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. 2019 Feb 15;120(5):512–521. doi: 10.1038/s41416-018-0373-6

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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. 4 — Axl modulates the motility and invasive capacity of immortalised hepatocellular carcinoma (HCC) cells and determines sensitivity to sorafenib in immortalised cell lines and in patients with HCC. a, b Inhibitory effect of shRNA-mediated Axl silencing on SKHep-1 and SKHep-1SR cell motility and invasion capacity. c Inhibitory effect of R428 on SKHep-1 and SKHep-1SR cell motility and invasion. d, e Wound healing assays confirming shRNA and R428-mediated repression of cell motility secondary to Axl inhibition. f Inhibition of Axl by shRNA augments the sensitivity of SKHep-1 and SKHep-1SR cells to sorafenib. g Incremental effect of R428 on sorafenib-induced apoptosis of SKHep-1 cells as measured by Caspase 3/7 activation ratios against controls. h The relationship between pre-sorafenib serum sAxl levels and cause of treatment discontinuation in patients receiving sorafenib for HCC (n = 40). i Patients with elevated sAxl levels had significantly shorter duration of sorafenib therapy with earlier discontinuation compared to patients with lower sAxl levels at baseline. j Kaplan–Meier curves showing the effect of high baseline sAxl levels in predicting for worse overall survival in patients with HCC undergoing sorafenib therapy