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. 2022 Sep 16;41:275. doi: 10.1186/s13046-022-02475-2

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© The Author(s) 2022

Open AccessThis 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. 8 — The combination of defactinib with capmatinib is effective in reducing ETV1-mediated HCC metastasis (A) The levels of ETV1, p-PTK2 (Tyr397), PTK2, p-c-MET (Tyr1234/1235), c-MET in PLC/PRF/5-ETV1 cells processed with a single agent or the combination of defactinib and capmatinib. (B) HCC cell invasion and migration was evaluated by transwell assay. The combination treatment of defactinib and capmatinib showed the greatest inhibitory effect among all the groups. (C) Schematic diagram of treatment in nude mice of four groups. (Group1: Vehicle, Group2: Defactinib, Group3: Capmatinib, Group4: Defactinib combined with Capmatinib) (D-I) In vivo metastatic assay. (D) The representative BLI images in the liver were shown 9 weeks after implantation with indicated cells. (E) The bioluminescent signals were used to show the growth rate of liver tumors. (F)The number of metastatic lesions in the lung tissues. (G) The occurrence of lung metastasis. (H) The OS of different groups of nude mice. (I) Representative images of H&E staining of lung samples (indicated by arrowheads) from each group. * Represented p < 0.05. All data were displayed as Mean ± SD. (J) Diagram illustrating the mechanisms underlying how ETV1 promotes HCC metastasis and a potential combination strategy. ETV1 mediates HCC metastasis through increasing PTK2 and c-MET expression. HGF upregulates ETV1 expression via c-MET-ERK1/2-ELK1, creating a positive feedback loop that continuously stimulates HCC development. PTK2 inhibition in combination with c-MET inhibition markedly mitigates ETV1-mediated HCC metastasis