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. 2021 May 5;11:9587. doi: 10.1038/s41598-021-88983-1

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© The Author(s) 2021

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/.

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Resminostat in combination with the MKi sorafenib or regorafenib reversed platelet-induced cellular invasion of HCC cells. (A) Schematic presentation of the kinase inhibitor profile of sorafenib, regorafenib, lenvatinib and crizotinib. (B) EC50 values for the anti-proliferative activities of kinase inhibitors sorafenib, regorafenib, crizotinib and lenvatinib in PLC/PRF/5 and SNU-475 cells. The data are presented as mean ± SD (n = 3). (C) Invasion assay of PLC/PRF/5 with platelets. Resminostat in combination with several kinase inhibitors; sorafenib, regorafenib, lenvatinib and crizotinib. A representative experiment is shown. (D) Model: Inhibition of platelet-mediated cancer-promoting effects by the drug combination of resminostat and the MKi sorafenib or regorafenib.