2-CM, HGF or anti-HGF antibody (aHGF) alone or combination affects the expression and phosphorylation of c-Met, ERK and AKT kinases in SMMC-7721 cells as measured by Western blots. GAPDH is a protein loading control. b Treatment with sorafenib, M2-CM, HGF or anti-HGF antibody (aHGF) alone or combination affects the expression and phosphorylation of c-Met, ERK, and AKT kinases in Hep3B cells as measured by Western blots. GAPDH is a protein loading control